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Carbohydrate metabolism and blood sugar levels

Carbohydrate metabolism and blood sugar levels

Eventually, however, Healthy sugar substitutes for smoothies beta metabolsim begin to fail. The EarlyBird study is a Understanding your metabolic rate, prospective cohort skgar, that recruited healthy UK children at age 5, and followed them annually throughout childhood for 12 years. Classification and diagnosis of diabetes: Standards in medical care in diabetes — GrossbardL.

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Where Crbohydrate have been noted, attention will be drawn to them. These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in via an institution.

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HansonR. HersH. Acta 37 HoltP. HommesF. JamdarS. JamesE. JohnsonJ. Its biology and history Adv. JostA. KatzJ. LardyH. LeaM. McCannM. MercierC. MiddletonM. MonteleoneJ. Studies of a kindred, Amer.

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: Carbohydrate metabolism and blood sugar levels

Carbohydrate metabolism

For individuals with diabetes in the fasting state, plasma glucose is derived from glycogenolysis and gluconeogenesis 1 under the direction of glucagon 2. Exogenous insulin 3 influences the rate of peripheral glucose disappearance 4 and, because of its deficiency in the portal circulation, does not properly regulate the degree to which hepatic gluconeogenesis and glycogenolysis occur 5.

For individuals with diabetes in the fed state, exogenous insulin 1 is ineffective in suppressing glucagon secretion through the physiological paracrine route 2 , resulting in elevated hepatic glucose production 3.

As a result, the appearance of glucose in the circulation exceeds the rate of glucose disappearance 4. The net effect is postprandial hyperglycemia 5.

Glucoregulatory hormones include insulin, glucagon, amylin, GLP-1,glucose-dependent insulinotropic peptide GIP , epinephrine, cortisol, and growth hormone. Of these, insulin and amylin are derived from theβ-cells, glucagon from the α-cells of the pancreas, and GLP-1 and GIP from the L-cells of the intestine.

The glucoregulatory hormones of the body are designed to maintain circulating glucose concentrations in a relatively narrow range. In the fasting state, glucose leaves the circulation at a constant rate. To keep pace with glucose disappearance, endogenous glucose production is necessary. For all practical purposes, the sole source of endogenous glucose production is the liver.

Renal gluconeogenesis contributes substantially to the systemic glucose pool only during periods of extreme starvation. Although most tissues have the ability to hydrolyze glycogen, only the liver and kidneys contain glucosephosphatase, the enzyme necessary for the release of glucose into the circulation.

In the bi-hormonal model of glucose homeostasis, insulin is the key regulatory hormone of glucose disappearance, and glucagon is a major regulator of glucose appearance. After reaching a post-meal peak, blood glucose slowly decreases during the next several hours, eventually returning to fasting levels.

In the immediate post-feeding state, glucose removal into skeletal muscle and adipose tissue is driven mainly by insulin. At the same time, endogenous glucose production is suppressed by 1 the direct action of insulin, delivered via the portal vein, on the liver, and 2 the paracrine effect or direct communication within the pancreas between the α- andβ-cells, which results in glucagon suppression Figure 1B.

Until recently, insulin was the only pancreatic β-cell hormone known to lower blood glucose concentrations. Insulin, a small protein composed of two polypeptide chains containing 51 amino acids, is a key anabolic hormone that is secreted in response to increased blood glucose and amino acids following ingestion of a meal.

Like many hormones, insulin exerts its actions through binding to specific receptors present on many cells of the body,including fat, liver, and muscle cells. The primary action of insulin is to stimulate glucose disappearance.

Insulin helps control postprandial glucose in three ways. Initially,insulin signals the cells of insulin-sensitive peripheral tissues, primarily skeletal muscle, to increase their uptake of glucose. Finally, insulin simultaneously inhibits glucagon secretion from pancreatic α-cells, thus signalling the liver to stop producing glucose via glycogenolysis and gluconeogenesis Table 1.

All of these actions reduce blood glucose. Insulin action is carefully regulated in response to circulating glucose concentrations.

Long-term release of insulin occurs if glucose concentrations remain high. While glucose is the most potent stimulus of insulin, other factors stimulate insulin secretion. These additional stimuli include increased plasma concentrations of some amino acids, especially arginine, leucine, and lysine;GLP-1 and GIP released from the gut following a meal; and parasympathetic stimulation via the vagus nerve.

Isolated from pancreatic amyloid deposits in the islets of Langerhans,amylin was first reported in the literature in Amylin, a 37—amino acid peptide, is a neuroendocrine hormone coexpressed and cosecreted with insulin by pancreatic β-cells in response to nutrient stimuli.

Studies in humans have demonstrated that the secretory and plasma concentration profiles of insulin and amylin are similar with low fasting concentrations and increases in response to nutrient intake. In subjects with diabetes,amylin is deficient in type 1 and impaired in type 2 diabetes.

Preclinical findings indicate that amylin works with insulin to help coordinate the rate of glucose appearance and disappearance in the circulation, thereby preventing an abnormal rise in glucose concentrations Figure 2.

Postprandial glucose flux in nondiabetic controls. Postprandial glucose flux is a balance between glucose appearance in the circulation and glucose disappearance or uptake.

Glucose appearance is a function of hepatic endogenous glucose production and meal-derived sources and is regulated by pancreatic and gut hormones. Glucose disappearance is insulin mediated. Calculated from data in the study by Pehling et al. Amylin complements the effects of insulin on circulating glucose concentrations via two main mechanisms Figure 3.

Amylin suppresses post-prandial glucagon secretion, 27 thereby decreasing glucagon-stimulated hepatic glucose output following nutrient ingestion. This suppression of post-prandial glucagon secretion is postulated to be centrally mediated via efferent vagal signals.

Importantly,amylin does not suppress glucagon secretion during insulin-induced hypoglycemia. Glucose homeostasis: roles of insulin, glucagon, amylin, and GLP The multi-hormonal model of glucose homeostasis nondiabetic individuals : in the fed state, amylin communicates through neural pathways 1 to suppress postprandial glucagon secretion 2 while helping to slow the rate of gastric emptying 3.

These actions regulate the rate of glucose appearance in the circulation 4. In addition, incretin hormones, such as GLP-1, glucose-dependently enhance insulin secretion 6 and suppress glucagon secretion 2 and, via neural pathways, help slow gastric emptying and reduce food intake and body weight 5.

Amylin exerts its actions primarily through the central nervous system. Animal studies have identified specific calcitonin-like receptor sites for amylin in regions of the brain, predominantly in the area postrema.

The area postrema is a part of the dorsal vagal complex of the brain stem. A notable feature of the area postrema is that it lacks a blood-brain barrier, allowing exposure to rapid changes in plasma glucose concentrations as well as circulating peptides, including amylin.

In summary, amylin works to regulate the rate of glucose appearance from both endogenous liver-derived and exogenous meal-derived sources, and insulin regulates the rate of glucose disappearance. Glucagon is a key catabolic hormone consisting of 29 amino acids.

It is secreted from pancreatic α-cells. Described by Roger Unger in the s,glucagon was characterized as opposing the effects of insulin. He further speculated that a therapy targeting the correction of glucagon excess would offer an important advancement in the treatment of diabetes.

Hepatic glucose production, which is primarily regulated by glucagon,maintains basal blood glucose concentrations within a normal range during the fasting state.

When plasma glucose falls below the normal range, glucagon secretion increases, resulting in hepatic glucose production and return of plasma glucose to the normal range. When coupled with insulin's direct effect on the liver, glucagon suppression results in a near-total suppression of hepatic glucose output Figure 4.

Insulin and glucagon secretion: nondiabetic and diabetic subjects. In nondiabetic subjects left panel , glucose-stimulated insulin and amylin release from the β -cells results in suppression of postprandial glucagon secretion. In a subject with type 1 diabetes, infused insulin does not suppress α -cell production of glucagon.

Adapted from Ref. EF38 In the diabetic state, there is inadequate suppression of postprandial glucagon secretion hyperglucagonemia 41 , 42 resulting in elevated hepatic glucose production Figure 4. Importantly,exogenously administered insulin is unable both to restore normal postprandial insulin concentrations in the portal vein and to suppress glucagon secretion through a paracrine effect.

This results in an abnormally high glucagon-to-insulin ratio that favors the release of hepatic glucose. The intricacies of glucose homeostasis become clearer when considering the role of gut peptides. By the late s, Perley and Kipnis 44 and others demonstrated that ingested food caused a more potent release of insulin than glucose infused intravenously.

Additionally, these hormonal signals from the proximal gut seemed to help regulate gastric emptying and gut motility. Several incretin hormones have been characterized, and the dominant ones for glucose homeostasis are GIP and GLP GIP stimulates insulin secretion and regulates fat metabolism, but does not inhibit glucagon secretion or gastric emptying.

GLP-1 also stimulates glucose-dependent insulin secretion but is significantly reduced postprandially in people with type 2 diabetes or impaired glucose tolerance. Derived from the proglucagon molecule in the intestine, GLP-1 is synthesized and secreted by the L-cells found mainly in the ileum and colon.

Circulating GLP-1 concentrations are low in the fasting state. However, both GIP and GLP-1 are effectively stimulated by ingestion of a mixed meal or meals enriched with fats and carbohydrates. GLP-1 has many glucoregulatory effects Table 1 and Figure 3.

In the pancreas,GLP-1 stimulates insulin secretion in a glucose-dependent manner while inhibiting glucagon secretion. Infusion of GLP-1 lowers postprandial glucose as well as overnight fasting blood glucose concentrations.

Yet while GLP-1 inhibits glucagon secretion in the fed state, it does not appear to blunt glucagon's response to hypoglycemia. Administration of GLP-1 has been associated with the regulation of feeding behavior and body weight. Of significant and increasing interest is the role GLP-1 may have in preservation of β-cell function and β-cell proliferation.

Our understanding of the pathophysiology of diabetes is evolving. Type 1 diabetes has been characterized as an autoimmune-mediated destruction of pancreaticβ-cells. Early in the course of type 2 diabetes, postprandial β-cell action becomes abnormal, as evidenced by the loss of immediate insulin response to a meal.

Abnormal gastric emptying is common to both type 1 and type 2 diabetes. The rate of gastric emptying is a key determinant of postprandial glucose concentrations Figure 5.

In individuals with diabetes, the absent or delayed secretion of insulin further exacerbates postprandial hyperglycemia. Both amylin and GLP-1 regulate gastric emptying by slowing the delivery of nutrients from the stomach to the small intestine.

Gastric emptying rate is an important determinant of postprandial glycemia. Abstract Classifying the glycemic responses of carbohydrate foods using the glycemic index GI requires standardized methodology for valid results.

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More from Oxford Academic. Allied Health Professions. Dietetics and Nutrition. Medicine and Health. So, the question can be raised as to why the body would create something it has just spent a fair amount of effort to break down?

Certain key organs, including the brain, can use only glucose as an energy source; therefore, it is essential that the body maintain a minimum blood glucose concentration.

When the blood glucose concentration falls below that certain point, new glucose is synthesized by the liver to raise the blood concentration to normal. Gluconeogenesis is not simply the reverse of glycolysis. There are some important differences Figure 7. Pyruvate is a common starting material for gluconeogenesis.

First, the pyruvate is converted into oxaloacetate. Oxaloacetate then serves as a substrate for the enzyme phosphoenolpyruvate carboxykinase PEPCK , which transforms oxaloacetate into phosphoenolpyruvate PEP. From this step, gluconeogenesis is nearly the reverse of glycolysis.

PEP is converted back into 2-phosphoglycerate, which is converted into 3-phosphoglycerate. Then, 3-phosphoglycerate is converted into 1,3 bisphosphoglycerate and then into glyceraldehydephosphate.

Two molecules of glyceraldehydephosphate then combine to form fructosebisphosphate, which is converted into fructose 6-phosphate and then into glucosephosphate. Finally, a series of reactions generates glucose itself.

In gluconeogenesis as compared to glycolysis , the enzyme hexokinase is replaced by glucosephosphatase, and the enzyme phosphofructokinase-1 is replaced by fructose-1,6-bisphosphatase. This helps the cell to regulate glycolysis and gluconeogenesis independently of each other.

As will be discussed as part of lipolysis, fats can be broken down into glycerol, which can be phosphorylated to form dihydroxyacetone phosphate or DHAP. DHAP can either enter the glycolytic pathway or be used by the liver as a substrate for gluconeogenesis.

Figure 7. Gluconeogenesis is the synthesis of glucose from pyruvate, lactate, glycerol, alanine, or glutamate. Changes in body composition, including reduced lean muscle mass, are mostly responsible for this decrease.

The most dramatic loss of muscle mass, and consequential decline in metabolic rate, occurs between 50 and 70 years of age. Loss of muscle mass is the equivalent of reduced strength, which tends to inhibit seniors from engaging in sufficient physical activity.

This results in a positive-feedback system where the reduced physical activity leads to even more muscle loss, further reducing metabolism. There are several things that can be done to help prevent general declines in metabolism and to fight back against the cyclic nature of these declines.

These include eating breakfast, eating small meals frequently, consuming plenty of lean protein, drinking water to remain hydrated, exercising including strength training , and getting enough sleep. These measures can help keep energy levels from dropping and curb the urge for increased calorie consumption from excessive snacking.

While these strategies are not guaranteed to maintain metabolism, they do help prevent muscle loss and may increase energy levels. Some experts also suggest avoiding sugar, which can lead to excess fat storage. Spicy foods and green tea might also be beneficial.

Because stress activates cortisol release, and cortisol slows metabolism, avoiding stress, or at least practicing relaxation techniques, can also help. Metabolic enzymes catalyze catabolic reactions that break down carbohydrates contained in food. The energy released is used to power the cells and systems that make up your body.

Excess or unutilized energy is stored as fat or glycogen for later use. Carbohydrate metabolism begins in the mouth, where the enzyme salivary amylase begins to break down complex sugars into monosaccharides. These can then be transported across the intestinal membrane into the bloodstream and then to body tissues.

In the cells, glucose, a six-carbon sugar, is processed through a sequence of reactions into smaller sugars, and the energy stored inside the molecule is released. The first step of carbohydrate catabolism is glycolysis, which produces pyruvate, NADH, and ATP.

Under anaerobic conditions, the pyruvate can be converted into lactate to keep glycolysis working. Under aerobic conditions, pyruvate enters the Krebs cycle, also called the citric acid cycle or tricarboxylic acid cycle. In addition to ATP, the Krebs cycle produces high-energy FADH 2 and NADH molecules, which provide electrons to the oxidative phosphorylation process that generates more high-energy ATP molecules.

For each molecule of glucose that is processed in glycolysis, a net of 36 ATPs can be created by aerobic respiration. Under anaerobic conditions, ATP production is limited to those generated by glycolysis.

While a total of four ATPs are produced by glycolysis, two are needed to begin glycolysis, so there is a net yield of two ATP molecules. In conditions of low glucose, such as fasting, starvation, or low carbohydrate diets, glucose can be synthesized from lactate, pyruvate, glycerol, alanine, or glutamate.

This process, called gluconeogenesis, is almost the reverse of glycolysis and serves to create glucose molecules for glucose-dependent organs, such as the brain, when glucose levels fall below normal. salivary amylase: digestive enzyme that is found in the saliva and begins the digestion of carbohydrates in the mouth.

cellular respiration: production of ATP from glucose oxidation via glycolysis, the Krebs cycle, and oxidative phosphorylation.

glycolysis: series of metabolic reactions that breaks down glucose into pyruvate and produces ATP. pyruvate: three-carbon end product of glycolysis and starting material that is converted into acetyl CoA that enters the. Krebs cycle: also called the citric acid cycle or the tricarboxylic acid cycle, converts pyruvate into CO 2 and high-energy FADH 2 , NADH, and ATP molecules.

citric acid cycle or tricarboxylic acid cycle TCA : also called the Krebs cycle or the tricarboxylic acid cycle; converts pyruvate into CO 2 and high-energy FADH 2 , NADH, and ATP molecules.

energy-consuming phase , first phase of glycolysis, in which two molecules of ATP are necessary to start the reaction. glucosephosphate: phosphorylated glucose produced in the first step of glycolysis.

Hexokinase: cellular enzyme, found in most tissues, that converts glucose into glucosephosphate upon uptake into the cell. Glucokinase: cellularenzyme, found in the liver, which converts glucose into glucosephosphate upon uptake into the cell.

energy-yielding phase: second phase of glycolysis, during which energy is produced. terminal electron acceptor: ATP production pathway in which electrons are passed through a series of oxidation-reduction reactions that forms water and produces a proton gradient. electron transport chain ETC : ATP production pathway in which electrons are passed through a series of oxidation-reduction reactions that forms water and produces a proton gradient.

oxidative phosphorylation: process that converts high-energy NADH and FADH 2 into ATP. Skip to main content. Module 8: Metabolism and Nutrition. Search for:. Carbohydrate Metabolism Learning Objectives By the end of this section, you will be able to: Explain the processes of glycolysis Describe the pathway of a pyruvate molecule through the Krebs cycle Explain the transport of electrons through the electron transport chain Describe the process of ATP production through oxidative phosphorylation Summarize the process of gluconeogenesis.

Watch this video to learn about glycolysis:. Watch this animation to observe the Krebs cycle.

Carbohydrate Metabolism and the Regulation of Blood Glucose | SpringerLink Low-carbohydrate-diet score and the risk of Diabetic retinopathy retinal imaging Carbohydrate metabolism and blood sugar levels disease in women. Similar articles in PubMed. The first step is Carbohydrate metabolism and blood sugar levels phosphorylation Carbojydrate fructose Cqrbohydrate fructose 1-phosphate by fructokinase. In the liver, Carbohdyrate 6-phosphate can be converted to glucose, whereas, in other tissues, it is metabolized through glycolysis. Which carbohydrates you choose to consume, how they are packaged in your diet, and how your body metabolizes carbohydrates will all affect metabolism and the combination of glucose, fats, or proteins your body burns for energy. CrossRef Medline Web of Science Google Scholar. The authors have no other dualities of interest to declare.
Carbohydrate Metabolism and the Regulation of Blood Glucose This Healthy sugar substitutes for smoothies recent znd led to a view of glucose homeostasis involving Intermittent fasting results pancreatic hormones. Lrvels you think this message was received Nut-free diet options error, please contact an administrator. Carbohyrate additional stimuli include increased plasma concentrations of some amino acids, especially arginine, leucine, and lysine;GLP-1 and GIP released from the gut following a meal; and parasympathetic stimulation via the vagus nerve. Knowing what the optimal number of calories you need and in what combination of fat, protein, and carbohydrates is the million-dollar question. Diabetes Care ; 28, Suppl 1: S72—9.
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Reducing glycemic responses by reducing carbohydrate intake increases postprandial serum free-fatty acids FFA and does not improve overall glycemic control in diabetic subjects. By contrast, low-GI diets reduce serum FFA and improve glycemic control.

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For technical feasibility and to ensure optimal data reproducibility for cohort analysis, a threshold of 1, blood serum samples e.

Metabolic profiling was carried out by means of proton nuclear magnetic resonance spectroscopy 1 H NMR spectroscopy, as reported previously 14 , Briefly, μL of blood serum were mixed with μL of deuterated phosphate buffer solution 0.

Based on an internal database of reference compounds, representative signals of metabolites were integrated. The signals are expressed in an arbitrary unit corresponding to a peak area normalized to total metabolic profiles.

This metabonomics approach targeted the major metabolic pathways, including central energy metabolism, amino acids, carboxylic acids, and lipoproteins and in a highly reproducible manner across more than 1, serum samples.

In particular, 1 H-NMR spectroscopy of human blood serum enables the monitoring of signals related to lipoprotein-bound fatty acyl groups found in triglycerides, phospholipids and cholesteryl esters, together with peaks from the glyceryl moiety of triglycerides and the choline head group of phosphatidylcholine.

Mixed effects modeling was used to assess the association between individual metabolites and fasting glucose, taking into account age, BMI z-scores, and physical activity.

Controlling for maturational and growth status is crucial in life course studies, and age at peak height velocity APHV is a key measure of maturity that was also taken into account.

Random intercepts were included as well as age categorized to allow for non-linear change in glucose over time , gender, BMI z-score, APHV, MVPA number of minutes spent in moderate-vigorous physical activity , and individual metabolites in separate models as fixed effects.

Each metabolite was transformed to a z-score i. Modeling was carried out in R software www. org using the lmer function in the package lme4 24 and p -values calculated using the Satterthwaite approximation implemented in the lmerTest package Both unadjusted and Bonferroni-adjusted p -values are presented.

Additional Spearman Correlation analysis was conducted between fasting glucose and serum metabolites, HOMA indexes, HbA1c, and respiratory exchange ratio. Clinical and anthropometric characteristics of the children for the year period are summarized in Table 1 and Supplementary Figure 1.

For both genders, there was an increase in fasting glucose throughout childhood, concomitant with increasing BMI-z-score and respiratory exchange ratio, and decreasing physical activity MVPA. As previously reported, fasting insulin and HOMA-IR decreased until around 8 years, and then increased during puberty until the age of 14 years, before decreasing until the age of 16 years.

This pattern was dependent on the time of APHV and BMI z-scores Mean fasting glucose concentrations increased from 4. Interestingly, these increases were marked by two plateaus, first between 8 and 11 years of age, then between 13 and 16 years of age Supplementary Figure 1.

Mirroring the changes in blood glucose concentrations, an evolving pattern was observed in the RER and age. RQ values reflect metabolic substrate utilization for energy production.

From age 5 to 7, RER values were around 0. Figure 1 describes the age-dependent changes in clinical and glycemic parameters in relation to male and female pubertal development. Parameters were plotted according to Tanner stage 21 , Tanner stage was self-reported at each time-point, and the same Tanner stage may be reported at more than one time-point.

Therefore, for each child, the parameter for each Tanner stage is represented once by selecting only the value at the first occurrence e.

Figure 1. Overview of main glycemic and physiological trajectories in childhood: longitudinal status according to pubertal stage in boys and girls. Data are plotted as mean ± standard error. Using data at all ages simultaneously, mixed effects modeling was applied to assess the association between fasting glucose concentrations and individual metabolites.

Several blood metabolites including amino acids, organic acids, and lipids showed statistically significant associations with fasting glucose concentrations in longitudinal models, independently of BMI z-score, physical activity, and APHV. Data are reported to statistical significance and in alphabetic order for different metabolic pathways and metabolites Table 2.

Table 2. Estimates and p -values from mixed effects models examining the association between metabolites and fasting glucose. Of note, the analysis described positive associations of alanine and lactate with fasting glucose. In addition, the LDL and VLDL-related blood lipid signature was positively associated with fasting glucose concentrations throughout childhood.

Most other amino acid metabolites, HDL and phosphocholine-related lipids were negatively associated with fasting glucose throughout childhood. The analysis also described how blood ketone bodies 3-D-hydroxybutyrate, acetoacetate , Krebs cycle intermediates citrate, formate , glycine-related metabolites dimethylglycine, creatine, creatinine were negatively associated with the fasting glucose trajectories.

Additional cross-sectional correlation analysis of metabolites, insulin traits, HbA1c, respiratory exchange ratio, and BMI-z-scores with fasting glucose for each year was conducted using Spearman rank correlation.

Data for the year period were reported using heatmaps in Figure 2 , for which the variables are ordered according to the temporal profile of their correlation with fasting glucose. Figure 2. Overview of spearman correlations between fasting glucose and other parameters as a function of chronological age.

MVPA, moderate to vigorous physical activity; RER, respiratory exchange ratio. The heatmap plot highlights the negative correlations of α-keto-isovalerate, 3-methyloxovalerate, 2-ketobutyrate, 3-D-hydroxybutyrate, acetoacetate, citrate, and leucine with fasting glucose at each age, throughout childhood.

In addition, positive associations of glucose with alanine, lactate, LDL, and VLDL related blood lipids were observed in the early years, between 5 and 9 years of age. The same correlation analysis using HbA1c as endpoint variable was also performed and reported in Supplementary Figure 2.

Fasting glucose and HbA1c showed positive correlations during childhood, and similar correlation patterns are observed between metabolites and fasting glucose and HbA1c.

Yet, fasting glucose shows stronger statistically significant correlation with metabolites, and with insulin and insulin resistance, than HbA1c during childhood. Major changes in levels of blood serum metabolites suggested changes in protein and amino acid levels, as well as lipid metabolic pathways.

Therefore, blood biochemical patterns involved in central carbon metabolism, branched chain amino acids BCAA , fatty acid oxidation, and ketogenesis were displayed according to their respective metabolic pathways Figure 3 , Supplementary Figures 3 — 5. Data are reported as a function of the pubertal stages for boys and girls.

Figure 3. Overview of central energy metabolic pathways with selected blood serum metabolite patterns according to pubertal stages.

Such a data visualization illustrates a rapid decrease in the level of ketogenesis from the early pubertal stages. These changes were associated with decreased levels of acetate, formate and the major Krebs cycle intermediate citrate, and are indicative of a profound remodeling of fatty acid oxidation in children's metabolism during the transition from early childhood to adolescence.

In contrast to the changes in lipid metabolism, glucose and alanine concentrations increased steadily during puberty, whilst lactate concentration increased primarily in the early period of pubertal development. Such variations in blood biochemical profiles probably reflect changes in energy and carbohydrate metabolism during puberty, with alanine and lactate concentrations reflecting changing activity in the Cori and Cahill cycles.

Throughout puberty, changes in amino acid metabolism are more complex. Overall, children show a decreased blood concentration of several compounds, including glutamate, arginine, and glycine. In addition, complex patterns in the metabolism of branched amino acids BCAA are described.

Whilst circulating levels of BCAA catabolic products decreased during puberty, circulating levels of BCAA evolved differently, and seemed to exhibit sexual dimorphism e. Of note, several other blood amino acid profiles displayed distinct differences between boys and girls in late puberty. For instance, boys showed a distinct increase in glutamine and proline in late puberty, whilst girls showed decreases in histidine, asparagine, and citrulline Supplementary Figure 4.

Finally, creatinine metabolism shows a consistent pattern throughout puberty, with creatinine concentrations increasing steadily, and more markedly in boys from mid-puberty Supplementary Figure 5.

As children grow and develop, changes in metabolism are directly related to total energy requirements e. Growth and development are associated with complex endocrine changes. This description of puberty-related changes in molecular processes and substrate utilization for energy production significantly extends the existing literature.

Although HbA1c retains a positive association with glucose throughout childhood in our cohort, it is weak, and their trends diverge from 10 years These findings therefore limit the interpretation of HbA1c for the diagnosis of impaired fasting glycemia during childhood and suggest that factors other than glycaemia systematically influence the variance of HbA1c in youth Our additional study reveals stronger associations of fasting glycemia with changes in insulin resistance as well as metabolites when compared to HbA1c, which suggests that analysis of temporal glycemic variations may encapsulate more comprehensively the changes in physiological and metabolite pathways during childhood.

In this uniquely well-characterized cohort of healthy children, the transition from childhood to adolescence was associated with increasing fasting glucose concentrations and a complex remodeling of central energy metabolism, including amino acid and fatty acid molecular pathways.

In the EarlyBird cohort, the gradual rise in the fasting respiratory exchange ratio describes an increased carbohydrate oxidation throughout childhood. Yet, these fasting respiratory exchange ratio values are high in comparison to adults, where fasting respiratory exchange ratio would remain between 0.

Higher fasting respiratory exchange ratio values in adults 29 and in adolescents 30 may be linked to reduced metabolic flexibility i. Whilst there is limited published literature on healthy children, in the Earlybird cohort, we did not see statistically significant differences in fasting respiratory exchange ratio between normoglycemic children and those with impaired fasting glycemia.

Since the maximum values are observed around 11—13 years of age, a period of height growth spurt and important growth in lean mass tissues, our observations may suggest a period of reduced metabolic flexibility during puberty. Finally, a potential limitation in the interpretation of the respiratory exchange ratio is that the measurements were conducted in the fasted state, and conclusions should not necessarily be extrapolated to the post-prandial state.

Prior to puberty, we identified that pre-pubertal children oxidize more fat relative to total energy expenditure than adults and pubertal children, an observation consistent with previous reports In addition, pre-pubertal children are known to oxidize fats preferentially over carbohydrates during low to moderate intensity exercise as well, when compared with post-pubertal children and adults 32 — Boisseau et al.

reported that higher fat oxidation in pre-pubertal children was associated with a distinctive metabolic phenotype, namely increased blood free fatty acid and glycerol, which are indicators of fat mobilization from peripheral stores and increased lipolysis Our study has also shown that pre-pubertal children have higher levels of ketogenesis, as noted by higher serum levels of ketones.

Two ketone bodies, namely 3-D-hydroxybutyrate and acetoacetate, decreased linearly during the first two pubertal stages for both sexes, to reach minima that remained constant throughout the rest of childhood. Ketogenesis is generally stimulated when fatty acid β-oxidation and production of acetyl-CoA exceeds the processing capacity of the Krebs cycle.

The decreased concentration of serum citrate and formate with puberty illustrates the decreased contribution of fatty acids to the pool of acetyl-coA entering the Krebs for energy production.

These patterns describe an overall decreasing fatty acid oxidation, via β-oxidation and ketogenesis, from pre-pubertal to pubertal stage. Whereas 3-D-hydroxybutyrate showed the largest decrease in concentration, levels of acetoacetate remained more stable constant levels , which suggests that there may be different contributions to ketogenesis from protein and lipid metabolism during puberty.

In addition, serum lipoprotein levels in childhood are known to vary with age, as a result of the hormonal changes of puberty, with reports of complex pattern and interactions according to age, gender and insulin resistance 36 — Some studies in normal weight children reported that levels of triglycerides mainly in VLDL increased whereas total cholesterol and LDL-cholesterol decreased during puberty in both sexes 36 , Other reports describe distinct and gender-specific patterns from mid-puberty, namely increased triglycerides and decreased HDL cholesterol in boys, and the opposite pattern in girls Our observations suggest that changes in the serum LDL and VLDL fatty acid signature are positively associated with fasting glycemia throughout childhood.

We previously reported how IR development in the Earlybird cohort was marked by decreased phospholipids mainly in HDL particles and increased LDL fatty acid signature in both males and females in the EarlyBird cohort Such an observation further illustrates the remodeling of lipid mobilization and metabolism that underpins structural growth and changing energy storage 36 , As puberty commences and progresses, there are major changes in many physiological processes, which in turn modify fuel mobilization and utilization 39 , Jones and Kostyak reported higher fat oxidation in children 5—10 years compared with adults—an adaptative process that might support normal growth requirements, such as higher rates of protein synthesis, lipid storage, and bone growth.

Such higher requirements are captured in dietary recommendations for fat consumption, which suggest reduction in fat intake from childhood to adulthood 40 , The novel molecular insights into lipid metabolism before and during puberty, revealed in the present study, may help to further refine the dietary recommendations in terms of quantity and quality of lipids required for optimal growth and development of children before and during puberty.

Girls and boys are indistinguishable in muscle strength until puberty, at which time strength and aerobic performance increases more rapidly in boys 7 , Our analysis also revealed that serum creatinine increased from mid puberty more rapidly in boys than in girls, whilst being negatively correlated with fasting glucose.

It is likely that the gender difference in muscle mass and function is driven primarily by the large difference in free testosterone concentrations that emerges with the onset of puberty However, boys are more insulin sensitive than girls, especially during puberty, and it is possible that differences in the action of insulin may also contribute to gender difference in muscle mass and function.

The gender-specific pattern of creatinine was associated with greater increases in serum leucine, valine, glutamine and proline in boys. Our observations agree with a recent report on whole blood amino acid patterns in puberty from the LIFE Child Cohort by Hirschel et al.

Serum creatinine is known to be affected by age, gender, ethnicity, dietary protein intake, and lean mass Amino acids play a major role as building blocks for protein synthesis and as regulators of key metabolic pathways for cell maintenance and growth Previous studies reported that during puberty, growth is driven by maintaining a greater rate of protein synthesis than that of breakdown 46 , Arslanian et al.

described lower protein oxidation and proteolysis during puberty when compared to pre-puberty, whereas protein synthesis was unchanged In addition, they showed that during puberty whole body proteolysis is resistant to suppression by insulin Blood amino acid concentrations reflect both the availability of amino acids and changes in amino acid influx or efflux between muscle and other tissues as a result of their utilization e.

In particular, proline, alanine, and glutamine are used as a source of energy metabolism through the anaplerotic pathway of the Krebs cycle in skeletal muscle Since the efficiency of carbohydrate oxidation increases during puberty, we may hypothesize that increasing glycolytic metabolism reduces the mobilization of these amino acids into the anaplerotic pathway, and further contributes to higher circulating concentrations.

The observed elevation of blood lactate and alanine concentrations with age reflects changes in the Cori and Cahill cycles. Since Cori and Cahill cycle shuttle lactate and alanine from the muscles to the liver, where the nitrogen enters the urea cycle for gluconeogenesis, this phenotype further illustrates the pubertal changes in glycolytic metabolism.

Last, several metabolites of one-carbon metabolism—glycine, dimethylglycine and creatine—showed a negative association with fasting glucose trajectories. This transmethylation pathway closely interconnects choline, betaine and homocysteine metabolism, and is of major importance for numerous cellular functions, such as DNA methylation, phosphatidylcholine, and protein synthesis 51 , Previous reports described how glycine and dimethylglycine metabolism is linked to glucose homeostasis and diabetes and may be genetically determined In particular, lower circulating levels were associated with lower insulin sensitivity and higher fasting glucose 53 , which is in agreement with our novel observations.

With a potential role of the one-carbon cycle in the developmental origins of T2D 54 , the biological implication of such a signature in the course of childhood would benefit from further clinical investigations. It is recognized that there are several potential limitations with the present study.

Importantly, the sample size was limited, and being an exploratory study, it was not possible to undertake an a priori power calculation.

Furthermore, while less-invasive methods for measuring IR, such as the HOMA are well-suited for repeat measurements in cohort studies of children, it is recognized that a potential limitation is that IR measured by HOMA correlates only modestly with clamp-derived measures of IR, and also that HOMA IR already correlates highly with fasting insulin in normoglycaemic subjects 55 , However, if fasting insulin secretion is impaired, the direction of error is that HOMA underestimates IR.

Despite these acknowledged limitations, HOMA is considered as a valid method for measuring IR in pediatric research This study demonstrates that normal pubertal growth and development is accompanied by complex and extensive remodeling of metabolism and fuel oxidation, reflecting the changing energy requirements of puberty.

The full complexity of this process is revealed by blood metabolic profiling. Fasting glycemia increases steadily throughout childhood and is accompanied by increasing concentration of insulin and rising respiratory exchange ratio.

As a result, the fuel economy shifts away from fatty acid oxidation and toward carbohydrate oxidation. The metabolic signatures indicate reduced fatty acid oxidation and ketogenesis, increased flux through Cori and Cahill cycles, and complex changes in amino acids with gender differences reflecting the emerging contrasts in body composition.

There are gradual rises in LDL and VLDL particles and remodeling of one carbon metabolism. All of these changes represent normal physiological development. These findings raise the important question at what point do physiological changes, such as increasing fasting glycemia begin to have pathophysiological consequences and raise concern for future cardiometabolic health?

It is possible to speculate that the metabolic changes we have observed, especially the shift away from fat oxidation, and reduced ketogenesis, is maladaptive in the context of obesity, and may also be liable to perpetuate the obese state.

Therefore, the reduced metabolic flexibility of puberty makes this a vulnerable period for excessive weight gain. Weight gain and obesity further exacerbate the physiological insulin resistance of puberty and fasting glycemia, and will favor atherogenic changes in the lipid profile and pathways, such as one carbon metabolism.

This is in line with our other findings which suggested that weight gain and increasing insulin resistance will exacerbate hyperglycaemia 15 in adolescence, especially in those who also have genetic impairment of pancreatic beta cell function 13 , Finally, these findings will have implications for guidance on child nutrition.

Since fat, protein, and carbohydrate requirements change during pubertal development, this study suggests that macronutrient requirements for optimum healthy growth and development and reduction in risk of cardiometabolic disease may need to take into account metabolic changes at puberty and gender differences.

We speculate that increasing respiratory exchange ratio and reduced ketogenesis may justify reduction in dietary fat relative to carbohydrate at adolescence, in order to reduce the risks of weight gain and insulin resistance. This nutritional change might be necessary earlier in girls, reflecting their earlier onset of puberty and growth spurt.

The avoidance of adolescent weight gain is also emphasized, in view of the maladaptive metabolic effects of insulin resistance, and in order to reduce long term cardiometabolic risks. Since growth and energy metabolism are dependent also on the presence of small quantities of several micronutrients, further analyses should explore the potential influence of key enzyme cofactors on metabonomic profiles and implications for cardiometabolic risk.

This knowledge has the potential to open-up the development of new and age-specific strategies for the prevention of cardiometabolic disease in children, through more evidence-based guidance on lifestyle and personalized dietary interventions.

The datasets presented in this article are not readily available because subject in particular, to ethical and privacy considerations. Requests to access the datasets should be directed to jonathan. pinkney plymouth. uk and francois-pierre. martin rd. The studies involving human participants were reviewed and approved by Plymouth Local Research Ethics Committee.

F-PM designed the study. AJ and F-PM were involved in the acquisition of the data. OC, F-PM, JH, and JP contributed to the analysis, data interpretation, and drafted the manuscript.

JP was guarantor of the work. All authors approved the final version. The authors declare that this study received funding from Bright Future Trust, The Kirby Laing Foundation, Peninsula Medical Foundation, Diabetes UK, the EarlyBird Diabetes Trust, and Nestlé Research.

Nestlé Research had the following involvement with the study: metabonomics data generation and analysis, interpretation of data, writing of this article and decision to submit it for publication.

The other funders were not involved in the study design, collection, analysis, interpretation of data, the writing of this article or the decision to submit it for publication. JH, JP, and AJ are employees of Plymouth University Peninsula School of Medicine and Dentistry.

F-PM and OC are employees of Nestlé Research. JH and AJ have received funding from Nestlé Research. The authors have no other dualities of interest to declare. We acknowledge the life and work of our former colleague Terence Wilkin — , Professor of Endocrinology and Metabolism, whose vision and original thinking led to the creation of the EarlyBird Study and the establishment of the collaboration that made possible the studies reported here.

We thank the EarlyBird children, their parents and all EarlyBird team members for their contribution to the study. We thank Ondine Walter for biobanking, sample handling and preparation at Nestlé, and for support for compliance with the Human Research Act.

We thank Christian Darimont and Jörg Hager for scientific discussion during the preparation of the manuscript. The EarlyBird study was supported by Bright Future Trust, The Kirby Laing Foundation, Peninsula Medical Foundation, Diabetes UK, and the EarlyBird Diabetes Trust.

JH and AJ have received funding from the Nestlé Group. The metabonomic analysis reported in this paper was funded by Nestlé Research. World Health Organization. Global Report on Diabetes. Geneva: World Health Organization Google Scholar.

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4. Regulation of Blood Glucose The odds ratio of the loci for the association with type 1A is only 1. The impact of diet, exercise, and body weight. This reaction is catalyzed by glucosephosphate dehydrogenase GPD. Department of Health and Human Services. Glucose in cerebrospinal fluid: suspected bacterial meningitis. May ;26 2
Carbohydrate metabolism Nutritional Booster the mtabolism of the metaboliem processes blpod for the metabolic formationbreakdown suga, and interconversion of carbohydrates in living organisms. Nut-free diet options Carbohyddate central to many essential metabolic pathways. Humans can consume a Weightlifting injury prevention of Carbohydrate metabolism and blood sugar levels, digestion breaks Carbohydfate complex carbohydrates into simple monomers monosaccharides : glucosefructosemannose and galactose. After resorption in the gutthe monosaccharides are transported, through the portal veinto the liver, where all non-glucose monosacharids fructose, galactose are transformed into glucose as well. Glycolysis is the process of breaking down a glucose molecule into two pyruvate molecules, while storing energy released during this process as adenosine triphosphate ATP and nicotinamide adenine dinucleotide NADH. Glycolysis consists of ten steps, split into two phases.

Carbohydrate metabolism and blood sugar levels -

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Kidney Int ; 5: 1— See also Section 3. The term hypoglycemia refers to a low blood glucose concentration associated with clinical symptoms. Hypoglycemia is the result of an imbalance between the inflow of glucose into the bloodstream due to decreased endogenous glucose production or deficient glucose uptake, and the consumption of glucose by the tissues.

The glucose threshold for a decrease in the blood insulin concentration is approx. Glucagon and catecholamines raise the blood glucose level within minutes by stimulating hepatic glycogenolysis and gluconeogenesis as well as renal gluconeogenesis. The substrates of gluconeogenesis are glycerol, free fatty acids, and amino acids.

Cortisol and growth hormone reduce the glucose consumption of insulin-sensitive tissues and lead to an increase in blood glucose within hours. The main source of energy for the brain is glucose, and there are protective mechanisms to maintain glucose homeostasis.

the sympathoadrenal nervous system is activated, leading to hypoglycemic symptoms such as anxiety, sweating, tremor, fast heartbeat, and hunger. These end-organ responses, also called autonomic symptoms, can progress to neuroglycopenic symptoms including behavioral changes, cognitive dysfunction, seizures, and coma.

However, the threshold for cognitive dysfunction depends on various clinical aspects and psychometric tests. The clinical symptoms associated with a decrease in glucose concentrations are shown in Fig. The aforementioned glucose levels are a highly specific criterion for hypoglycemia. If levels are below the thresholds suggested by Whipple, further clinical investigations are necessary, even in the absence of hypoglycemia symptoms.

Hypoglycemia is not a diagnosis but a pathological state, the cause of which must be determined. The most common diagnoses at admission in patients presenting with hypoglycemia are diabetes mellitus, alcoholism, sepsis, and reactive hypoglycemia. Insulinomas are very rare, with a prevalence of 4 cases per 1 million population per year.

For evaluation refer to Section 3. Iatrogenic hypoglycemia in diabetics is evaluated based on medical history. Hypoglycemia syndromes which are due to an insulinoma predominantly occur in the fasting state, rarely in the fasting plus postprandial state, and very rarely only in the postprandial state.

Postprandial symptoms, which occur 2—4 h after meals are classified as food-stimulated and those which occur more than 5 h after meals are classified as food-deprived. Autonomous symptoms without hypoglycemia, also known as pseudo-hypoglycemia, which occur after meals usually cannot confirmed as arising from hypoglycemia.

The flow chart in Fig. Blood glucose: detection of hypoglycemia. In this case, the h fast or another functional test should be performed. Findings on hypoglycemia in adults and drug-associated hypoglycemia and their diagnostic significance are listed in Tab.

Detection and differentiation of hypoglycemia by determination of insulin, C-peptide and β-hydroxy butyrate Tab. C-peptide suppression test, intravenous tolbutamide test, glucagon test: these tests are performed if the h fast is not conclusive. Following enteral feeding, blood glucose levels cycle, with a peak occurring about 1 h after food intake.

If hypoglycemia is suspected, a blood sample should be taken just before the second food intake. Low glucose levels in the first 24—48 h are not uncommon in normally developing newborns who are breast-fed. Every year, approx. The main etiologies are infections, drug-induced intoxications, seizures, and metabolic disorders.

For the molecular basis of glucose homeostasis and incidence of congenital hypoglycemia see Ref. Rosen SG, Clutter WE, Berk MA, Shah SD, Cryer PE. Epinephrine supports the post absorptive plasma glucose concentration and prevents hypoglycemia when glucagon secretion is deficient in man.

Mitrakou A, Ryan C, Veneman T, et al. Hierarchy of glycemic thresholds for counter regulatory hormone secretion, symptoms, and cerebral dysfunction. Am J Physiol ; E 67— Brun JF, Baccara MT, Blacon C, Orsetti A. Comparaison avec des hypoglycemies reactionelles Abstract.

Diabetes Metab ; 21 A. Marks V. Glycemic stability in healthy subjects: fluctuations in blood glucose during day. In: Andreani D, Marks V, Lefebvre PJ, eds. New York; Raven Press 19— Brun JF, Fedou C, Mercier J. Postprandial reactive hypoglycemia. Diabetes and Metabolism Paris ; — Whipple AO.

The surgical therapy of hyperinsulinism. J Internat Chirol ; 3: Heller SR. Diabetic hypoglycemia. Service FJ. Hypoglycemic disorders. Comi RJ. Approach to acute hypoglycemia. Blood glucose measurements during symptomatic episodes in patients with suspected postprandial hypoglycemia.

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Defining and reporting hypoglycemia in diabetes: a report from the American Diabetes Association Workgroup on Hypoglycemia. Diabetes Care ; —9. Weitzman ER, Kelemen S, Quinn M, Eggleston EM, Mandl KD.

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N Engl J Med ; 22 : —6. This must be taken into account during the clinical evaluation. A blood glucose test is a measure of glucose concentration present in an the blood of an individual at a given point of time. Diagnostic laboratory tests for diabetes are Tab.

Principle: the enzyme glucose oxidase catalyzes the oxidation of glucose to gluconic acid and H 2 O 2. In the subsequent peroxidase-mediated indicator reaction, H 2 O 2 oxidizes a reduced chromogen to produce a colored compound, which is measured using a photometer.

Principle: hexokinase in the presence of ATP phosphorylates glucose to form glucosephosphate. The latter reacts with NADP to form 6-phosphogluconate and NADPH 2. This reaction is catalyzed by glucosephosphate dehydrogenase GPD.

The measurand is NADPH 2 , the increase in NADPH 2 is measured at the endpoint of the reaction. The increase in absorbance determined is proportional to the glucose concentration in the test sample. Principle: glucose is oxidized to gluconolactone by Gluc-DH. The hydrogen released in the reaction is transferred to NAD, producing NADH 2.

The increase in NADH 2 is measured using the principle of continuous absorbance registration. The increase in absorbance is proportional to the glucose concentration in the test sample. In contrast to the end point method addition of mutarotase to the reagents is not necessary.

Gluc-DH only reduces β-D-glucose. In aqueous solution, glucose is present in the α- and β-form. As the β-D-glucose is consumed, an equilibrium between the two forms is established again as a function of time.

To prevent this reaction from becoming the determining factor for the speed of the Gluc-DH reaction, the reagent contains mutarotase. This enzyme accelerates the rate at which equilibrium is reached. Biosensors are analytical devices that incorporate a biological material e.

Principle of the glucose sensor: in the first step, glucose reacts with the oxidized form of the enzyme glucose oxidase GOD to form gluconic acid. In this process, two electrons and two protons are released, and GOD is reduced. In the second step, O 2 which is present in the surrounding fluid reacts with GOD accepting the aforementioned electrons and protons leading to form H 2 O 2 and regenerating oxidized GOD, which is ready to react once more with glucose.

The glucose concentration in the test sample determines the amount of H 2 O 2. This is detected following oxidation at the surface of a platinum electrode which causes a change in the electrochemical potential.

Analyzers in which glucose is determined using readable strip and reflectance photometer are used for:. With the photometric measurement, glucose is enzymatically oxidized to gluconolactone by the enzymes glucose peroxidase or glucose dehydrogenase.

The optimal sample is capillary blood. Modern glucose meters for the self-monitoring of blood glucose allow the storage and processing of the measured values and the calculation of mean blood glucose MBG and mean amplitude of glucose excursions MAGE.

Continuous glucose monitoring CGM systems have been recognized as the ideal monitoring systems for glycemic control of diabetic patients. The CGM system measures blood glucose levels in subcutaneous tissue by attaching a CGM sensor to the skin, allowing the patient to make appropriate modifications to their medical interventions according to experience or empirically derived algorithms.

The principles of glucose sensing employed in the commercially available CGM systems are mainly electrochemical and employ the enzyme glucoseoxidase as the glucose sensing molecule with the combination of hydrogen peroxide monitoring or with the combination of redox mediator harboring hydrogel.

The blood level of glucose depends on the metabolic state of an individual. The following states are possible Tab. and the diagnostic significance of glucose in the fasting and postprandial state in:. This is due to intraindividual variations of blood glucose levels which are greater than those of other blood parameters as they are influenced by physical activity and the length of time since the last food intake.

The biological variability of plasma glucose is thus higher than the analytical imprecision. Moreover, the fasting plasma glucose concentration increases continuously with age from the third to the sixth decade of life.

Dysregulations such as insulin resistance, hyperinsulinism and diabetes as well as pregnancy further increase the variations. In newly diagnosed type 2 diabetics, the intraindividual variation of fasting glucose is The interpretation of blood glucose levels also depends on the type of sample examined.

The GI is a measure of how much 50 g of carbohydrate from a specific food raises the blood glucose level. The lower the GI, the less the concentration of blood glucose increases. After consuming a certain food it is usually measured how high the increase of glucose is. A diet with a high GI is associated with an increased risk of cardiovascular disease and death.

The glycemic load GL is the product of GI and the consumed carbohydrates and a measure of insulin needs.

The GL is calculated by multiplying the mean net carbohydrate intake as measured in grams per day by the GI and then dividing by Test procedure: Blood glucose increase is measured several times after ingestion of the specific food within 2 hours and compared with blood glucose increase after ingestion of 50 g glucose.

The assessment of GI is as follows:. The concentration of glucose in blood depends on the type of sample examined.

Arterial whole blood has a higher glucose concentration than venous blood; the glucose concentration of capillary whole blood sampled from the finger tip is in between the two. Measurements in capillary whole blood and venous plasma result in similar glucose levels within the reference interval.

The following types of specimen are used in the different countries for determining blood glucose in routine diagnosis: Capillary whole blood, venous whole blood, and plasma from venous whole blood.

Capillary whole blood: samples should be collected by skin puncture from the finger or from the heel infants only. In the fasting state there is no arteriovenous difference between arterial and venous blood. Therefore, the concentrations measured in venous and capillary whole blood are nearly identical.

Compared to glucose measured in plasma, the glucose concentration in whole blood is influenced by the hematocrit Hct , by proteins, lipoproteins and other dissolved and corpuscular components. Venous plasma: the molality of glucose in whole blood and plasma is identical.

Sensor variability in continuous glucose monitoring CGM : substantial variation is observed within sensors over time and across 2 different sensors worn simultaneously on the same individuals.

When comparing the same sensor at two different time points two 2-week periods, 3 months apart , the within-person coefficient of variation CVw in mean glucose was CVw for percent time in range was A constant factor of 1.

This applies to a Hct of 0. In the case of higher Hct values, as are typical in neonates, this factor must be increased by multiplication by the following correction factor cf :.

With a Hct of 0. According to the IFCC, it is possible to convert whole blood glucose and biosensor glucose to plasma glucose, but not whole blood glucose to biosensor glucose Fig. According to recommendations of the WHO, the cutoffs for fasting glucose and for the oral glucose tolerance test are identical for capillary whole blood and venous plasma.

Fasting glucose : sampling 7 a. after at least 8 h of fasting. Capillary whole blood: only draw blood if blood circulation is good; finger must be warm. Venous blood: is analyzed in the form of whole blood, plasma, and serum.

In plasma and serum following blood collection is recommended in separator tubes. The collection tubes for determining glucose in whole blood contain NaF to prevent glycolysis, and potassium oxalate or Na 2 EDTA to inhibit clotting.

NaF acts by inhibiting glycolytic enzymes, in particular enolase, although the effect is minor in the first 2 h after blood collection. A better effect than with NaF alone is achieved by cooling the sample, by acidifying it, or by using citrate tubes for blood collection.

The reference method is the hexokinase method, or in some countries the glucose oxidase method. Possible methodological errors are shown in Tab. However, small amounts of icodextrin can get into the bloodstream via the lymphatic system.

In the bloodstream it is hydrolyzed to glucose oligomers such as maltose and maltotriose. These oligomers cause falsely high glucose readings in some point-of-care glucometers. At 4 °C there is only a slight decrease during the first 2 h and approx.

In EDTA-coated collection tubes there is no significant decrease within 24 h in the presence of maleinimide. At 4 °C blood deproteinized by perchloric acid gives stable values in the supernatant, obtained by centrifugation, for at least 5 days.

In newborns, measurement of blood glucose should be performed as soon as possible after blood collection, since the rate of glycolysis of erythrocytes in newborns is considerably higher than in adults so that the glycolysis inhibitors cannot be as effective.

The biological variation in plasma glucose levels results from complex interaction of genetically anchored metabolic processes that are subject to strict hormone-controlled regulation.

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A quantitative appraisal of interference by icodextrin metabolites in point-of-care glucose analysis. Clin Chem Lab Med ; —8. Miller SA, Wallace RJ, Musker DM, Septimus EJ, Kohl S, Baughn R. Hypoglycemia as a manifestation of sepsis.

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Handling of blood specimens for blood glucose analysis. J Clin Chem Clin Biochem ; —6. Fernandez L, Jee P, Klein MJ, Fischer P, Brooks SPJ. Clin Biochem ; —8. Tate PF, Clemens CA, Walters JE. Accuracy of home blood glucose monitoring.

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N Engl J Med ; DOI Özcürümez M, Arzideh F, Torge A, Figge A, Haeckel R, Streichert T. The influence of sampling time on indirect reference limits, and the estimation of biological variation of random plasma glucose concentrations.

J Lab Med ; 45 2 : —9. Selvin E, Wang D, Rooney MR, Fang M, Echouffo-Tcheugui JB, Zeger S, et al. Within person and between-sensor variability in continuous glucose monitoring metrics. Clin Chem ; 69 2 : —8. Increased exercise duration and intensity can speed up fat metabolism.

Decreased sleep quality or quantity can lead to insulin resistance, increased ghrelin hunger hormone , decreased leptin fullness hormone , decreased physical activity, and increased inflammation. These changes can increase your risk of diabetes, obesity, and cardiovascular disease.

Several inherited lipid metabolism disorders affect how fats are used and stored in the body. Although fat, glucose, and protein metabolism all contribute to metabolic health, the two factors with the greatest impact on metabolism are maintaining stable blood sugar and getting enough exercise.

Insulin and exercise are anabolic. Insulin aids in storing excess energy as glycogen or fat. Exercise helps build muscle from protein. Which carbohydrates you choose to consume, how they are packaged in your diet, and how your body metabolizes carbohydrates will all affect metabolism and the combination of glucose, fats, or proteins your body burns for energy.

Insulin resistance disrupts metabolism because glucose stays in your bloodstream instead of entering cells to be used for energy. Increased insulin levels lead to fat storage and weight gain. Blood sugar is a key indicator of how well your metabolism is functioning. When you have metabolic flexibility , average and fasting glucose levels stay within an optimal range, and you experience minimal glucose spikes after eating.

In this state, your metabolism is functioning well. Optimally, you supply your body with the nutritional calories it needs to function without providing excess calories that are stored as fat.

Excess calories contribute to obesity, a chronic disease that adversely affects metabolic health. Knowing what the optimal number of calories you need and in what combination of fat, protein, and carbohydrates is the million-dollar question.

Each person's metabolic response is unique, and it may fluctuate throughout the day in response to triggers such as diet, exercise, and stress. Your basal metabolic rate BMR is the minimum number of calories your body needs to function at rest.

People with a fast metabolism burn more calories at rest. Therefore, they have a higher BMR. Conversely, people with a slow metabolism burn fewer calories at rest and have a lower BMR. However, having a higher BMR does not mean you will be thin. Carrying excess body weight makes your body work harder and therefore increases BMR.

Besides your BMR, your body's metabolic rate is determined by the thermic effect of food and energy used during physical activity. But, of course, this depends on how active you are. Slower metabolism lower BMR means that you burn fewer calories at rest, which can increase your propensity for weight gain, but does it affect insulin resistance and blood sugar?

In one animal study, researchers found that mice with lower BMRs had metabolism-specific pathways that increased their risk of developing insulin resistance and type 2 diabetes.

More research is needed to see if this also applies to humans. The biggest factors affecting your BMR are your fat-free mass FFM and fat mass FM. Having a faster metabolism is at least partially due to increased FFM. Exercise also helps control blood sugar.

More research is needed to determine if there are any stronger links between fast metabolism and blood sugar. Metabolic disorders affect how your body obtains energy from food.

Metabolic disorders can be inherited or acquired. Insulin resistance, prediabetes, and type 2 diabetes are on the spectrum of disorders that affect glucose metabolism and blood sugar. The World Health Organization classifies type 2 diabetes as a metabolic disorder.

Obesity is a risk factor for insulin resistance, prediabetes, and type 2 diabetes and is also classified as a metabolic disorder. Glycogen storage disease is an example of an inherited metabolic disorder that primarily affects glucose metabolism. Inherited metabolic diseases are usually due to a missing enzyme or vitamin that is essential for metabolism.

Metabolic syndrome is a cluster of risk factors that are specific to cardiovascular disease. Metabolic syndrome increases the risk of diabetes, heart disease, and stroke.

Obesity is the primary risk factor for metabolic syndrome. Metabolic syndrome is diagnosed when three of the following five health markers are no longer in the optimal range:. These five markers are used to make a diagnosis of metabolic syndrome.

Metabolic syndrome does not cause high blood sugar, but high blood sugar is one marker of metabolic syndrome.

Metabolic health is defined by having all five markers in an optimal range without needing any medications to correct them. When fat, muscle, and liver cells become insensitive to insulin, the pancreas works harder to pump out more insulin.

Eventually, the insulin-producing cells in the pancreas will burn out as they cannot keep up with the demand. As a result, blood glucose levels rise, inflammation increases, and when the pancreas can no longer compensate, type 2 diabetes develops.

Muscle cells absorb the majority of excess blood glucose, as long as they are sensitive to insulin. When muscle cells become inflamed from excess fatty acids, the liver picks up excess glucose. If glycogen stores are full, excess glucose in the liver is stored as fat.

Free fatty acids increase in the blood, which makes the liver and muscle more insulin resistant. Diet, exercise, and body weight all impact metabolic health and metabolism.

Since diet and exercise affect body weight and blood sugar, it is important to work on all three as you journey towards better metabolic health. A healthy diet can reduce post-meal glucose spikes.

Dietary tips for better glucose control: Exercise reduces stress, improves insulin sensitivity, and helps with weight management. Even walking can help with weight loss. The American College of Sports Medicine ACSM 18 and the U. Department of Health and Human Services Physical Activity Guidelines 19 jointly recommend the following:.

Even small amounts of weight loss can improve your metabolic health and blood sugar. Weight management tips: 20, If you can only improve in one of these areas, start with your diet. You can't out-exercise a bad diet. Learn more in this podcast with Nicole Aucoin from Healthy Steps Nutrition.

Track your progress towards better metabolic health and blood sugar using a continuous glucose monitor CGM.

Leann Poston, MD, is a licensed physician in Ohio who holds an MBA and an M. She is a medical writer and educator who researches and writes about medicine, education, and healthcare administration.

Please note: The Signos team is committed to sharing insightful and actionable health articles that are backed by scientific research, supported by expert reviews, and vetted by experienced health editors.

The Signos blog is not intended to diagnose, treat, cure or prevent any disease. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider. Read more about our editorial process and content philosophy here.

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Abstract Classifying the glycemic responses of carbohydrate foods using the glycemic index GI requires standardized methodology for valid results.

carbohydrate , glucose , glycemic index , metabolism , methodology. Issue Section:. Download all slides. Views 2, More metrics information. Total Views 2, Email alerts Article activity alert. Advance article alerts. New issue alert. Receive exclusive offers and updates from Oxford Academic.

Carbohydrates are Nut-free diet options molecules composed of carbon, hydrogen, metaboilsm oxygen atoms. The family Post-workout nutrition carbohydrates includes both simple and complex bloo. Glucose merabolism fructose are examples of simple Nut-free diet options, and starch, glycogen, and cellulose are all examples of complex sugars. The complex sugars are also called polysaccharides and are made of multiple monosaccharide molecules. Polysaccharides serve as energy storage e. During digestion, carbohydrates are broken down into simple, soluble sugars that can be transported across the intestinal wall into the circulatory system to be transported throughout the body.

Carbohydrate metabolism and blood sugar levels -

After research showed that BG levels are influenced by intestinal hormones in addition to insulin and glucagon, incretin mimetics became a new class of medications to help balance BG levels in people who have diabetes. Two types of incretin hormones are GLP-1 glucagon-like peptide and GIP gastric inhibitory polypeptide.

Each peptide is broken down by naturally occurring enzymes called DDP-4, dipeptidyl peptidase Exenatide Byetta , an injectable anti-diabetes drug, is categorized as a glucagon-like peptide GLP-1 and directly mimics the glucose-lowering effects of natural incretins upon oral ingestion of carbohydrates.

The administration of exenatide helps to reduce BG levels by mimicking the incretins. Both long- and short-acting forms of GLP-1 agents are currently being used.

A new class of medications, called DPP4 inhibitors, block this enzyme from breaking down incretins, thereby prolonging the positive incretin effects of glucose suppression. An additional class of medications called dipeptidyl peptidase-4 DPP-4 inhibitors—note hyphen , are available in the form of several orally administered products.

These agents will be discussed more fully later. People with diabetes have frequent and persistent hyperglycemia, which is the hallmark sign of diabetes.

For people with type 1 diabetes, who make no insulin, glucose remains in the blood plasma without the needed BG-lowering effect of insulin.

Another contributor to this chronic hyperglycemia is the liver. When a person with diabetes is fasting, the liver secretes too much glucose, and it continues to secrete glucose even after the blood level reaches a normal range Basu et al.

Another contributor to chronic hyperglycemia in diabetes is skeletal muscle. After a meal, the muscles in a person with diabetes take up too little glucose, leaving blood glucose levels elevated for extended periods Basu et al.

The metabolic malfunctioning of the liver and skeletal muscles in type 2 diabetes results from a combination of insulin resistance, beta cell dysfunction, excess glucagon, and decreased incretins. These problems develop progressively. Early in the disease the existing insulin resistance can be counteracted by excess insulin secretion from the beta cells of the pancreas, which try to address the hyperglycemia.

The hyperglycemia caused by insulin resistance is met by hyperinsulinemia. Eventually, however, the beta cells begin to fail. Hyperglycemia can no longer be matched by excess insulin secretion, and the person develops clinical diabetes Maitra, How would you explain to your patient what lifestyle behaviors create insulin resistance?

In type 2 diabetes, many patients have body cells with a decreased response to insulin known as insulin resistance. This means that, for the same amount of circulating insulin, the skeletal muscles, liver, and adipose tissue take up and metabolize less glucose than normal.

Insulin resistance can develop in a person over many years before the appearance of type 2 diabetes. People inherit a propensity for developing insulin resistance, and other health problems can worsen the condition. For example, when skeletal muscle cells are bathed in excess free fatty acids, the cells preferentially use the fat for metabolism while taking up and using less glucose than normal, even when there is plenty of insulin available.

In this way, high levels of blood lipids decrease the effectiveness of insulin; thus, high cholesterol and body fat, overweight and obesity increase insulin resistance. Physical inactivity has a similar effect. Sedentary overweight and obese people accumulate triglycerides in their muscle cells.

This causes the cells to use fat rather than glucose to produce muscular energy. Physical inactivity and obesity increase insulin resistance Monnier et al. For people with type 1 diabetes, no insulin is produced due to beta cells destruction.

Triggers of that autoimmune response have been linked to milk, vaccines, environmental triggers, viruses, and bacteria. For people with type 2 diabetes, a progressive decrease in the concentration of insulin in the blood develops.

Not only do the beta cells release less insulin as type 2 diabetes progresses, they also release it slowly and in a different pattern than that of healthy people Monnier et al. Without sufficient insulin, the glucose-absorbing tissues—mainly skeletal muscle, liver, and adipose tissue—do not efficiently clear excess glucose from the bloodstream, and the person suffers the damaging effects of toxic chronic hyperglycemia.

At first, the beta cells manage to manufacture and release sufficient insulin to compensate for the higher demands caused by insulin resistance.

Eventually, however, the defective beta cells decrease their insulin production and can no longer meet the increased demand. At this point, the person has persistent hyperglycemia.

A downward spiral follows. The hyperglycemia and hyperinsulinemia caused by the over-stressed beta cells create their own failure. In type 2 diabetes, the continual loss of functioning beta cells shows up as a progressive hyperglycemia.

How would you explain insulin resistance differently to someone with type 1 diabetes and someone with type 2 diabetes? Together, insulin resistance and decreased insulin secretion lead to hyperglycemia, which causes most of the health problems in diabetes.

The acute health problems—diabetic ketoacidosis and hyperosmolar hyperglycemic state—are metabolic disorders that are directly caused by an overload of glucose. In comparison, the chronic health problems—eye, heart, kidney, nerve, and wound problems—are tissue injury, a slow and progressive cellular damage caused by feeding tissues too much glucose ADA, Hyperglycemic damage to tissues is the result of glucose toxicity.

There are at least three distinct routes by which excess glucose injures tissues:. If you are attending a virtual event or viewing video content, you must meet the minimum participation requirement to proceed.

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Diabetes Type 2: Nothing Sweet About It Page 6 of Fuels of the Body To appreciate the pathology of diabetes, it is important to understand how the body normally uses food for energy.

Hormones of the Pancreas Regulation of blood glucose is largely done through the endocrine hormones of the pancreas, a beautiful balance of hormones achieved through a negative feedback loop. The glucose becomes syrupy in the bloodstream, intoxicating cells and competing with life-giving oxygen.

Optimal health requires that: When blood glucose concentrations are low, the liver is signaled to add glucose to the circulation. Convergence of genetic and environmental factors in the immunopathogenesis of type 1 diabetes mellitus.

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Yarandi R, Vaismoradi M, Panahi MH, Kymre IG, Behoudi-Gandevani S. Mild gestational diabetes and adverse pregnancy outcome. a systemic review and meta-analysis. Frontiers in Medicine ; doi: Ryan EA. Pregnancy in diabetes. Gestational diabetes mellitus. Diabetes Care ; S74—S Aguilar-Bryan L, Bryan J.

Neonatal diabetes mellitus. Mayer-Davis E, Lawrence JM, Dabelea D, Divers J, Isom S, Dolan L, et al. Incidence trends of type 1 and type 2 diabetes among youths, — N Engl J Med ; — Vidal J, Kahn SE. Regulation of insulin secretion in vivo.

In Lowe WL, Jr, ed. Genetics of diabetes mellitus. Boston; Kluwer — Kolb H, Mandrup-Poulsen T. The global diabetes epidemic as a consequence of lifestyle-induced low-grade inflammation. Diabetologia ; 10— Larsen S. Diabetes mellitus secondary to chronic pancreatitis. Danish Medical Bulletin ; — Müller MJ, Pirlich M, Balks HJ, Selberg O, Glucose intolerance in liver cirrhosis: role of hepatic and non-hepatic influences.

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Clin Endocrinol ; —6. Schlaghecke R. Diabetes mellitus bei verschiedenen endokrinologischen Erkrankungen. In: Berger M, ed. Diabetes mellitus. München; Urban and Schwarzenberg — Feig DS, Donovan LE, Corcoy R, Murphy KE, Amiel SA, Hunt KF, et al. Continuous glucose monitoring in pregnant women with type 1 diabetes Concept : a multicentre international randomised controlled trial.

Lancet ; : — Implications of the diabetes control and complications trial. Diabetes Care ; S24—S Cornblath M, Schwartz R. Hypoglycemia in the neonate. J Pediatr Endocrinol ; 6: — Silverman BL, Metzger BE, Cho NH, et al. Impaired glucose tolerance in adolescent offspring of diabetic mothers. Shohat M, Merlob P, Reisner SH.

Neonatal polycythemia: I. Early diagnosis and incidence relating to time of sampling. Pediatrics ; 7— Shohat M, Reisner SH, Mimouni M, Merlob P. Neonatal polycythemia: II. Definition related to time of sampling.

Pediatrics ; 11—3. Kerner W. Klassifikation and Diagnose des Diabetes mellitus. Dtsch Ärztebl ; B—8. Sacks DB, Bruns DE, Goldstein DE, MacLaren K, McDonald JM, Parrott M.

Guidelines and recommendations for laboratory analysis in the diagnosis and management of diabetes mellitus. Hyperglycaemia and risk of adverse perinatal outcomes: £systematic review and meta-analysis. The NICE-SUGAR Study investigators. Intensive versus conventional glucose control in critically ill patients.

Cheung BM, Ong KL, Cherny SS, Sham PC, Tso AW, Lam KS. Diabetes prevalence and therapeutic target achievement in the United States, — Am J Med ; — Gourdy P. Diabetes and oral conception. Clin Endocrinol and Metab ; 67— Braunwald E.

Gliflozins in the management of cardiovascular disease. N Engl J Med ; 21 : — DeBoer IH, Khunti K, Sadusky T, Rosas SE, Rossing P, et al. Diabetes management in chronic kidney disease: a consensus report by the American Diabetes Association ADA and Kidney Disease: Improving Global Outcomes KDIGO.

Kidney Int ; 5: 1— See also Section 3. The term hypoglycemia refers to a low blood glucose concentration associated with clinical symptoms. Hypoglycemia is the result of an imbalance between the inflow of glucose into the bloodstream due to decreased endogenous glucose production or deficient glucose uptake, and the consumption of glucose by the tissues.

The glucose threshold for a decrease in the blood insulin concentration is approx. Glucagon and catecholamines raise the blood glucose level within minutes by stimulating hepatic glycogenolysis and gluconeogenesis as well as renal gluconeogenesis. The substrates of gluconeogenesis are glycerol, free fatty acids, and amino acids.

Cortisol and growth hormone reduce the glucose consumption of insulin-sensitive tissues and lead to an increase in blood glucose within hours. The main source of energy for the brain is glucose, and there are protective mechanisms to maintain glucose homeostasis.

the sympathoadrenal nervous system is activated, leading to hypoglycemic symptoms such as anxiety, sweating, tremor, fast heartbeat, and hunger. These end-organ responses, also called autonomic symptoms, can progress to neuroglycopenic symptoms including behavioral changes, cognitive dysfunction, seizures, and coma.

However, the threshold for cognitive dysfunction depends on various clinical aspects and psychometric tests. The clinical symptoms associated with a decrease in glucose concentrations are shown in Fig.

The aforementioned glucose levels are a highly specific criterion for hypoglycemia. If levels are below the thresholds suggested by Whipple, further clinical investigations are necessary, even in the absence of hypoglycemia symptoms.

Hypoglycemia is not a diagnosis but a pathological state, the cause of which must be determined. The most common diagnoses at admission in patients presenting with hypoglycemia are diabetes mellitus, alcoholism, sepsis, and reactive hypoglycemia.

Insulinomas are very rare, with a prevalence of 4 cases per 1 million population per year. For evaluation refer to Section 3. Iatrogenic hypoglycemia in diabetics is evaluated based on medical history.

Hypoglycemia syndromes which are due to an insulinoma predominantly occur in the fasting state, rarely in the fasting plus postprandial state, and very rarely only in the postprandial state. Postprandial symptoms, which occur 2—4 h after meals are classified as food-stimulated and those which occur more than 5 h after meals are classified as food-deprived.

Autonomous symptoms without hypoglycemia, also known as pseudo-hypoglycemia, which occur after meals usually cannot confirmed as arising from hypoglycemia. The flow chart in Fig. Blood glucose: detection of hypoglycemia.

In this case, the h fast or another functional test should be performed. Findings on hypoglycemia in adults and drug-associated hypoglycemia and their diagnostic significance are listed in Tab. Detection and differentiation of hypoglycemia by determination of insulin, C-peptide and β-hydroxy butyrate Tab.

C-peptide suppression test, intravenous tolbutamide test, glucagon test: these tests are performed if the h fast is not conclusive. Following enteral feeding, blood glucose levels cycle, with a peak occurring about 1 h after food intake.

If hypoglycemia is suspected, a blood sample should be taken just before the second food intake. Low glucose levels in the first 24—48 h are not uncommon in normally developing newborns who are breast-fed. Every year, approx.

The main etiologies are infections, drug-induced intoxications, seizures, and metabolic disorders. For the molecular basis of glucose homeostasis and incidence of congenital hypoglycemia see Ref. Rosen SG, Clutter WE, Berk MA, Shah SD, Cryer PE. Epinephrine supports the post absorptive plasma glucose concentration and prevents hypoglycemia when glucagon secretion is deficient in man.

Mitrakou A, Ryan C, Veneman T, et al. Hierarchy of glycemic thresholds for counter regulatory hormone secretion, symptoms, and cerebral dysfunction. Am J Physiol ; E 67— Brun JF, Baccara MT, Blacon C, Orsetti A. Comparaison avec des hypoglycemies reactionelles Abstract. Diabetes Metab ; 21 A.

Marks V. Glycemic stability in healthy subjects: fluctuations in blood glucose during day. In: Andreani D, Marks V, Lefebvre PJ, eds. New York; Raven Press 19— Brun JF, Fedou C, Mercier J. Postprandial reactive hypoglycemia. Diabetes and Metabolism Paris ; — Whipple AO. The surgical therapy of hyperinsulinism.

J Internat Chirol ; 3: Heller SR. Diabetic hypoglycemia. Service FJ. Hypoglycemic disorders. Comi RJ. Approach to acute hypoglycemia. Blood glucose measurements during symptomatic episodes in patients with suspected postprandial hypoglycemia.

N Engl J Med ; —5. Deshpande S, Platt MW. The investigation and management of neonatal hypoglycemia. Wendel U. Diagnostisches Vorgehen bei kindlichen Hypoglykämien.

Monatsschr Kinderheilkd ; —6. Mechanisms of hypoglycemia-associated autonomic failure and its component syndromes in diabetes. American Diabetes Association Workgroup on Hypoglycemia. Defining and reporting hypoglycemia in diabetes: a report from the American Diabetes Association Workgroup on Hypoglycemia.

Diabetes Care ; —9. Weitzman ER, Kelemen S, Quinn M, Eggleston EM, Mandl KD. Participatory surveillance of hypoglycemia and harms in an online social network. JAMA Intern Med ; — Service GJ, Thompson GB, Service FJ, Andrews JC, Collazo-Clavell ML, Lloyd RV. Hyperinsulinemic hypoglycemia with nesidioblastosis after gastric-bypass surgery.

Toft-Nielsen M, Madsbad S, Holst JJ. Exaggerated secretion of glucagon-like peptide-1 GLP-1 could cause reactive hypoglycaemia. Diabetologica ; —6. Bergman RN. Toward physiological understanding of glucose tolerance. Minimal model approach.

Ahmadpour S, Kabadi UM. Pancreatic alpha-cell function in idiopathic reactive hypoglycemia. Metabolism ; — Sasaki M, Moki T, Wada Y, Hirosawa I, Koizumi A.

An endemic condition of biochemical hypoglycemia among male volunteers. Ind Health ; — Marimee TJ, Tyson JE. Hypoglycemia in men. Pathologic and physiologic variants. Diabetes ; —5.

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White Jr JR, Campbell RK. Dangerous and common drug interactions in patients with diabetes mellitus. Bonham JR. The investigation of hypoglycemia during childhood. Gesellschaft für Neonatologie, pädiatrische Intensivmedizin, et al. Betreuung von Neugeborenen diabetischer Mütter. AWMF-Leitlinie Roe TF, NG WG, Smit PGA.

Disorders of carbohydrate and glycogen metabolism. In: Blau N, Duran M, Blaskovics ME, Gibson KM, eds. Berlin; Springer ; — Duran M. Disorders of mitochondrial fatty acid oxidation and ketone body handling.

Berlin, Springer ; — Birkebaek NH, Simonsen H, Gregersen N. Acta Paediatr ; —6. Ryan C, Gurtunca S, Becker D. Hypoglycemia: a complication of diabetes therapy in children. Pediatr Clin N Am ; — Diabetes Control and and Complications Trial Research Group.

Hypoglycemia in the Diabetes Control and Complications Trial. Bowker R, Green A, Bonham JR. Guidelines for the investigation and management of reduced level of consciousness in children: implications for clinical biochemistry laboratories.

Lang TF. Update on investigating hypoglycemia in childhood. Haverkamp GLG, Ijzerman RG, Kooter J, Krul-Poel YHM. The after-dinner dip. N Engl J Med ; 22 : —6. This must be taken into account during the clinical evaluation. A blood glucose test is a measure of glucose concentration present in an the blood of an individual at a given point of time.

Diagnostic laboratory tests for diabetes are Tab. Principle: the enzyme glucose oxidase catalyzes the oxidation of glucose to gluconic acid and H 2 O 2. In the subsequent peroxidase-mediated indicator reaction, H 2 O 2 oxidizes a reduced chromogen to produce a colored compound, which is measured using a photometer.

Principle: hexokinase in the presence of ATP phosphorylates glucose to form glucosephosphate. The latter reacts with NADP to form 6-phosphogluconate and NADPH 2. This reaction is catalyzed by glucosephosphate dehydrogenase GPD. The measurand is NADPH 2 , the increase in NADPH 2 is measured at the endpoint of the reaction.

The increase in absorbance determined is proportional to the glucose concentration in the test sample. Principle: glucose is oxidized to gluconolactone by Gluc-DH. The hydrogen released in the reaction is transferred to NAD, producing NADH 2.

The increase in NADH 2 is measured using the principle of continuous absorbance registration. The increase in absorbance is proportional to the glucose concentration in the test sample. In contrast to the end point method addition of mutarotase to the reagents is not necessary.

Gluc-DH only reduces β-D-glucose. In aqueous solution, glucose is present in the α- and β-form. As the β-D-glucose is consumed, an equilibrium between the two forms is established again as a function of time.

To prevent this reaction from becoming the determining factor for the speed of the Gluc-DH reaction, the reagent contains mutarotase. This enzyme accelerates the rate at which equilibrium is reached.

Biosensors are analytical devices that incorporate a biological material e. Principle of the glucose sensor: in the first step, glucose reacts with the oxidized form of the enzyme glucose oxidase GOD to form gluconic acid.

In this process, two electrons and two protons are released, and GOD is reduced. In the second step, O 2 which is present in the surrounding fluid reacts with GOD accepting the aforementioned electrons and protons leading to form H 2 O 2 and regenerating oxidized GOD, which is ready to react once more with glucose.

The glucose concentration in the test sample determines the amount of H 2 O 2. This is detected following oxidation at the surface of a platinum electrode which causes a change in the electrochemical potential.

Analyzers in which glucose is determined using readable strip and reflectance photometer are used for:. With the photometric measurement, glucose is enzymatically oxidized to gluconolactone by the enzymes glucose peroxidase or glucose dehydrogenase. The optimal sample is capillary blood.

Modern glucose meters for the self-monitoring of blood glucose allow the storage and processing of the measured values and the calculation of mean blood glucose MBG and mean amplitude of glucose excursions MAGE.

Continuous glucose monitoring CGM systems have been recognized as the ideal monitoring systems for glycemic control of diabetic patients. The CGM system measures blood glucose levels in subcutaneous tissue by attaching a CGM sensor to the skin, allowing the patient to make appropriate modifications to their medical interventions according to experience or empirically derived algorithms.

The principles of glucose sensing employed in the commercially available CGM systems are mainly electrochemical and employ the enzyme glucoseoxidase as the glucose sensing molecule with the combination of hydrogen peroxide monitoring or with the combination of redox mediator harboring hydrogel.

The blood level of glucose depends on the metabolic state of an individual. The following states are possible Tab. and the diagnostic significance of glucose in the fasting and postprandial state in:. This is due to intraindividual variations of blood glucose levels which are greater than those of other blood parameters as they are influenced by physical activity and the length of time since the last food intake.

The biological variability of plasma glucose is thus higher than the analytical imprecision. Moreover, the fasting plasma glucose concentration increases continuously with age from the third to the sixth decade of life.

Dysregulations such as insulin resistance, hyperinsulinism and diabetes as well as pregnancy further increase the variations. In newly diagnosed type 2 diabetics, the intraindividual variation of fasting glucose is The interpretation of blood glucose levels also depends on the type of sample examined.

The GI is a measure of how much 50 g of carbohydrate from a specific food raises the blood glucose level. The lower the GI, the less the concentration of blood glucose increases.

After consuming a certain food it is usually measured how high the increase of glucose is. A diet with a high GI is associated with an increased risk of cardiovascular disease and death. The glycemic load GL is the product of GI and the consumed carbohydrates and a measure of insulin needs.

The GL is calculated by multiplying the mean net carbohydrate intake as measured in grams per day by the GI and then dividing by Test procedure: Blood glucose increase is measured several times after ingestion of the specific food within 2 hours and compared with blood glucose increase after ingestion of 50 g glucose.

The assessment of GI is as follows:. The concentration of glucose in blood depends on the type of sample examined.

Arterial whole blood has a higher glucose concentration than venous blood; the glucose concentration of capillary whole blood sampled from the finger tip is in between the two.

Measurements in capillary whole blood and venous plasma result in similar glucose levels within the reference interval.

The following types of specimen are used in the different countries for determining blood glucose in routine diagnosis: Capillary whole blood, venous whole blood, and plasma from venous whole blood. Capillary whole blood: samples should be collected by skin puncture from the finger or from the heel infants only.

In the fasting state there is no arteriovenous difference between arterial and venous blood. Therefore, the concentrations measured in venous and capillary whole blood are nearly identical. Compared to glucose measured in plasma, the glucose concentration in whole blood is influenced by the hematocrit Hct , by proteins, lipoproteins and other dissolved and corpuscular components.

Venous plasma: the molality of glucose in whole blood and plasma is identical. Sensor variability in continuous glucose monitoring CGM : substantial variation is observed within sensors over time and across 2 different sensors worn simultaneously on the same individuals.

When comparing the same sensor at two different time points two 2-week periods, 3 months apart , the within-person coefficient of variation CVw in mean glucose was CVw for percent time in range was A constant factor of 1. This applies to a Hct of 0. In the case of higher Hct values, as are typical in neonates, this factor must be increased by multiplication by the following correction factor cf :.

With a Hct of 0. According to the IFCC, it is possible to convert whole blood glucose and biosensor glucose to plasma glucose, but not whole blood glucose to biosensor glucose Fig. According to recommendations of the WHO, the cutoffs for fasting glucose and for the oral glucose tolerance test are identical for capillary whole blood and venous plasma.

Fasting glucose : sampling 7 a. after at least 8 h of fasting. Capillary whole blood: only draw blood if blood circulation is good; finger must be warm. Venous blood: is analyzed in the form of whole blood, plasma, and serum.

In plasma and serum following blood collection is recommended in separator tubes. The collection tubes for determining glucose in whole blood contain NaF to prevent glycolysis, and potassium oxalate or Na 2 EDTA to inhibit clotting.

NaF acts by inhibiting glycolytic enzymes, in particular enolase, although the effect is minor in the first 2 h after blood collection. A better effect than with NaF alone is achieved by cooling the sample, by acidifying it, or by using citrate tubes for blood collection.

The reference method is the hexokinase method, or in some countries the glucose oxidase method. Possible methodological errors are shown in Tab. However, small amounts of icodextrin can get into the bloodstream via the lymphatic system.

In the bloodstream it is hydrolyzed to glucose oligomers such as maltose and maltotriose. These oligomers cause falsely high glucose readings in some point-of-care glucometers.

At 4 °C there is only a slight decrease during the first 2 h and approx. In EDTA-coated collection tubes there is no significant decrease within 24 h in the presence of maleinimide. At 4 °C blood deproteinized by perchloric acid gives stable values in the supernatant, obtained by centrifugation, for at least 5 days.

In newborns, measurement of blood glucose should be performed as soon as possible after blood collection, since the rate of glycolysis of erythrocytes in newborns is considerably higher than in adults so that the glycolysis inhibitors cannot be as effective.

The biological variation in plasma glucose levels results from complex interaction of genetically anchored metabolic processes that are subject to strict hormone-controlled regulation. The amplitude of glucose levels decreased with increasing concentrations. Between 6. Blood glucose: its measurement and clinical importance.

Clin Chim Acta ; 3— Weiner K. Whole blood glucose. What are we actually measuring. Ann Clin Biochem ; 1—8.

Reljic R, Ries M, Anic N, Ries B. New chromogen for assay of glucose in serum. Clin Chem ; —5. Kunst A, Draeger B, Ziegenhorn J.

UV-methods with hexokinase and glucosephosphate dehydrogenase. In: Bergmeyer HU, ed. Methods of enzymatic analysis. Weinheim: Verlag Chemie, Vol IV, — Vormbrock R. UV-method with glucose dehydrogenase. Weinheim: Verlag Chemie, Vol IV, —8. Turner APF, Chen B, Piletschy SA.

In vitro diagnostics in diabetes: meeting the challenge. Monnier L. Is postprandial glucose a neclected cardiovascular risk factor in type 2 diabetes? Eur J Clin Invest ; 30, Suppl 2: 3— Mensing C, Boucher J, Cypress M, Weinger K, Mulcahy K, Barta P, et al.

National standards for diabetes self-management education. Diabetes Care ; 28, Suppl 1: S72—9. Schlebusch H. Dezentrale Blutglucosebestimmungen im Krankenhaus. DG Klin Chem Mitt ; 91— Oliver NS, Toumazou C, Cass AEG, Johnston DG.

Glucose sensors: a review of current and emerging technology. Diabetic Medicine ; — Heck LJ, Erenberg A. Serum glucose levels in term neonates during the first 48 hours of life. J Pediatr ; — Diabetes Care ; 37, Suppl 1: S14—S Sacks DB, Bruns DE, Goldstein DE, Maclaren NK, McDonald JM, Parrott M.

Decreased sleep quality or quantity can lead to insulin resistance, increased ghrelin hunger hormone , decreased leptin fullness hormone , decreased physical activity, and increased inflammation.

These changes can increase your risk of diabetes, obesity, and cardiovascular disease. Several inherited lipid metabolism disorders affect how fats are used and stored in the body. Although fat, glucose, and protein metabolism all contribute to metabolic health, the two factors with the greatest impact on metabolism are maintaining stable blood sugar and getting enough exercise.

Insulin and exercise are anabolic. Insulin aids in storing excess energy as glycogen or fat. Exercise helps build muscle from protein.

Which carbohydrates you choose to consume, how they are packaged in your diet, and how your body metabolizes carbohydrates will all affect metabolism and the combination of glucose, fats, or proteins your body burns for energy.

Insulin resistance disrupts metabolism because glucose stays in your bloodstream instead of entering cells to be used for energy. Increased insulin levels lead to fat storage and weight gain.

Blood sugar is a key indicator of how well your metabolism is functioning. When you have metabolic flexibility , average and fasting glucose levels stay within an optimal range, and you experience minimal glucose spikes after eating. In this state, your metabolism is functioning well.

Optimally, you supply your body with the nutritional calories it needs to function without providing excess calories that are stored as fat. Excess calories contribute to obesity, a chronic disease that adversely affects metabolic health.

Knowing what the optimal number of calories you need and in what combination of fat, protein, and carbohydrates is the million-dollar question. Each person's metabolic response is unique, and it may fluctuate throughout the day in response to triggers such as diet, exercise, and stress.

Your basal metabolic rate BMR is the minimum number of calories your body needs to function at rest. People with a fast metabolism burn more calories at rest. Therefore, they have a higher BMR.

Conversely, people with a slow metabolism burn fewer calories at rest and have a lower BMR. However, having a higher BMR does not mean you will be thin. Carrying excess body weight makes your body work harder and therefore increases BMR.

Besides your BMR, your body's metabolic rate is determined by the thermic effect of food and energy used during physical activity. But, of course, this depends on how active you are.

Slower metabolism lower BMR means that you burn fewer calories at rest, which can increase your propensity for weight gain, but does it affect insulin resistance and blood sugar? In one animal study, researchers found that mice with lower BMRs had metabolism-specific pathways that increased their risk of developing insulin resistance and type 2 diabetes.

More research is needed to see if this also applies to humans. The biggest factors affecting your BMR are your fat-free mass FFM and fat mass FM. Having a faster metabolism is at least partially due to increased FFM.

Exercise also helps control blood sugar. More research is needed to determine if there are any stronger links between fast metabolism and blood sugar. Metabolic disorders affect how your body obtains energy from food. Metabolic disorders can be inherited or acquired.

Insulin resistance, prediabetes, and type 2 diabetes are on the spectrum of disorders that affect glucose metabolism and blood sugar. The World Health Organization classifies type 2 diabetes as a metabolic disorder.

Obesity is a risk factor for insulin resistance, prediabetes, and type 2 diabetes and is also classified as a metabolic disorder. Glycogen storage disease is an example of an inherited metabolic disorder that primarily affects glucose metabolism. Inherited metabolic diseases are usually due to a missing enzyme or vitamin that is essential for metabolism.

Metabolic syndrome is a cluster of risk factors that are specific to cardiovascular disease. Metabolic syndrome increases the risk of diabetes, heart disease, and stroke.

Obesity is the primary risk factor for metabolic syndrome. Metabolic syndrome is diagnosed when three of the following five health markers are no longer in the optimal range:.

These five markers are used to make a diagnosis of metabolic syndrome. Metabolic syndrome does not cause high blood sugar, but high blood sugar is one marker of metabolic syndrome. Metabolic health is defined by having all five markers in an optimal range without needing any medications to correct them.

When fat, muscle, and liver cells become insensitive to insulin, the pancreas works harder to pump out more insulin.

Eventually, the insulin-producing cells in the pancreas will burn out as they cannot keep up with the demand. As a result, blood glucose levels rise, inflammation increases, and when the pancreas can no longer compensate, type 2 diabetes develops.

Muscle cells absorb the majority of excess blood glucose, as long as they are sensitive to insulin. When muscle cells become inflamed from excess fatty acids, the liver picks up excess glucose.

If glycogen stores are full, excess glucose in the liver is stored as fat. Free fatty acids increase in the blood, which makes the liver and muscle more insulin resistant.

Diet, exercise, and body weight all impact metabolic health and metabolism. Since diet and exercise affect body weight and blood sugar, it is important to work on all three as you journey towards better metabolic health.

A healthy diet can reduce post-meal glucose spikes. Dietary tips for better glucose control: Exercise reduces stress, improves insulin sensitivity, and helps with weight management.

Even walking can help with weight loss. The American College of Sports Medicine ACSM 18 and the U. Department of Health and Human Services Physical Activity Guidelines 19 jointly recommend the following:.

Even small amounts of weight loss can improve your metabolic health and blood sugar. Weight management tips: 20, If you can only improve in one of these areas, start with your diet. You can't out-exercise a bad diet. Learn more in this podcast with Nicole Aucoin from Healthy Steps Nutrition.

Track your progress towards better metabolic health and blood sugar using a continuous glucose monitor CGM. Leann Poston, MD, is a licensed physician in Ohio who holds an MBA and an M. She is a medical writer and educator who researches and writes about medicine, education, and healthcare administration.

Please note: The Signos team is committed to sharing insightful and actionable health articles that are backed by scientific research, supported by expert reviews, and vetted by experienced health editors.

The Signos blog is not intended to diagnose, treat, cure or prevent any disease. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider. Read more about our editorial process and content philosophy here. Take control of your health with data-backed insights that inspire sustainable transformation.

Your body is speaking; now you can listen.

gov means Speed enhancement tips official. Federal Healthy sugar substitutes for smoothies websites often end in. gov or. Before Carbohyrate sensitive information, make sure you're on a federal government site. The site is secure. NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

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