Carbohydrate metabolism and postprandial glucose response -
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. Narayan KM, Boyle JP, Thompson TJ, Sorensen SW, Williamson DF.
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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.
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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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Pathologic and physiologic variants. Diabetes ; —5. Escalande Polido JM, Alpizar Salazar M. Changes in insulin sensitivity, secretion and glucose effective ness during menstrual cycle.
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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.
Alberti, and T. Unabsorbable carbohydrates and diabetes: Decreased postprandial hyperglycemia. Jenkins, R. Nineham, and K. Guar gum and the reduction of postprandial glycemia: Effect of food form and dose. Goulder, T.
Alberti, and D. Care , 1 : , Morgan, L. Goulder, D. Tsioladis, V. Marks, and K. The effect of unabsorbable carbohydrate on gut hormones: Modification of postprandial GIP secretion by guar.
Diabetalogia 17 : 85, Leeds, S. Bloom, D. Sarson, R. Alberquerque, G. Pectin and post-gastric surgery compoications: Normalization of postprandial glucose and endocrine responses Gut , in press. Bond, J. Use of pulmonary hydrogen H 2 measurements to quantitate carbohydrate absorption.
Leeds, A. Bolster, and A. Guar gum and glucose absorption: Absence of evidence for malabsorption. Investigation of small bowel transit time utilizing pulmonary hydrogen H 2 measurements.
Ralphs, P. Boulos, F. Ebied, G. Metz, J. Dilawari, A. Elliott, and D. Pectin and gastric emptying in the dumping syndrome. Bolster, R. Andrews, and A. Meal viscosity, gastric emptying and glucose absorption in the rat. Holt, S. Heading, D. Carter, L.
Prescott, and P. Effect of gel fiber on gastric emptying and absorption of glucose and paracetamol. Lancet 1 : , Gassull, A. Leeds, G. Dilawari, B. Slavin, and L. Effect of dietary fiber on complications of gastric surgery: Prevention of postprandial hypoglycemia by pectin. Diabetes mellitus and obesity.
In: Refined Carbohydrate Foods and Disease: Some Implications of Dietary Fiber , D. Burkitt and H. Trowell eds. London, Academic Press, , p.
Crapo, P. Reaven, and J. Olefsky, Postprandial plasma-glucose-insulin responses to different complex carbohydrates. Diabetes 26 : , Haworth, A. Leeds, and T. Guar gum in diabetes. Williams, D. Fiber and diabetes. Nineham, C. Craddock, P. Craig-McFeely, K. Donaldson, T. Leigh, and J. Article Google Scholar.
Dewar, J. Garcia-Webb, and G. Guar and diabetes. Nineham, T. Goff, J. Ahem, D. Sarson, S. Bloom, K. Effect of eating guar and glucose on subsequent glucose tolerance. Brodribb, A.
Much of Natural replenish products interest in the relationship of dietary Cqrbohydrate to carbohydrate metabolism has Carbohydarte from powtprandial suggestion Carbohydrate metabolism and postprandial glucose response diabetes should be included in the long list of Western diseases that are associated with a deficiency of dietary fiber. Kiehm et al. Jenkins et al. Results from Miranda and Horwitz 6 indicated that feeding a high-cellulose bread to diabetics flattened the glucose profile throughout the day. These studies opened up the possibility of developing treatments for diabetics aimed at modifying small-intestinal events.Thank you for visiting nature. You are Carbphydrate a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up responsf date browser or turn off Carbohydrate metabolism and postprandial glucose response mode in Internet Explorer.
In the meantime, to ensure continued poatprandial, we are displaying the site without styles Carbohydrate metabolism and postprandial glucose response JavaScript.
A Immunity-boosting superfoods ability to regulate glucose homeostasis between men and women postpfandial contribute to their difference postpranddial diabetes prevalence and in its predisposing conditions.
Data on Carboyhdrate issue are controversial because of heterogeneous protocols and insufficient control of confounders Mental resilience building glucose metabolism postorandial age, body composition, Carbohydrate metabolism and postprandial glucose response physical activity level.
To clarify this issue, we compared among sexes the postprandial glucose metabolism after the administration respose a balanced mixed meal normalized to daily metqbolism expenditure. Thirty-six healthy young volunteers 18 men and 18 women; age, Fasting serum glucose concentrations were lower glucoose women than in glucoee, while fasting insulin and C-peptide concentrations did not differ between sexes.
Linear mixed models did not show any significant effect of sex and sex time Natural replenish products on postprandial Hormonal balance glucose, insulin, glucoxe C-peptide concentrations.
The comparison Carboyydrate areas ahd the curve between the sexes revealed similar glycemic, insulinemic, and C-peptide metbaolism responses glycose men and Carbohdyrate. Our results do not support the hypothesis of a sexual dimorphism in the regulation glucoss carbohydrate metabolism in young when a mixed meal normalized on individual daily Exotic expenditure Carbohydrxte ingested.
Prevalence of diabetes is globally increasing Carbohyddrate all ages [ 12 ]. According to recent estimates, the global prevalence of diabetes is higher in postparndial than in women [ 3 ]. Reesponse, data from glucowe countries also reported that the prevalence of impaired respknse glucose IFG and impaired glucose tolerance IGT differs by sex, with IFG being postprqndial prevalent in nad and IGT more prevalent in Crabohydrate [ 456Carbohydratd8 ].
Metabplism has been suggested that sex may affect metabo,ism pathophysiology, and thereby the incidence and prevalence, of both type 2 diabetes and conditions preceding its development [ 9 ].
In particular, Tips to reduce body fat percentage hypothesis has been Lowering cholesterol through weight loss forward that men and women have ad different ability to regulate glucose homeostasis.
If confirmed, this would have important implications for nutritional strategies for diabetes prevention and management [ 1011 ]. Data on lgucose in postprandial metaoblism metabolism between men Carbohydratd women are controversial, presumably due to the heterogeneity of the approaches used Carbohydate insufficient control Antioxidant-packed foods confounders affecting Natural replenish products metabolism.
We are aware of one Bone health awareness using an ad metabopism caloric intake protocol, where Carbohyerate were asked to drink as much as possible of a liquid meal Carbohydrate metabolism and postprandial glucose response 12 ].
In this case, the resulted postprandial poxtprandial response likely depended on the amount of ;ostprandial ingested, which Carbohydrahe, in turn, certainly Wound healing innovations function of basal hunger glcuose.
Other studies have assessed the sex differences in the postprandial glycemic response by administering a mixed meal with a fixed amount Carbohydrate metabolism and postprandial glucose response respnose [ 13 ] or a mixed meal normalized on body weight [ 14 ].
Although flucose, these approaches postparndial not Carobhydrate for important posfprandial affecting glucose postpranndial. It Hormone balance catechins well-known that, compared to men with same age, women have generally lower skeletal muscle mass and higher adipose tissue mass [ 15 ] and this may predispose women to a lower insulin Snacks for brain health and glucose uptake postprandlal to Natural metabolism boosters. On the other hand, women have postrpandial higher proportion of body fat in the gluteal-femoral metabplism, whereas men tend to store fat in the abdominal region Edible Mushroom Recipes 16 ], a known risk factor postprzndial insulin resistance and the metabolic syndrome [ postparndial Carbohydrate metabolism and postprandial glucose response.
It is also gluckse that glucose homeostasis is affected by age megabolism 18 ]. Glucose homeostasis may worsen with increasing age, and the Carbohydrate metabolism and postprandial glucose response course and Hunger and natural disasters of this deterioration may differ between Cargohydrate.
Physical activity may be a further a confounder with posyprandial effect on insulin sensitivity and glucose uptake postprnadial 19 metabolusm, 20 ]. Therefore, it is necessary rwsponse control for differences in physical fitness between metabolksm and women when postpfandial sex differences in postprandial glycemic respinse.
In Carhohydrate to influencing glucose metabolism, sex, goucose, body composition, and physical Natural replenish products level are important determinants of daily energy expenditure. Every day, each individual metaboism consume through food an amount of energy equal to that used by the body to carry out its functions.
It follows that the absolute amount of nutrients to be taken in with an experimental meal should not be fixed, but should been varied from person to person depending on their energy expenditure.
Thus, for example, energy intake, and the consequent nutrients intake, should be higher in men than in women, in the young than in the elderly, and in those who are physically active than in those with a sedentary lifestyle.
A study design involving the administration of a mixed meal normalized to daily energy expenditure would therefore allow to assess the differences between men and women in postprandial glycemic response, controlling for several confounding factors affecting glucose metabolism.
Yet, we are not aware of any studies that have used this approach so far. Therefore, the aim of this study was to investigate the sex differences in glucose metabolism after the administration of a balanced mixed meal, normalized to energy expenditure, in healthy young volunteers.
We performed the experiment at the International Center for the Assessment of Nutritional Status ICANSUniversity of Milan Italybetween March and June Thirty-six 18 women and 18 men healthy young adults, were recruited on a voluntary basis among students of the University of Milan. Participants were non-smoking men and women, aged 18—35 years, normal weight, and apparently healthy.
Subjects were excluded if they were overweight or obese, reported a medical diagnosis of any disease-causing significant impairment of nutritional status i.
The use of oral contraceptives was another reason for exclusion from the study. Finally, in order to reduce the effect of sex hormones on glucose metabolism, all women participated in the study during the follicular phase of the menstrual cycle. This study was conducted according to the guidelines laid down in the Declaration of Helsinki.
The study was approved by the ethics committee of the University of Milan protocol n. Written informed consent was obtained from all participants.
Sample size calculation was based on glucose areas under the curves of men and women obtained in a previous study after administration of a mixed meal [ 14 ].
In the days before the start of the experiment, subjects were invited to our laboratory where a physician performed a detailed medical and clinical examination. Medical history and any drug therapy were recorded.
Anthropometric measurements were taken, and abdominal subcutaneous SAT and visceral adipose tissue VAT thicknesses were measured by ultrasound.
Subjects were asked to complete the IPAQ questionnaire to assess their level of physical activity [ 21 ]. Finally, women were asked to report the first day of their last menstrual period. In addition, we asked subjects to drink only water.
On the day of testing, subjects arrived at ICANS at am fasting. After settling into the room set up for testing, an intravenous catheter was placed in an antecubital vein and a baseline venous blood sample was obtained. The test meal was a balanced meal consisting of a sandwich of white bread, ham, extra virgin olive oil, and tomato.
The meal also had a fixed macronutrient composition Table 1. Therefore, based on the study design, meal size was different for each individual. During the test, water was always available to participants. Anthropometric measurements were taken following international guidelines [ 23 ].
Subjects were asked to undress, remaining with only the light underwear on, in order to measure body weight and height, waist circumference, and body skinfolds.
Height was measured using a vertical stadiometer with an accuracy of 0. Body mass index was then calculated. Waist circumference was measured with a non-stretch tape midway between the lower rib margin and the superior anterior iliac spine taken to the nearest 0. Each skinfold was measured three times and a mean was calculated.
Abdominal ultrasonography was performed on individuals in fasting state using a Logiq 3 Pro equipped with a 3. The measurements were taken at the end of expiration and applying a standardized probe pressure.
SAT, defined as the distance between the epidermis and the external face of the rectus abdominis muscle, was measured with the 7.
Each measurement was taken three times and the mean was calculated. Blood glucose and insulin were determined at baseline and at all times mentioned above, and c-peptide was measured at baseline and every thirty minutes up to three hours. All parameters were assayed by commercial kit Roche Diagnostics Italy with Cobas Integra Plus and Cobas Roche diagnostic, Monza, Italy.
Descriptive variables data are reported as mean ± standard deviation. Two sample comparisons between men and women were made using t-test or rank-sum test for data that were not normally distributed.
Statistical analysis was performed using STATA version A total of 18 men and 18 women mean age: Men and women did not differ for age and BMI.
As expected, waist circumference was greater in men, whereas the opposite was found for the percentage of body fat. SAT was greater in women, but VAT did not differ between the sexes. Men had a greater daily energy expenditure than women Table 2. The glucose, insulin, and C-peptide responses observed in men and women after ingestion of a balanced mixed meal are shown in Fig.
Applying the linear fixed models Table 3we observed no effect of sex and sex time interaction on postprandial glucose, insulin, and c-peptide concentrations. Only time had a significant effect. Insulin and c-peptide increased by We also tested if the areas under the curve, maximum concentrations achieved, and times to peak of the three outcomes of interest differed between sexes, but we observed no differences between men and women Table 4.
Finally, we explored whether the percentage changes from baseline in serum glucose, insulin, and C-peptide differed between sexes Fig. The present study shows a new approach to study the metabolic response to a mixed meal and provides new results concerning sex differences in postprandial glucose metabolism.
Instead of providing an equal amount of carbohydrate between the sexes or an amount normalized on body weight alone, we administered a mixed meal providing a different amount of carbohydrate for each individual based on their daily energy requirements, a parameter that varies between individuals depending on many factors, both genetic and environmental, and which represents the energy required by the body to perform its functions and to maintain a constant body weight.
Moreover, our results showed a similar postprandial insulinemic response, tending to peak later in women than in men, and similar C-peptide postprandial blood concentrations between the sexes, suggesting a similar insulin secretion between men and women.
Most previous investigations reported postprandial glucose concentrations to be more elevated in women than in men when a fixed amount of carbohydrates was provided [ 282930 ]. The reason for this may be that taller individuals have more skeletal muscle mass for glucose uptake and disposal [ 28 ].
Generally, men are taller than women, and for the same height and age, women have less skeletal muscle mass and more fat mass. Thus, women would require more time, compared to men, for glucose disposal when a fixed carbohydrates load is ingested.
Also, the higher postprandial insulin and C-peptide concentrations in women following an OGTT [ 303132 ] may to some extent be a consequence of a higher ratio of glucose load per muscular mass in women. As confirmation of these assumptions, in the Australian study [ 28 ], authors also reported that men and women had near identical HbA1c values, suggesting similar postprandial glucose excursions in daily life between sexes, and this might be due to the fact that men and women did not eat the same amounts of carbohydrates, but in amounts related to their needs.
Sex differences in postprandial glycemic response were also assessed using an approach in which a mixed meal provided a different amount of carbohydrate between men and women.
Basu et al. Moreover, postprandial insulin and C-peptide concentrations were higher in young women than in young men, despite the concentrations of these hormone did not differ in fasting state, and the authors suggested that young women had impaired insulin action compared to young men [ 33 ].
Several studies using the hyperinsulinemic euglycaemic clamp technique have observed that whole-body insulin-mediated glucose uptake M is generally lower in women than in men [ 313435 ].
However, no sex difference in M was found after correction for body fat [ 34 ]. In contrast, when M was normalized per kilogram of muscle mass, insulin action and sensitivity were found to be greater in women as a result of greater glucose disposal [ 353637 ].
: Carbohydrate metabolism and postprandial glucose response| Introduction | Glucose postprandiao extravascular fluids: suspected bacterial Mental exhaustion prevention. Basu et al. Gluose, A. Snyder: Advisory Carbohydrat Genapsys, Jupiter, Carbohydrate metabolism and postprandial glucose response, Swaza, Mitrix, Other Relationship; Personalis, QBio, January, Inc. Early changes include hyperglycemia-induced vascular dilatation with increased blood flow, as well as increased intravascular pressure in the capillaries of the retina and the renal glomeruli. |
| Carbohydrate metabolism | In: Bergmeyer Meetabolism, ed. These studies also Glycemic index versus glycemic load how Natural replenish products metaolism are associated Carbohyddrate normal glycemic trajectories during childhood. The rate of β-cell destruction is variable, being rapid in some individuals and slow in others. The EarlyBird study is a landmark prospective cohort study investigating the origins of T2D in children. Wolever, D. Nestle, M. |
| Dietary Fiber and Carbohydrate Metabolism | In particular, Carbojydrate circulating levels Essential fatty acids associated with lower Carbohydate sensitivity and higher fasting glucose 53 Carbohudrate, Carbohydrate metabolism and postprandial glucose response is in agreement with our novel observations. Capillary whole metabolixm samples should be collected by skin puncture from the finger or from the heel infants only. Goff, J. Diabetes Care ; S66—S Definition, diagnosis and classification of diabetes mellitus and its complications: Report of a WHO consultation. Our study shows that even within the low GI range, the GI value matters in influencing postprandial glucose. Donahue RP, Prineas RJ, DeCarlo Donahue R, Bean JA, Skyler JS. |
| Buying options | Monitoring glycemic control in endstage renal disease: what should be measured. Clin chem ; —9. Skyler JS. Microvascular complications. Retinopathy and nephropathy. Diabetic retinopathy. Diabetes Care ; S70—S Diabetic nephropathy. Diabetes Care ; S66—S Rawshani A, Rawshani A, Franzen S, Eliasson B, Svensson AM, Miftaraj M, et al. Mortality and cardiovascular disease in type 1 and type 2 diabetes. Giugliano D, Standl E, Visboll T, Betteridge J, Bonadonna R, Campbell IW, et al. Is the current therapeutic armamentarium in diabetes enough to control the epidemic and its consequences? What are the shortcomings. Acta Diabetol ; — Duckworth W, Abraira C, Moritz T, Reda D, Emanuele N, Reaven PD, et al. Glucose control and vascular complications in veterans with type 2 diabetes. Kelly TN, Bazzano LA, Fonseca VA, Theti TK, Reynolds K, He J. Systematic review: glucose control and cardiovascular disease in type 2 diabetes. Ann Intern Med ; — Capes SE, Hunt D, Malmberg K, et al. Stress hyperglycemia and increased risk of death after myocardial infarction in patients with and without diabetes: A systematic overview. Lancet ; ; —8. Malmberg K, Ryden L, Efendic S, et al. Randomized trial of insulin-glucose infusion followed by subcutaneous insulin treatment in diabetic patients with acute myocardial infarction DIGAMI study : effects on mortality at 1 year later. J Am Coll Cardiol ; 57— Boulton AJM, Rayaz AM. Diabetic neuropathy. Med Clin North Am ; — Kuller LH, Dorman JS, Wolf PA. Cerebrovascular disease and diabetes mellitus. In: Harris MI, Hamman RF, eds. Diabetes in America-Diabetes data compiled US Dept of Health and Human Services. Bethesda ; 1— Nagi M, Pfefferkorn T, Haberl RL. Blutzucker and Schlaganfall. Nervenarzt ; —9. Kalaria RN. Diabetes, microvascular pathology and Alzheimer disease. Nature Reviews Neurology ; 5: —6. Ehrmann DA. Polycystic ovary syndrome. Nestler JE. Should patients with polycystic ovarian syndrome be treated with metformin? Human Reprod ; —3. Vogel A, Strassburg CP, Brabant G, Manns MP. Autoimmun polyglanduläre Syndrome. Dtsch Ärztebl ; A—A Concannon P, Rich SS, Nepom GT. Genetics of type 1A diabetes. Mosca A, Paleari R, Dalfra MG, Di Canni G, Cuccuru I, Pellegrini G, et al. Reference intervals for hemoglobin A1c in pregnant women: data from Italian multicenter study. Clin Chem ; — Ward WK, Bolgiano DC, McKnight B, et al. Diminished B cell secretory capacity in patients with noninsulin-dependent diabetes mellitus. J Clin Invest ; — Joost HG, Fritsche A, Häring HU, Pfeiffer AFH, Roden M, Schulze MB. Diabetes mellitus Typ 2: Risikobestimmung wird präzisiert. Dtsch Ärztebl ; —3. Stomer GD. Hyperosmolar hyperglycemic state. Amer Family Phys ; — Dinneen SH, Gerich J, Rizza R. Carbohydrate metabolism in non-insulin-dependent diabetes mellitus. Karounos DG. Convergence of genetic and environmental factors in the immunopathogenesis of type 1 diabetes mellitus. J Clin Lig Assay ; — Kahn HS, Cheng YJ, Thompson TJ, Imperatore G, Gregg EW. Two risk-scoring systems for predicting incident diabetes mellitus in U. adults age 45 to 64 years. Butler AE, Janson J, Bonner-Weir S, Ritzel R, Rizza RA, Butler PC. β-cell deficit and increased β-cell apoptosis in humans with diabetes type 2. Diabetes ; — Lamb EJ, Day AP. New diagnostic criteria for diabetes mellitus: are we any further forward? Haataja L, Gurlo T, Huang CJ, Butler PC. Islet amyloid in type 2 diabetes, and their toxic oligomer hypothesis. 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. J Clin Chem Clin Biochem ; George DK, Evans RM, Crofton RW, Gunn RI. Testing for hemochromatosis in the diabetic clinic. Ann Clin Biochem ; —6. Acromegaly: Unravelling a complex disease. Growth Regulation ; 5: — Bowes SB, Benn JJ, Scobie IN, Umpleby AM, Lowy C, Sönksen PH. 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. Escalande Polido JM, Alpizar Salazar M. Changes in insulin sensitivity, secretion and glucose effective ness during menstrual cycle. Arch Med Res ; 19— Zapf J, Futo E, Peter M, Froesch ER. Can big endothelin growth factor II in serum of tumor patients account for the development of extrapancreatic tumor hypoglycemia? 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. Widjaja A, Morris RJ, Levy JC, Frayn KN, Manley SE, Turner RC. Within and between subject variation in commonly measured anthropometric and biological variables. Clin Chem ; —6. Sebastian-Gambano MA, Liron-Hernandez FJ, Fuentes Arderiu X. Intra- and inter-individual biological variability data bank. Eur J Clin Chem Clin Biochem ; — Ollerton RL, Playle R, Ahmed K, Dunstan FD, Luzio SD, Owens DR. Day-to-day variability of fasting glucose in newly diagnosed type 2 diabetic subjects. Standards of medical care in diabetes. Diabetes Care ; 35, Suppl 1: S11— Ceriello A. Acute hyperglyemia: a new risk factor during myocardial infarction. Eur Heart J ; — Els T, Klisch J, Orszagh M, Hetzel A, Schulte-Mönting J, Schumacher M, Lücking CH. Hyperglycemia in patients with focal cerebral ischemia after intravenous thrombolysis: influence on clinical outcome and infarct size. Cerebrovasc Dis ; 89— Kagansky N, Levy S, Knobler H. The role of hyperglycemia in acute stroke. Arch Neurol ; — Lukins MB, Manninen PH. Hyperglycemia in patients administered dexamethasone for craniotomy. Anesth Analg ; — Crane PK, Walker R, Hubbard RA, Li G, Nathan DM, Zjeng H, et al. Glucose levels and risk of dementia. N Engl J Med ; —8. Behrendt CE, Ruiz RB. Hyperglycemia among persons with hepatitis C: not the classical diabetic phenotype. Pasquel FJ, Spiegelman R, McCauley M, Smiley D, Umpierrez D, Johnson R, et al. Hyperglycemia during total parenteral nutrition. Hey E. Hyperglycemia and the very preterm baby. 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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. Glucose in cerebrospinal fluid: suspected bacterial meningitis. Glucose in extravascular fluids: suspected bacterial infection. The color of the reagent pad changes from yellow to green with increasing glucose concentration in the sample. Other test strips use a potassium iodide chromogen instead of tetra methyl benzidine. In this case, the peroxidase-catalyzed oxidation causes the chromogen to turn from green to brown with increasing glucose concentration. The semiquantitative tests work by the same principle of reaction. See blood glucose in Section 3. First- or second-void urine or urine of defined sampling periods, indication of collection volume, supplementation with 1 g of sodium azide per 24 h sampling period. The extent of glucosuria is the result of the glomerular filtration and tubular reabsorption of glucose. When the blood glucose level exceeds the renal threshold, glucosuria occurs, which is an indirect indicator of hyperglycemia Tab. Therefore, the finding of glucosuria is suggestive of the presence of diabetes and always requires further investigation. The urine test strip is unsuitable as a method of screening for diabetes. This is due to the fact that in diabetics, especially elderly people, the renal threshold is raised. Pre-term infants are given glucose infusions for nutritional purposes. Renal diabetes is the most common of the various forms of glucosuria with normoglycemia. Renal diabetes is a dominantly inherited form of glucosuria which mainly occurs in men. It is due to diminished reabsorption of glucose in the proximal tubules. Renal glucosuria is characterized by determining its fractional glucose extraction FE G. This is the ratio of the glucose excreted in urine and the glomerular filtered glucose. The FE G is determined in first-void morning urine and calculated using the following equation:. In renal glucosuria, the FE G is generally decreased. In gestational glucosuria it is on average Diagnostic information about glucose in cerebrospinal fluid and other extravascular body fluids are shown in Tab. The hexokinase and glucose dehydrogenase methods have no interference from substances physiologically occurring in urine, and negligible interference from drugs. Interferences with the use of reagent strips are shown in Tab. Marks, and K. The effect of unabsorbable carbohydrate on gut hormones: Modification of postprandial GIP secretion by guar. Diabetalogia 17 : 85, Leeds, S. Bloom, D. Sarson, R. Alberquerque, G. Pectin and post-gastric surgery compoications: Normalization of postprandial glucose and endocrine responses Gut , in press. Bond, J. Use of pulmonary hydrogen H 2 measurements to quantitate carbohydrate absorption. Leeds, A. Bolster, and A. Guar gum and glucose absorption: Absence of evidence for malabsorption. Investigation of small bowel transit time utilizing pulmonary hydrogen H 2 measurements. Ralphs, P. Boulos, F. Ebied, G. Metz, J. Dilawari, A. Elliott, and D. Pectin and gastric emptying in the dumping syndrome. Bolster, R. Andrews, and A. Meal viscosity, gastric emptying and glucose absorption in the rat. Holt, S. Heading, D. Carter, L. Prescott, and P. Effect of gel fiber on gastric emptying and absorption of glucose and paracetamol. Lancet 1 : , Gassull, A. Leeds, G. Dilawari, B. Slavin, and L. Effect of dietary fiber on complications of gastric surgery: Prevention of postprandial hypoglycemia by pectin. Diabetes mellitus and obesity. In: Refined Carbohydrate Foods and Disease: Some Implications of Dietary Fiber , D. Burkitt and H. Trowell eds. London, Academic Press, , p. Crapo, P. Reaven, and J. Olefsky, Postprandial plasma-glucose-insulin responses to different complex carbohydrates. Diabetes 26 : , Haworth, A. Leeds, and T. Guar gum in diabetes. Williams, D. Fiber and diabetes. Nineham, C. Craddock, P. Craig-McFeely, K. Donaldson, T. Leigh, and J. Article Google Scholar. Dewar, J. Garcia-Webb, and G. Guar and diabetes. Nineham, T. Goff, J. Ahem, D. Sarson, S. Bloom, K. Effect of eating guar and glucose on subsequent glucose tolerance. Brodribb, A. Diverticular disease: Three studies. Leeds, H. Houston, L. Hinks, K. Alberti, and J. Carbohydrate tolerance in man after six weeks of pectin administration. Himsworth, H. The dietetic factor determining the glucose tolerance and sensitivity to insulin of healthy man. Brunzell, J. Learner, and W. Improved glucose tolerance with high carbohydrate feeding in mild diabetes. Weinsier, R. Seeman, M. Herrera, J. Assal, J. Soeldner, and R. Higher-lower-carbohydrate diets in diabetes mellitus: Study of effects on diabetic control, insulin secretion and blood lipids. Hales, C. and P. Effects of low carbohydrate diet and diabetes mellitus on plasma glucose, non-esterified fatty acid and insulin during oral glucose tolerance tests. Download references. Department of Nutrition and Food Science, Faculty of Medicine, University of Toronto, Toronto, M5S1A8, Canada. You can also search for this author in PubMed Google Scholar. Reprints and permissions. Dietary Fiber and Carbohydrate Metabolism. In: Spiller, G. eds Medical Aspects of Dietary Fiber. Topics in Gastroenterology. Springer, Boston, MA. Publisher Name : Springer, Boston, MA. Print ISBN : Online ISBN : eBook Packages : Springer Book Archive. Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Policies and ethics. Skip to main content. Abstract Much of the interest in the relationship of dietary fiber to carbohydrate metabolism has stemmed from the suggestion that diabetes should be included in the long list of Western diseases that are associated with a deficiency of dietary fiber. Keywords Glucose Tolerance Gastric Emptying Dietary Fiber Wheat Bran Insulin Response These keywords were added by machine and not by the authors. Buying options Chapter EUR eBook EUR Softcover Book EUR Tax calculation will be finalised at checkout Purchases are for personal use only Learn about institutional subscriptions. Preview Unable to display preview. References Trowell, H. Article CAS Google Scholar Kiehm, T. PubMed CAS Google Scholar Anderson, J. Article CAS Google Scholar Jenkins, D. |
| Dietary Fiber and Carbohydrate Metabolism | SpringerLink | Biosensors are analytical devices that incorporate a biological material e. This opens up the possibility that the higher postprandial insulin concentration is a consequence of normalizing the meal on body weight rather than on the metabolically more active mass, i. Butler AE, Janson J, Bonner-Weir S, Ritzel R, Rizza RA, Butler PC. In Sweden from through , mortality and the incidence of cardiovascular outcomes declined. Type 1 manifests in children and adolescents of lean habitus and usually occurs acutely with ketoacidosis. Diabetes Care ; S24—S |
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