The Disposal of an Oral Glucose Load in Healthy Subjects: A Quantitative Study

Ferrannini, Eleuterio; Björkman, Ola; Reichard, George A.; Pilo, A.; Olsson, Maggie; Wahren, John; DeFronzo, Ralph A.

doi:10.2337/diab.34.6.580

Cited by 318 publications

(113 citation statements)

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“…On the other hand, tissue-specific glucose utilisation may differ between insulin-resistant and insulin-sensitive individuals. For instance, splanchnic glucose disposal is mostly driven by hyperglycaemia [15], which will increase the proportion of glucose taken up by this tissue. Then insulin-resistant individuals, having elevated glycaemia, may have increased splanchnic glucose disposal compared with insulin-sensitive individuals.…”

Section: Discussionmentioning

confidence: 99%

Postprandial whole-body glycolysis is similar in insulin-resistant and insulin-sensitive non-diabetic humans

Galgani

Ravussin

2011

Diabetologia

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Aims/hypothesis Insulin resistance is characterised by impaired glucose utilisation when measured by a euglycaemic–hyperinsulinaemic clamp. We hypothesised that, in response to postprandial conditions, non-diabetic individuals would have similar intracellular glycolytic and oxidative glucose metabolism independent of the degree of insulin resistance. Methods Fourteen (seven male) sedentary, insulin-sensitive participants (mean±SD: BMI 25±4 kg/m2; age 39±10 years; glucose disposal rate 9.4±2.1 mg [kg estimated metabolic body size]−1 min−1) and 14 (six male) sedentary, non-diabetic, insulin-resistant volunteers (29±4 kg/m2; 34±13 years; 5.3±1.2 mg [kg estimated metabolic body size]−1 min−1) received after a 10 h fast 60 g glucose plus 15 g [6,6-2H2]glucose. Serum glucose and insulin concentrations, plasma 2H enrichment and whole-body gas exchange were determined before glucose ingestion and hourly thereafter for 4 h. Plasma 2H2O production is an index of glycolytic disposal. On day 2, participants received a weight-maintenance diet. On day 3, a euglycaemic–hyperinsulinaemic clamp was performed. Results Insulin-resistant individuals had about a twofold higher postprandial insulin response than insulin-sensitive individuals (p=0.003). Resting metabolic rate was similar in the two groups before (p=0.29) and after (p=0.33–0.99 over time) glucose ingestion, whereas a trend for blunted glucose-induced thermogenesis was observed in insulin-resistant vs insulin-sensitive individuals (p=0.06). However, over the 4 h after the 75 g glucose ingestion, glycolytic glucose disposal was the same in insulin-sensitive and insulin-resistant individuals (36.5±3.7 and 36.2±6.4 mmol, respectively; p=0.99). Similarly, whole-body carbohydrate oxidation did not differ between the groups either before or after glucose ingestion (p=0.41). Conclusions/interpretation Postprandial hyperinsulinaemia and modest hyperglycaemia overcome insulin resistance by enhancing tissue glucose uptake and intracellular glucose utilisation.

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Section: Discussionmentioning

confidence: 99%

Postprandial whole-body glycolysis is similar in insulin-resistant and insulin-sensitive non-diabetic humans

Galgani

Ravussin

2011

Diabetologia

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“…Parameters were set assuming that kinetics for 13 C-glucose appearance in blood after ingestion of a 13 C-labelled glucose load apply to the ingestion of a 13 C-labelled fructose load, as well [23]. …”

Section: Methodsmentioning

confidence: 99%

Metabolic Fate of Fructose Ingested with and without Glucose in a Mixed Meal

et al. 2014

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Ingestion of pure fructose stimulates de novo lipogenesis and gluconeogenesis. This may however not be relevant to typical nutritional situations, where fructose is invariably ingested with glucose. We therefore assessed the metabolic fate of fructose incorporated in a mixed meal without or with glucose in eight healthy volunteers. Each participant was studied over six hours after the ingestion of liquid meals containing either 13C-labelled fructose, unlabeled glucose, lipids and protein (Fr + G) or 13C-labelled fructose, lipids and protein, but without glucose (Fr), or protein and lipids alone (ProLip). After Fr + G, plasma 13C-glucose production accounted for 19.0% ± 1.5% and 13CO2 production for 32.2% ± 1.3% of 13C-fructose carbons. After Fr, 13C-glucose production (26.5% ± 1.4%) and 13CO2 production (36.6% ± 1.9%) were higher (p < 0.05) than with Fr + G. 13C-lactate concentration and very low density lipoprotein VLDL 13C-palmitate concentrations increased to the same extent with Fr + G and Fr, while chylomicron 13C-palmitate tended to increase more with Fr + G. These data indicate that gluconeogenesis, lactic acid production and both intestinal and hepatic de novo lipogenesis contributed to the disposal of fructose carbons ingested together with a mixed meal. Co-ingestion of glucose decreased fructose oxidation and gluconeogenesis and tended to increase 13C-pamitate concentration in gut-derived chylomicrons, but not in hepatic-borne VLDL-triacylglycerol (TG). This trial was approved by clinicaltrial. gov. Identifier is NCT01792089.

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“…5 ), knowledge of the mechanisms that mediate the postprandial suppression of both processes is relevant to understanding the hyperglycaemia observed in diabetes mellitus. Net hepatic glucose uptake, as measured by splanchnic arteriovenous balance and tracer methods, is estimated to be approximately one-third of a moderate enteral glucose load in humans and dogs 2,4,6–9 . However, the liver also contributes to the systemic disposal of an enteral glucose load through the suppression of glucose output, thus facilitating the consumption of residual exogenous glucose by extrahepatic tissues, such as skeletal muscle and adipose tissue.…”

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confidence: 99%

Regulation of hepatic glucose metabolism in health and disease

2017

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The liver is crucial for the maintenance of normal glucose homeostasis — it produces glucose during fasting and stores glucose postprandially. However, these hepatic processes are dysregulated in type 1 and type 2 diabetes mellitus, and this imbalance contributes to hyperglycaemia in the fasted and postprandial states. Net hepatic glucose production is the summation of glucose fluxes from gluconeogenesis, glycogenolysis, glycogen synthesis, glycolysis and other pathways. In this Review, we discuss the in vivo regulation of these hepatic glucose fluxes. In particular, we highlight the importance of indirect (extrahepatic) control of hepatic gluconeogenesis and direct (hepatic) control of hepatic glycogen metabolism. We also propose a mechanism for the progression of subclinical hepatic insulin resistance to overt fasting hyperglycaemia in type 2 diabetes mellitus. Insights into the control of hepatic gluconeogenesis by metformin and insulin and into the role of lipid-induced hepatic insulin resistance in modifying gluconeogenic and net hepatic glycogen synthetic flux are also discussed. Finally, we consider the therapeutic potential of strategies that target hepatosteatosis, hyperglucagonaemia and adipose lipolysis.

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The Disposal of an Oral Glucose Load in Healthy Subjects: A Quantitative Study

Cited by 318 publications

References 0 publications

Postprandial whole-body glycolysis is similar in insulin-resistant and insulin-sensitive non-diabetic humans

Postprandial whole-body glycolysis is similar in insulin-resistant and insulin-sensitive non-diabetic humans

Metabolic Fate of Fructose Ingested with and without Glucose in a Mixed Meal

Regulation of hepatic glucose metabolism in health and disease

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