Glucose flux in controlled hyperglycaemia before and after oral glucose ingestion in men with mild type 2 diabetes

AimsThis study aimed to determine how insufficiently suppressed endogenous glucose production vs. reduced peripheral glucose uptake contribute to postprandial hyperglycaemia in type 2 diabetes (T2D).MethodsEight men with T2D (age: 52 ± 7 years; BMI: 26.6 ± 2.3 kg/m²; fasting glycaemia: 7.1 ± 1.5 mmol/L) were compared with eight non-diabetic controls (age: 51 ± 5 years; BMI: 24.6 ± 2.9 kg/m²; fasting glycaemia: 4.9 ± 0.4 mmol/L). Their glucose turnover rates and hepatic glucose cycles were measured by monitoring 2H7]glucose infusion, with m+7 and m+6 enrichment, 3 h before and 4 h after the ingestion of 6,6-2H2]-labelled glucose, while maintaining glycaemia at 10 mmol/L using the pancreatic clamp technique.ResultsOf the 700 mg/kg oral glucose load, 71% appeared in the systemic circulation of the T2D patients vs. 63% in the controls (NS). Endogenous glucose production and hepatic glucose cycles did not differ from normal either before or after oral glucose ingestion, while peripheral glucose uptake was reduced by 40% in the T2D group both before (P < 0.01) and after (P < 0.05) ingestion of oral glucose.ConclusionWhen T2D patients were compared with non-diabetic subjects with similarly controlled levels of hyperglycaemia after oral glucose ingestion, they essentially differed only in peripheral glucose uptake, whereas endogenous glucose production was apparently unaltered.