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

Abstract Aims This study aimed to determine how insufficiently suppressed endogenous glucose production vs. reduced peripheral glucose uptake contribute to postprandial hyperglycaemia in type 2 diabetes (T2D). Methods Eight men with T2D (age: 52±7 years; BMI: 26.6±2.3kg/m 2 ; fasting glycaemia: 7.1±1.5mmol/L) were compared with eight non-diabetic controls (age: 51±5 years; BMI: 24.6±2.9kg/m 2 ; fasting glycaemia: 4.9±0.4mmol/L). Their glucose turnover rates and hepatic glucose cycles were measured by monitoring [2H7]glucose infusion, with m+7 and m+6 enrichment, 3h before and 4h after the ingestion of [6,6-2H2]-labelled glucose, while maintaining glycaemia at 10mmol/L using the pancreatic clamp technique. Results Of the 700mg/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 Conclusion When 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.