Effect of somatostatin-induced insulinopenia on glucose oxidation in man

In the basal state the body utilizes glucose at a rate of 2.2-2.3 mg· kg^-1·min^-1; of this approximately 1.2-1.3 mg · kg^-1 · min^-1 is oxidized, while the remaining 1.0 mg · kg^-1·min^-1 must be utilized by non-oxidative pathways. Little information is, however, available concerning the insulin dependency of these processes. To examine the role of basal insulin levels on glucose oxidation, glucose storage and total body glucose uptake, somatostatin (10 μg/min) was infused for 2 h in nine volunteers while maintaining plasma glucose concentration constant at basal levels by an exogenous glucose infusion. Basal plasma insulin fell by about 50% (13±2 to 7±1mU/l, p<0.01). Total body glucose metabolism (³H-3-glucose) declined from 2.3±0.1 to 1.9±0.1mg· kg^-1·min^-1 (p<0.01). This decrease was entirely accounted for by a fall in basal glucose oxidation (measured by indirect calorimetry) from 1.3±0.1 to 0.7±0.1 mg·kg^-1·min^-1 (p< 0.001). To assess the specific role of insulin deficiency in the decline in glucose oxidation, subjects were restudied with somatostatin plus basal insulin replacement (0.07 mg ·kg^-1· min^-1). Fasting insulin concentration (14±1 mU/1) remained constant during somatostatin plus insulin infusion (13±1mU/l) and basal rates of glucose oxidation (1.2±0.1 mg · kg^-1·min^-1) and total body glucose uptake did not change significantly. After 2 h, the basal insulin infusion was stopped and somatostatin was continued. Over the subsequent hour, glucose oxidation declined by 0.4±0.1 mg· kg^-1 · min^-1. This decrease was associated with a parallel decrease in total body glucose uptake of 0.4±0.1 mg·kg^-1 ·min^-1. These results indicate that approximately 50% of basal glucose oxidation is dependent upon basal insulin secretion. Non-oxidative pathways of glucose metabolism under basal conditions appear to be insulin independent.