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 microgram/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 +/- 1 mU/l, p less than 0.01). Total body glucose metabolism (3H-3-glucose) declined from 2.3 +/- 0.1 to 1.9 +/- 0.1 mg.kg-1.min-1 (p less than 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 less than 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/l) remained constant during somatostatin plus insulin infusion (13 +/- 1 mU/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.(ABSTRACT TRUNCATED AT 250 WORDS)