BASAL PLASMA-INSULIN LEVELS EXERT A QUALITATIVE BUT NOT QUANTITATIVE EFFECT ON GLUCOSE-MEDIATED GLUCOSE-UPTAKE

We assessed the effect of hyperglycemia on glucose uptake in the presence of normal basal insulin levels or somatostatin-induced hypoinsulinemia in seven normal volunteers during a 200-min hyperglycemic clamp (+9 mmol/l) carried out with [3-H-3]glucose and indirect calorimetry. Hyperglycemia increased glucose uptake to 22.4 +/- 2.6 and 21.3 +/- 1.6 mu mol . kg(-1). min(-1) with and without insulin replacement, respectively. Normoinsulinemia increased glucose oxidation (Delta = +4.5 +/- 0.6 mu mol . kg(-1). min(-1)) and nonoxidative glucose metabolism (Delta = +5.2 +/- 1.7 mu mol . kg(-1). min(-1)), whereas with insulinopenia, glucose oxidation did not change (Delta = -0.3 +/- 0.6 mu mol . kg(-1). min(-1)), and nonoxidative glucose metabolism increased (Delta = +8.7 +/- 0.8 mu mol . kg(-1). min(-1)). Nonoxidative glucose metabolism was higher during insulinopenic (13.5 +/- 1.8 mu mol . kg(-1). min(-1)) than normoinsulinemic hyperglycemia (9.8 +/- 2.7 mu mol . kg(-1). min(-1); P < 0.01). Plasma FFA concentration and lipid oxidation were higher with insulinopenia. Blood lactate and alanine concentrations were greater with normoinsulinemia. In conclusion: I)hyperglycemia promotes glucose uptake by stimulating both nonoxidative and oxidative glucose disposal; 2) the ability of hyperglycemia to enhance total body glucose uptake is similar with and without normoinsulinemia; 3) although acute insulinopenia does not impair the ability of hyperglycemia to stimulate glucose uptake, it plays a critical role in determining the intracellular metabolic fate of glucose taken up in response to hyperglycemia.