NON-INSULIN-MEDIATED GLUCOSE-UPTAKE IN HUMAN IMMUNODEFICIENCY VIRUS-INFECTED MEN

1. One of the metabolic features of acquired immunodeficiency syndrome is increased tissue glucose uptake documented by euglycaemic-hyperinsulinaemic clamp studies, suggesting increased insulin sensitivity. However, these results may also be related to the confounding effect of increased non-insulin-mediated glucose uptake in acquired immunodeficiency syndrome, which will result in an erroneously presumed increased insulin sensitivity. To study the contribution of non-insulin-mediated glucose uptake to total tissue glucose uptake in acquired immunodeficiency syndrome, we conducted a hypoinsulinaemic clamp study in clinically stable human immunodeficiency virus-infected (Centers for Disease Control class IV) men (n=7) and healthy subjects (n=5). Glucose uptake was measured by a primed, continuous infusion of [3-H-3]glucose in the postabsorptive state and during somatostatin-induced insulinopenia at euglycaemic (almost-equal-to 5.3 mmol/l) and hyperglycaemic (almost-equal-to 11 mmol/l) glucose concentrations. 2. Basal glucose concentration (patients, 5.2+/-0.1 mmol/l; control subjects, 5.3+/-0.1 mmol/1) and basal glucose tissue uptake (patients, 15.9+/-0.5 mumol min-1 kg-1 fat-free mass; control subjects, 15.2+/-0.4 mumol min-1 kg-1 fat-free mass) were not different between the two groups. 3. Euglycaemic glucose uptake during somatostatin infusion, reflecting non-insulin-mediated glucose uptake, decreased to 82+/-3% in patients and 78+/-2%) in control subjects (not significant). Under hyperglycaemic (almost-equal-to 11 mmol/l) conditions with sustained insulinopenia, no differences in glucose uptake existed between the two groups (patients, 16.8+/-0.6 mumol min-1 kg-1 fat-free mass, control subjects, 16.1+/-0.3 mumol min-1 kg-1 fat-free mass). 4. Our results indicate that non-insulin-mediated glucose uptake is not increased in acquired immunodeficiency syndrome. Therefore the previously described increase in insulin sensitivity in acquired immunodeficiency syndrome during hyperinsulinaemia is explained by a real increase in insulin sensitivity and not by augmented non-insulin-mediated glucose uptake.