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 [3-3H]glucose in the postabsorptive state and during somatostatin-induced insulinopenia at euglycaemic (≈5.3 mmol/l) and hyperglycaemic (≈11 mmol/l) glucose concentrations.
2. Basal glucose concentration (patients, 5.2 ± 0.1 mmol/l; control subjects, 5.3 ± 0.1 mmol/l) and basal glucose tissue uptake (patients, 15.9 ± 0.5 μmol min−1 kg−1 fat-free mass; control subjects, 15.2 ± 0.4 μmol 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 (≈11 mmol/l) conditions with sustained insulinopenia, no differences in glucose uptake existed between the two groups (patients, 16.8 ± 0.6 μmol min−1 kg−1 fat-free mass; control subjects, 16.1 ± 0.3 μmol 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.