Insulin resistance

Perriello et al. (263-OR) performed hyperinsulinemic clamps in five normal individuals from 5:00 to 8:00 a.m. and from 5:00 to 8:00 p.m., on both occasions after a 9-h fast (abstract numbers refer to the Abstracts of the 61st Annual Meeting of the American Diabetes Association, Diabetes 50 [Suppl. 2]:1-A649). Insulin action decreased 27% in the evening, partially explaining the decrease in glucose tolerance in the afternoon versus early morning hours. Zaccaro et al. (301-PP) compared insulin sensitivity calculated from the frequently sampled intravenous glucose tolerance test with surrogate measures based on fasting insulin and glucose levles in 1,118 persons in the family members in the Insulin Resistance Atherosclerosis Study (IRAS), showing a greater degree of genetic contribution to specifically measured insulin sensitivity than to the measurement of fasting insulin alone, the product of fasting insulin and fasting glucose divided by 22.5 (the “homeostasis model” [HOMA] measure), or the reciprocal of the product of fasting insulin and glucose (the “Bennet index”). These surrogate measures of insulin sensitivity may therefore be less useful than previously thought. Mather et al. (9-LB) reported that the T786C variant of the endothelial isoform of nitric oxide synthase was associated with insulin resistance, perhaps contributing to its association with endothelial dysfunction. Meyer et al. (198-OR) compared hepatic and renal glucose production, which were 10.3 and 3.6 μmol · kg⁻¹ · min⁻¹, respectively, in 10 type 2 diabetic patients and 8.4 and 2.16 μmol · kg⁻¹ · min⁻¹ in 12 nondiabetic control subjects, using tritiated glucose turnover and renal vein glucose measurement. During hyperinsulinemic-euglycemic clamps, …