Insulin binding and responsiveness in fat cells from patients with reduced glucose tolerance and type II diabetes.

Adipose tissue was obtained from 66 individuals including 21 patients with type II diabetes of different severity (16 SU-treated and 5 diet-treated only) as well as 9 obese subjects with reduced glucose tolerance. Adipocyte insulin binding, antilipolytic effect of insulin, and glucose incorporation into triglycerides were measured in the diabetic and the obese subjects and the data compared with that of normal controls of similar age and relative weight. Insulin binding per cell was normal in the diabetic patients and was significantly increased at low insulin concentrations in the obese patients with reduced glucose tolerance, suggesting increased affinity. Furthermore, insulin binding correlated negatively with age but, when age was corrected for, did not correlate significantly with fasting insulin or glucose levels, relative body weight, or fat cell size. Insulin sensitivity, measured as the antilipolytic effect of insulin, was similar in all patient groups. Patients with the most severe type II diabetes (SU-treated group) demonstrated, in contrast to the less severely diabetic patients, a marked reduction in both basal and insulin-stimulated glucose incorporation into triglycerides showing the presence of a pronounced postreceptor defect. The insulin effect on glucose incorporation correlated negatively with the fasting glucose levels, suggesting that the postreceptor defect seen in the adipocyte reflects perturbations in other organs, like muscle or liver, of greater importance for glucose homeostasis.