Insulin Binding In Adipocytes Research Articles

The relation between insulin and adipocyte insulin receptors during treatment of human obesity.

Seventeen obese patients were submitted to 1 week's severe then 3 months moderate dietary restriction. The glycaemic and insulinaemic response to oral glucose was measured at baseline, after 1 week and at 3 months, and the results related to adipocyte insulin receptors estimated from fat biopsies taken on each occasion and to the weight lost. Adipocyte insulin binding was found to be significantly inversely correlated with the insulinaemic response to oral glucose (r = -0.54, P less than 0.05), an inverse relationship maintained even after weight loss had been achieved and displayed within as well as between subjects. Variation of 125I-insulin binding to adipocytes was related to receptor number and not to receptor affinity and could not be accounted for by differences in 125I-insulin degradation. Adipose cell size did not correlate significantly either with the insulinaemic response or with cell surface receptor density. The findings suggest: (1) that a significant proportion of obese subjects are not hyperinsulinaemic and that their metabolic response to weight reduction may differ from that of those who are hyperinsulinaemic; (2) that reduced insulin binding to adipocytes in the obese reflects hyperinsulinaemia, when present, and not adiposity as such; (3) that the degree of insulinaemia is a major determinant of the cell surface receptor density.

Insulin binding and glucose metabolism in adipocytes of streptozotocin-diabetic rats.

To investigate the mechanism of the cellular insulin insensitivity of diabetic rats, insulin binding, glucose transport, and glucose oxidation were studied in adipocytes from streptozotocin-diabetic rats. Increased insulin binding was found in cells from diabetic rats, and this was due to an increased number of insulin receptors rather than a change in receptor affinity. Basal and insulin-stimulated glucose oxidation was decreased in adipocytes from diabetic rats when the data are expressed in absolute terms or as percent increased above basal. Although the absolute rate of basal and insulin-stimulated glucose transport was decreased in adipocytes from diabetic rats, the percent increase above basal of insulin-stimulated glucose transport was not decreased. In conclusion, although the cellular insulin insensitivity exists in adipocytes from diabetic rats, the number of insulin receptors was increased, coupling between insulin receptors and the glucose transport system is intact in adipocytes from diabetic rats, and a defect in intracellular glucose metabolism rather than glucose transport plays a major role in the insulin insensitivity of adipocytes from diabetic rats.

Insulin binding and insulin response of adipocytes from rats adapted to fat feeding

The effect of fat feeding on adipocyte insulin binding was examined to expand a study of adaptive changes in plasma membrane functions. Cells from rats fed a high fat (L) diet for five to seven days bound less insulin and showed a decreased response to insulin (glucose oxidation) compared to those from rats fed a high glucose (G) diet. Both high and low affinity sites were influenced; the extent of the binding difference increased as increasing concentrations of insulin were present in the assay medium. Diet did not change hormone degradation on the capacity of phospholipase C to increase binding. Concanavalin A effects on fat cells were also decreased by L diet both in inhibition of insulin binding and its insulin-like effect on glucose oxidation. Spermine, which had no effect on insulin binding, also had a smaller insulin-like effect on glucose oxidation by L cells than by G cells. Serum insulin was significantly lower (30 +/- 3.7 muU/ml) in L than in G (43 +/- 3.1 muU/ml) groups. Dietary fat produces alterations in fat cells that decrease insulin binding as a part of a complex overall adaptation to the diet.