Insulin binding and hexose transport in rat adipocytes

Abstract

Insulin binding, initial velocity of [14C]methylglucose transport, uptake of [14C]deoxyglucose and conversion of [U-14C]glucose to CO2, glyceride-glycerol and fatty acids were measured at 37 degrees C in adipocytes from rats of different weights (135-450 g) and therefore with different mean cell volumes (53-389 pl). Insulin binding per cell increased with increasing cell size and binding was 2.3 times higher in the largest cells than in the smallest cells with tracer alone. The difference was largely accounted for by an increase in the apparent affinity. Influx of methylglucose per cell increased with increasing cell size in the absence of insulin and remained constant as a function of cell size in its presence. The effect of insulin ranged from 11 fold in small cells to 3.5 fold in large cells. The rat of conversion of [U-14C]glucose to CO2 and lipids was about half of the rate of methylglucose transport under all conditions. In contrast, the uptake of deoxyglucose in insulin-stimulated cells decreased markedly with increasing cell size. Increasing cell size caused a small decrease in sensitivity which could be explained by a smaller amont of insulin bound per unit surface area. The results show that increasing cell size/animal weight causes changes in insulin binding which may explain changes in sensitivity. In addition, the hexose transport system is modified in a way which is not explained by changes in insulin binding. Finally, changes in deoxyglucose uptake with cell size do not parallel changes in methylglucose transport.

The effect of N6‐phenylisopropyladenosine on the regulation of fat cell hexose transport, glucose oxidation and fatty acid release by insulin and catecholamines

“…These results: (1) support the concept of different regulatory processes for 2-DC and 3-OMG transport as suggested in [19,20]; (2) strongly implicate a role for the R-site in modulation of hexose transport as modified by hormonal treatment.…”

Expression of thyrotropin and thyroid hormone receptors in adipose tissue of patients with morbid obesity and/or type 2 diabetes: effects of weight loss

“…Thus, one could speculate that hypertrophy changes the cellular phenotype of the adipocyte, reducing the expression of these receptors in much the same way as with adiponectin receptors 27 or insulin sensitivity. 28 As a consequence of the downregulation in the thyroid hormone and TSHR expression, plasma TSH and FT 3 concentrations could increase to cope with peripheral hormone resistance. This sequence of events would be TSH and TH receptors expression in fat depots M Nannipieri et al reversed by weight loss, which restores the size and function of mature adipocytes.…”

In vitro insulin resistance of human adipocytes isolated from subjects with noninsulin-dependent diabetes mellitus.

“…The cell suspension was incubated at 370C for 1 h with continuous shaking at 40 cycles/min. The incubation was terminated by centrifuging a 400-Mil aliquot in a 550-Ml microfuge tube (23), and the amount of radioactivity associated with the adipocytes (as well as the total radioactivity in the incubation medium) determined by liquid scintillation counting. Under these conditions, -20% of the adipocyteassociated activity was water soluble, with the remainder being recovered as triglyceride.…”