The uptake of 2-deoxy-D-[-14C]-glucose, in the presence and absence of insulin, was measured in adipocytes from normal and streptozotocin-diabetic animals, over a wide temperature range (25–45°C). Optimum temperatures for uptake in the presence of maximally stimulating insulin concentrations occurred near physiologic temperatures. Both high and low temperatures lead to progressive inhibition of insulin-sensitive uptake, whereas basal uptake was only marginally affected. It is possible that the apparent “resistance” to insulin action at high (febrile) temperatures may have pathologic significance.

The magnitude of 2-deoxy-D-glucose uptake at all temperatures in the diabetic adipocytes was much reduced, both in the presence and absence of insulin, on a per cell basis, compared with cells from age-matched control animals. However, the fold stimulation of uptake caused by insulin at 35°C is comparable in both normal and diabetic adipocytes (approximately 2–3-fold).

Photomicrographs of adipocytes were used to estimate the cell diameters of the average normal (50 μm) and diabetic (37 μm) cells. The diabetic adipocytes are not “resistant” to insulin action in terms of 2-deoxy-D-glucose uptake since the basal and insulin-stimulated uptake magnitudes per μm2 membrane surface area are identical in both normal and diabetic cells (within experimental error). It is possible that the decreased diabetic cell size reflects the reduced antilipolytic effects of chronic hypoinsulinemia rather than any inherent resistance to insulin action in the cell itself.

The basal and insulin-stimulated overall removal of glucose from the incubation medium by adipocytes, isolated from the normal and streptozotocin-treated rats, was also measured. Both the overall glucose uptake magnitude per μm2 membrane surface area and the fold increase in glucose uptake due to insulin were identical between cells obtained from the two groups of animals. Any intracellular metabolic resistance to the effects of exogenous insulin that may be present in cells from the diabetic rats does not appear to grossly interfere with the accelerated net utilization of glucose induced by exposure to the hormone in vitro.

Purified plasma membranes from normal and diabetic adipocytes were examined in spin label studies. No differences in the flexibility of either the 5-nitroxide stearate or the cholestane (cholesterol-like) spin labels were noted between the two animal groups at any temperature between 15 and 40°C Although the diabetic membrane may well exhibit differing structural/functional properties compared with controls, our data do not support the concept that gross alterations in the lipid structure of the membrane occur in this hyperglycemie condition.

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