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Insulin-stimulated glucose transport in cultured fibroblasts from normal and noninsulin-dependent (type II) diabetic human subjects.

We have studied the effects of insulin on glucose transport in cultured fibroblasts obtained from six normal subjects and six patients with type II or noninsulin-dependent diabetes mellitus. Initial rates of glucose transport were determined by measurement of 2-deoxy-D-glucose uptake. In both normal and diabetic fibroblasts, insulin stimulated the uptake of 2-deoxy-D-glucose in a dose-dependent manner. The maximal level of insulin stimulation of 2-deoxy-D-glucose uptake (approximately 35% over basal uptake values) and the half-maximally effective insulin concentration (approximately 1 nM) were essentially the same for both the normal and diabetic fibroblasts. Furthermore, the absolute basal and maximally insulin-stimulated 2-deoxy-D-glucose uptake values were also the same. These results demonstrate that cultured fibroblasts from patients with noninsulin-dependent diabetes mellitus have normal basal and insulin-stimulated glucose transport capacities. Thus, the postreceptor defects in the glucose transport system previously demonstrated in vivo and in freshly isolated adipocytes from type II diabetic patients are most likely due to in vivo environmental factors rather than to an intrinsic (genetic) cellular defect(s).