Abstract
Upon interaction with phospholipid vesicles containing phosphatidylserine, isolated rat adipocytes demonstrate an inhibition of insulin-stimulated hexose uptake. In order to elucidate the mechanism of this effect, adipocytes were treated with agents, alone or in combination with vesicles, which affected the insulin-sensitive response at the receptor and post-receptor level. The effect of vesicles at a maximal inhibitory concentration proved to be non-additive with dexamethasone, suggesting that vesicles may act in a manner similar to this agent. In contrast, fat cells treated with vesicles and N-ethylmaleimide (NEM) or trypsin at submaximally effective concentrations demonstrate a partially additive inhibition of insulin-stimulated 2-deoxyglucose uptake. Vesicle treatment of adipocytes before stimulation with agents which mimic insulin, such as Con A and H2O2, demonstrates the same effects as insulin with respect to hexose uptake. These results support the contention that vesicles inhibit insulin action at least partially at the post-receptor level, and may directly interfere with the hexose transport site.
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