Rosen O M, Smith C J, Fung C, Rubin C S
J Biol Chem. 1978 Oct 25;253(20):7579-83.
Exposure of insulin-responsive, differentiated 3T3-L1 cells (adipocytes) to 0.1 to 1.0 microgram/ml of insulin for 3 to 48 h resulted in a persistent state of enhanced 2-deoxy-D-glucose and 3-O-methyl-D-glucose uptake. Elevated basal transport activity was retained under conditions where 125I-insulin binding activity remained unchanged and exchangeable insulin was dissociated from cell surface receptors. The appearance of enhanced hexose transport activity was prevented by cycloheximide and could be distinguished from the activation of the glucose transport system observed in these and other cells during glucose deprivation. Rigorously washed adipocytes, exhibiting insulin-induced elevations in basal transport activity, were refractory to further stimulation by insulin during hexose uptake assays. Insulin-unresponsive 3T3-L1 preadipocytes failed to increase hexose uptake activity when treated under conditions that elicited an optimal response in adipocytes.
将胰岛素反应性、已分化的3T3-L1细胞(脂肪细胞)暴露于0.1至1.0微克/毫升的胰岛素中3至48小时,会导致2-脱氧-D-葡萄糖和3-O-甲基-D-葡萄糖摄取增强的持续状态。在125I-胰岛素结合活性保持不变且可交换胰岛素从细胞表面受体解离的条件下,基础转运活性仍保持升高。环己酰亚胺可阻止己糖转运活性增强的出现,并且这种增强可与在葡萄糖剥夺期间这些细胞和其他细胞中观察到的葡萄糖转运系统的激活区分开来。经过严格洗涤的脂肪细胞,其基础转运活性因胰岛素诱导而升高,在己糖摄取试验期间对胰岛素的进一步刺激无反应。胰岛素无反应的3T3-L1前脂肪细胞在能引起脂肪细胞最佳反应的条件下处理时,无法增加己糖摄取活性。