van Putten J P, Wieringa T, Krans H M
Diabetologia. 1985 Jan;28(1):51-6. doi: 10.1007/BF00277000.
Observations in vivo suggest that insulin acts as a long-term regulator of hexose uptake in fat cells. In the present study, we examined the long-term effect of insulin on hexose uptake in vitro. Exposure of fully differentiated mouse 3T3-L1 adipocytes to insulin induced a time-, concentration-, and protein synthesis-dependent increase in basal 2-deoxyglucose uptake (up to 40%) and a decrease in the 'acute' insulin response. The decrease in insulin effect was due to post-receptor alterations, since insulin binding was not substantially altered. The increase in basal 2-deoxyglucose uptake was due to an increase in the apparent Vmax of the transport system rather than to the observed increase (30%) in hexokinase activity, since the concentration of non-phosphorylated 2-deoxyglucose inside the cell was far below the extracellular concentration. The increase in apparent Vmax was most likely due to a protein synthesis-dependent increase in de novo synthesis of hexose transporters. Glucose was not essential for the effect. The mechanism responsible for the loss in insulin response remains to be solved. It can be concluded that insulin has the ability to act as a long-term regulator of hexose uptake in fat cells in vitro.
体内观察结果表明，胰岛素作为脂肪细胞中己糖摄取的长期调节因子。在本研究中，我们检测了胰岛素在体外对己糖摄取的长期影响。将完全分化的小鼠3T3-L1脂肪细胞暴露于胰岛素中，可诱导基础2-脱氧葡萄糖摄取呈时间、浓度和蛋白质合成依赖性增加（高达40%），并降低“急性”胰岛素反应。胰岛素作用的降低是由于受体后改变，因为胰岛素结合没有实质性改变。基础2-脱氧葡萄糖摄取的增加是由于转运系统的表观Vmax增加，而不是由于观察到的己糖激酶活性增加（30%），因为细胞内非磷酸化2-脱氧葡萄糖的浓度远低于细胞外浓度。表观Vmax的增加最可能是由于己糖转运蛋白从头合成的蛋白质合成依赖性增加。葡萄糖对该效应并非必需。胰岛素反应丧失的机制仍有待解决。可以得出结论，胰岛素能够在体外作为脂肪细胞中己糖摄取的长期调节因子。
