EFFECT OF INSULIN AND GLUCOCORTICOIDS ON GLUCOSE TRANSPORTERS IN RAT ADIPOCYTES
EFFECT OF INSULIN AND GLUCOCORTICOIDS ON GLUCOSE TRANSPORTERS IN RAT ADIPOCYTES
复制标题
DOI：
10.1152/ajpendo.1987.252.4.e441
复制
发表时间：
1987-04-01
影响因子：
--
通讯作者：
OKAMOTO, K
中科院分区：
文献类型：
--
作者：
CARTERSU, C;OKAMOTO, K
糖皮质激素改变胰岛素对葡萄糖转运的影响的能力在完整的分离大鼠脂肪细胞和从激素处理的脂肪细胞分离的膜中进行了研究。在完整的脂肪细胞中，地塞米松（一种强效的合成糖皮质激素）在所有胰岛素浓度（0-2,000 . μ u /ml）下都能抑制胰岛素刺激的3- o -甲基葡萄糖转运。胰岛素敏感性，以及对胰岛素的最大反应，在没有改变胰岛素结合的情况下，地塞米松降低。不管哪一种激素先起作用，这种抑制作用都被放线菌素D阻断，并且是由于Vmax的降低而不是运输Kt的增加。在从胰岛素处理的脂肪细胞分离的质膜中，葡萄糖转运活性和以[3H]细胞松弛素B共价标记的葡萄糖转运蛋白的数量以剂量依赖的方式平行增加。在低密度微粒体分数（LDMF）中标记转运蛋白的数量以互惠的方式减少。相反，在胰岛素刺激的细胞中添加地塞米松导致质膜中转运活性和标记转运蛋白的数量下降。这伴随着LDMF中葡萄糖转运蛋白中[3H]细胞松弛素B的少量增加。这些结果与胰岛素和糖皮质激素改变葡萄糖转运蛋白在质膜和LDMF之间的分布方向相反是一致的。
The ability of glucocorticoids to modify the effect of insulin on glucose transport was investigated in both intact isolated rat adipocytes and in membranes isolated from hormone-treated adipocytes. In intact adipocytes, dexamethasone, a potent synthetic glucocorticoid, inhibited insulin-stimulated 3-O-methylglucose transport at all concentrations of insulin tested (0-2,000 .mu.U/ml). Insulin sensitivity, as well as the maximal response to insulin, was decreased by dexamethasone in the absence of a changing in insulin binding. The inhibition was observed regardless of which hormone acted first, was blocked by actinomycin D, and resulted from a decrease in Vmax rather than an increase in Kt of transport. In plasma membranes isolated from insulin-treated adipocytes, glucose transport activity and the amount of glucose transporter covalently labeled with [3H]cytochalasin B were increased in parallel in a dose-dependent fashion. The amount of labeled transporter in a low-density microsomal fraction (LDMF) was decreased in a reciprocal fashion. In contrast, addition of dexamethasone to insulin-stimulated cells caused decreases in both transport activity and amount of labeled transporter in the plasma membranes. This was accompanied by a small increase in the amount of [3H]cytochalasin B incorporated into the glucose transporter in the LDMF. These results are consistent with both insulin and glucocorticoids altering the distribution of glucose transporters between the plasma membrane and LDMF, in opposite directions.