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首页> 外文期刊>Journal of cellular biochemistry. >Combined use of insulin and endothelin-1 causes decrease of protein expression of beta-subunit of insulin receptor, insulin receptor substrate-1, and insulin-stimulated glucose uptake in rat adipocytes.
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Combined use of insulin and endothelin-1 causes decrease of protein expression of beta-subunit of insulin receptor, insulin receptor substrate-1, and insulin-stimulated glucose uptake in rat adipocytes.

机译：胰岛素和内皮素-1的联合使用会导致大鼠脂肪细胞中胰岛素受体β亚基，胰岛素受体底物1和胰岛素刺激的葡萄糖摄取的蛋白质表达下降。

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摘要

Previously, we reported that insulin-stimulated glucose uptake (ISGU) can be inhibited by endothelin (ET-1). However, the mechanism by which ET-1 impairs ISGU in adipocytes remains unclear. This study investigated the effects of ET-1 on insulin action in rat adipocytes in order to elucidate the molecular mechanism of action of ET-1 on ISGU. The results show that ISGU was increased fivefold after 3-h treatment with 1 nM insulin. Treatment with 100 nM ET-1 had no effect on basal glucose uptake. However, ET-1 inhibited approximately 25% of ISGU and 20% of insulin binding after 3-h treatment in the presence of 1 nM insulin. Expression of the beta-subunit of the insulin receptor (IRbeta) and the insulin receptor substrate-1 (IRS-1) in adipocytes was not significantly affected by 1 nM insulin or by 100 nM ET-1, even after 3-h treatment. However, expressions of IRbeta and IRS-1 were dramatically decreased in a dose- and time-dependent manner when adipocytes were treated with both insulin and ET-1. Approximately 50% of IRbeta and 65% of IRS-1 expression levels were suppressed when adipocytes were simultaneously treated with both 1 nM insulin and 100 nM ET-1 for 3 h. These results suggest that the inhibitory effect of ET-1 on ISGU may be mediated via the insulin receptor and suppression of IRbeta/IRS-1 expression. Copyright 2000 Wiley-Liss, Inc.
机译：以前，我们报道了内皮素（ET-1）可以抑制胰岛素刺激的葡萄糖摄取（ISGU）。但是，ET-1损害脂肪细胞中ISGU的机制仍不清楚。这项研究调查了ET-1对大鼠脂肪细胞中胰岛素作用的影响，以阐明ET-1对ISGU的作用的分子机制。结果表明，用1 nM胰岛素治疗3小时后，ISGU增加了五倍。用100 nM ET-1处理对基础葡萄糖摄取没有影响。但是，在1 nM胰岛素存在下进行3小时治疗后，ET-1抑制了大约25％的ISGU和20％的胰岛素结合。即使在3小时的治疗后，1 nM胰岛素或100 nM ET-1也不会显着影响脂肪细胞中胰岛素受体（IRbeta）和胰岛素受体底物1（IRS-1）的β亚基的表达。但是，当同时用胰岛素和ET-1处理脂肪细胞时，IRbeta和IRS-1的表达以剂量和时间依赖性显着降低。当同时用1 nM胰岛素和100 nM ET-1共同处理脂肪细胞3小时时，约50％的IRbeta和65％的IRS-1表达水平受到抑制。这些结果表明，ET-1对ISGU的抑制作用可能是通过胰岛素受体和IRbeta / IRS-1表达的抑制来介导的。版权所有2000 Wiley-Liss，Inc.

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