Cellular mechanisms in selected states of insulin resistance: human obesity, glucocorticoid excess, and chronic renal failure.
Cellular mechanisms in selected states of insulin resistance: human obesity, glucocorticoid excess, and chronic renal failure.
复制标题
胰岛素抵抗选定状态下的细胞机制：人类肥胖、糖皮质激素过量和慢性肾功能衰竭。
DOI：
10.1002/dmr.5610010304
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Lockwood,DH
中科院分区：
文献类型：
--
作者：
Amatruda,JM;Livingston,JN;Lockwood,DH
在过去的13年中，我们实验室的研究一直关注正常和胰岛素抵抗状态下细胞和亚细胞水平上的胰岛素作用。我们对胰岛素抵抗改变的理解，大部分来自于我们对胰岛素作用机制的理解的快速增长。随着20世纪70年代早期胰岛素受体的发现，在几乎所有已知的胰岛素作用改变状态下，这种实体的状态都受到了密切关注，这并不奇怪。虽然胰岛素结合在许多但肯定不是所有的抵抗病例中被证明是减少的，但通常不考虑结合异常对胰岛素作用受损的实际贡献。最近，许多研究更彻底地研究了胰岛素在有和没有结合异常的抵抗状态下的作用。在许多情况下，后结合机制似乎在胰岛素抵抗中起主要作用。在这篇文章中，我们回顾了我们和其他人已经详细研究过的三种胰岛素抵抗状态。人类肥胖是令人感兴趣的，因为现有的信息表明，结合后的改变在脂肪组织和受体中起作用。
During the past 13 years, investigations in our laboratories have been concerned with insulin action at the cellular and subcellular levels in normal and insulin-resistant states. Much of our understanding of the alterations responsible for insulin resistance has resulted from a rapid proliferation of our understanding of the mechanisms of insulin action. With the discovery of the insulin receptor in the early 1970s, it was not surprising that the status of this entity was closely scrutinized in virtually every known state of altered insulin action. Although insulin binding was shown to be reduced in many but certainly not all cases of resistance, the actual contribution of binding abnormalities to impaired insulin action was not generally considered. Recently, many investigations have studied insulin action more thoroughly in those resistant states with and without binding abnormalities. In many situations it appears that postbinding mechanisms play a major role in insulin resistance. In this article, we review three selected states of insulin resistance that we and others have studied in some detail. Human obesity is of interest because available information indicates that postbinding alterations are operative in adipose tissue and receptor