蛋白激酶C参与胰岛素刺激的己糖摄取的直接证据。

Direct evidence for protein kinase C involvement in insulin-stimulated hexose uptake.

作者信息

Cooper D R, Watson J E, Hernandez H, Yu B, Standaert M L, Ways D K, Arnold T T, Ishizuka T, Farese R V

机构信息

Research Service, James A. Haley Veterans Administration Hospital, Tampa, FL 33612.

出版信息

Biochem Biophys Res Commun. 1992 Oct 15;188(1):142-8. doi: 10.1016/0006-291x(92)92361-z.

DOI:10.1016/0006-291x(92)92361-z

PMID:1417838

Abstract

Insulin has been reported to translocate protein kinase C (PKC) in rat adipocytes, and activation of PKC by phorbol esters is known to increase hexose uptake in these cells (1.2). To test the hypothesis that PKC may participate in insulin-stimulated hexose uptake, adipocytes were partially depleted of protein kinase C by overnight phorbol ester treatment, thereby impairing insulin effects on hexose uptake. Purified PKC was then introduced into these PKC-depleted adipocytes by electropermeabilization, and this fully restored insulin-stimulated hexose uptake. These findings provide direct evidence that PKC is required for insulin-stimulated hexose uptake.

摘要

据报道，胰岛素可使大鼠脂肪细胞中的蛋白激酶C（PKC）发生易位，并且已知佛波酯激活PKC可增加这些细胞中的己糖摄取（1,2）。为了验证PKC可能参与胰岛素刺激的己糖摄取这一假说，通过过夜佛波酯处理使脂肪细胞中的蛋白激酶C部分缺失，从而损害胰岛素对己糖摄取的作用。然后通过电穿孔将纯化的PKC导入这些PKC缺失的脂肪细胞中，这完全恢复了胰岛素刺激的己糖摄取。这些发现提供了直接证据，表明PKC是胰岛素刺激的己糖摄取所必需的。