Parathyroid hormone suppresses insulin signaling in adipocytes

被引：63

作者：

Chang, Eugene ^{[1
]}

Donkin, Shawn S. ^{[1
]}

Teegarden, Dorothy ^{[1
]}

机构：

[1] Purdue Univ, Interdept Nutr Program, W Lafayette, IN 47907 USA

来源：

MOLECULAR AND CELLULAR ENDOCRINOLOGY | 2009年 / 307卷 / 1-2期

关键词：

Insulin receptor; Insulin receptor substrate-1; Glucose; Parathyroid hormone; NECROSIS-FACTOR-ALPHA; KAPPA-B ACTIVATION; 3T3-L1; ADIPOCYTES; PRIMARY HYPERPARATHYROIDISM; RECEPTOR SUBSTRATE-1; GLUCOSE-INTOLERANCE; TNF-ALPHA; EXPRESSION; RESISTANCE; PHOSPHORYLATION;

D O I：

10.1016/j.mce.2009.03.024

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Previous reports suggest that parathyroid hormone (PTH) is associated with insulin resistance. This research investigated the effects of PTH on insulin signaling in differentiated 3T3-L1 adipocytes. PTH (10 nM, 24 h) treatment induced a reduction in insulin-stimulated glucose uptake, AKT activity (phosphorylated AKT/total AKT protein expression) and a decrease in GLUT4 and IRS-1 protein expression compared to vehicle treated controls in differentiated adipocytes. PTH treatment also induced increased phosphorylation of IRS-1 on serine 307, which suppresses insulin signaling. In addition, treatment of cells with adenyl cyclase inhibitor SQ52236 ameliorated the effects of PTH on insulin-stimulated glucose uptake, whereas inhibition of phospholipase C alpha (U73122) did not significantly alter the effects of PTH. Thus, PTH treatment of differentiated 3T3-L1 adipocytes suppresses insulin-stimulated glucose uptake and insulin signaling via cAMP pathway, potentially through the phosphorylation of IRS-1 at serine 307. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

引用

页码：77 / 82

页数：6

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