CL 316, 243 mediated reductions in blood glucose are enhanced in RIP140-/- mice independent of alterations in lipolysis

被引：5

作者：

Peppler, Willem T. ^{[1
]}

Miotto, Paula M. ^{[1
]}

Holloway, Graham P. ^{[1
]}

Wright, David C. ^{[1
]}

机构：

[1] Univ Guelph, Dept Human Hlth & Nutr Sci, 50 Stone Rd E, Guelph, ON N1G 2W1, Canada

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2017年 / 486卷 / 02期

基金：

加拿大自然科学与工程研究理事会;

关键词：

CL; 316; 243; Adipose; Glucose; RIP140; Mouse; Lipolysis; TRANSCRIPTIONAL COREPRESSOR RIP140; WHITE ADIPOSE-TISSUE; BETA-3-ADRENERGIC RECEPTOR; MOLECULAR CHARACTERIZATION; MITOCHONDRIAL CONTENT; OXIDATIVE-METABOLISM; BROWN ADIPOCYTES; SKELETAL-MUSCLE; KNOCKOUT MICE; HEXOKINASE-II;

D O I：

10.1016/j.bbrc.2017.03.067

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The beta-3 adrenergic agonist CL 316, 243 acutely lowers blood glucose through a mechanism thought to involve fatty-acid induced insulin release. The purpose of this study was to determine if ablation of the nuclear receptor, receptor-inactivating protein 140 (RIP140), altered this response. Here, we used a single injection of CL 316, 243 (1 mg/kg) and found that whole body RIP140(-/-) mice had a greater decline in blood glucose over 2 h. This occurred alongside increased hexokinase II (HKII) protein content in adipose tissue and skeletal muscle, but independent of changes in circulating insulin or indices of lipolysis. These data indicate that RIP140 has a unique role in the acute effect of beta-3 adrenergic receptor activation using CL 316, 243. (C) 2017 Elsevier Inc. All rights reserved.

引用

页码：486 / 491

页数：6

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