Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

Ghrelin induces abdominal obesity via GHS-R-dependent lipid retention

Davies, Jeffrey Stephens, Kotokorpi, Pia, Eccles, Sinan R., Barnes, Sarah K., Tokarczuk, Pawel Franciszek, Allen, Sophie Katharine, Whitworth, Hilary S., Guschina, Irina, Evans, Bronwen Alice James, Mode, Agneta, Zigman, Jeffrey M. and Wells, Timothy 2009. Ghrelin induces abdominal obesity via GHS-R-dependent lipid retention. Molecular Endocrinology 23 (6) , pp. 914-924. 10.1210/me.2008-0432

Full text not available from this repository.

Abstract

Circulating ghrelin elevates abdominal adiposity by a mechanism independent of its central orexigenic activity. In this study we tested the hypothesis that peripheral ghrelin induces a depot-specific increase in white adipose tissue (WAT) mass in vivo by GH secretagogue receptor (GHS-R1a)-mediated lipolysis. Chronic iv infusion of acylated ghrelin increased retroperitoneal and inguinal WAT volume in rats without elevating superficial sc fat, food intake, or circulating lipids and glucose. Increased retroperitoneal WAT mass resulted from adipocyte enlargement probably due to reduced lipid export (ATP-binding cassette transporter G1 mRNA expression and circulating free fatty acids were halved by ghrelin infusion). In contrast, ghrelin treatment did not up-regulate biomarkers of adipogenesis (peroxisome proliferator-activated receptor-γ2 or CCAAT/enhancer binding protein-α) or substrate uptake (glucose transporter 4, lipoprotein lipase, or CD36) and although ghrelin elevated sterol-regulatory element-binding protein 1c expression, WAT-specific mediators of lipogenesis (liver X receptor-α and fatty acid synthase) were unchanged. Adiposity was unaffected by infusion of unacylated ghrelin, and the effects of acylated ghrelin were abolished by transcriptional blockade of GHS-R1a, but GHS-R1a mRNA expression was similar in responsive and unresponsive WAT. Microarray analysis suggested that depot-specific sensitivity to ghrelin may arise from differential fine tuning of signal transduction and/or lipid-handling mechanisms. Acylated ghrelin also induced hepatic steatosis, increasing lipid droplet number and triacylglycerol content by a GHS-R1a-dependent mechanism. Our data imply that, during periods of energy insufficiency, exposure to acylated ghrelin may limit energy utilization in specific WAT depots by GHS-R1a-dependent lipid retention.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Medicine
Subjects: R Medicine > R Medicine (General)
Publisher: The Endocrine Society
ISSN: 0888-8809
Last Modified: 07 Dec 2019 03:46
URI: http://orca.cf.ac.uk/id/eprint/8914

Citation Data

Cited 92 times in Google Scholar. View in Google Scholar

Cited 113 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item Edit Item