HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Raichur, S. Articles by Muscat, G. E O Search for Related Content PubMed PubMed Citation Articles by Raichur, S. Articles by Muscat, G. E O

¹ Institute for Molecular Bioscience, University of Queensland St Lucia, 4072, Queensland, Australia
² Departement d’Atherosclerose, Institut Pasteur de Lille, Inserm, U545, Lille F-59019, France
³ Faculte de Pharmacie et Faculte de Medecine, Universite de Lille 2, Lille F-59019, France

(Requests for offprints should be addressed to G E O Muscat; Email: g.muscat{at}imb.uq.edu.au)

Retinoid-related orphan receptor (ROR) is an orphan nuclear hormone receptor (NR) that is preferentially expressed in skeletal muscle and several other tissues, including pancreas, thymus, prostate, liver and testis. Surprisingly, the specific role of ROR in skeletal muscle, a peripheral tissue, has not been examined. Muscle is one of the most energy demanding tissues which accounts for ~40% of the total body mass and energy expenditure, >75% of glucose disposal and relies heavily on ß-oxidation of fatty acids. We hypothesize that ROR regulates metabolism in this major mass lean tissue. This hypothesis was examined by gain and loss of function studies in an in vitro mouse skeletal muscle cell culture model. We show that ROR mRNA and protein are dramatically induced during skeletal muscle cell differentiation. We utilize stable ectopic over-expression of VP16-ROR (gain of function), native ROR and RORH12 (loss of function) vectors to modulate ROR mRNA expression and function. Ectopic VP16 (herpes simplex virus transcriptional activator)-ROR and native ROR expression increases ROR mRNA expression. Candidate-driven expression profiling of lines that ectopically express the native and variant forms of ROR suggested that this orphan NR has a function in regulating the expression of genes that control lipid homeostasis (fatty acid-binding protein 4, CD36 (fatty acid translocase), lipoprotein lipase and uncoupling protein 3), carbohydrate metabolism (GLUT5 (fructose transporter), adiponectin receptor 2 and interleukin 15 (IL-15)) and muscle mass (including myostatin and IL-15). Surprisingly, the investigation revealed a function for ROR in the pathway that regulates production of reactive oxygen species.

This article has been cited by other articles:

				V. Douard and R. P. Ferraris Regulation of the fructose transporter GLUT5 in health and disease Am J Physiol Endocrinol Metab, August 1, 2008; 295(2): E227 - E237. [Abstract] [Full Text] [PDF]

				L. S. Quinn Interleukin-15: A muscle-derived cytokine regulating fat-to-lean body composition J Anim Sci, April 1, 2008; 86(14_suppl): E75 - E83. [Abstract] [Full Text] [PDF]