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Induction of uncoupling protein-1 in mouse embryonic fibroblast-derived adipocytes by retinoic acid.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mercader, Josep Palou, Andreu Bonet, M. Luisa
Description	Country affiliation: Spain Author Affiliation: Mercader J ( Laboratory of Molecular Biology, Nutrition and Biotechnology, Universitat de les Illes Balears, Palma de Mallorca, Spain.)
Abstract	The uncoupling protein-1 (UCP1) is the molecular effector of thermogenesis in brown adipocytes, a process in which there is a renewed interest after the recent recognition of its relevance in adult humans. Typical white adipocytes do not express UCP1. We investigated the capacity of retinoic acid (RA), the carboxylic acid form of vitamin A and a known positive regulator of UCP1 gene transcription in brown adipocytes, to stimulate UCP1 expression in adipocytes differentiated in culture from primary mouse embryonic fibroblasts (MEFs), which are commonly used as white adipocyte model cells. Exposure to all-trans RA (ATRA), but not to rosiglitazone or isoproterenol, potently induced UCP1 expression at both the mRNA and protein level in MEF-derived adipocytes, in a dose-dependent manner. The effect on UCP1 mRNA was reproduced by retinoid receptor agonists and by retinaldehyde, required p38 mitogen-activated protein kinase activity (p38 MAPK), and appeared to be dissociated from increases in mitochondria biogenesis and oxidative capacity. MEF-derived adipocytes exhibited a high mRNA expression level of the brown fat determination factor PRDM16. The results highlight a specific potential of retinoids to induce UCP1 gene expression in adipose cells, and may have implications for the elucidation of the signaling pathways to the UCP1 gene, as well as for research using MEF-derived adipocytes.
File Format	HTM / HTML
ISSN	19307381
Issue Number	4
Volume Number	18
e-ISSN	1930739X
Journal	Obesity
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2010-04-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Endocrinology Adipocytes Drug Effects Adipose Tissue, Brown Metabolism Fibroblasts Ion Channels Membrane Proteins Mitochondria Mitochondrial Proteins Tretinoin Pharmacology Animals Cells, Cultured Dna-binding Proteins Genetics Dose-response Relationship, Drug Embryo, Mammalian Mice Oxidation-reduction Rna, Messenger Receptors, Retinoic Acid Retinaldehyde Transcription Factors P38 Mitogen-activated Protein Kinases Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Nutrition and Dietetics Endocrinology, Diabetes and Metabolism Endocrinology

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