Journal
BMC CELL BIOLOGY
Volume 14, Issue -, Pages -Publisher
BMC
DOI: 10.1186/1471-2121-14-41
Keywords
Adipogenesis; ATRA; Brown adipocyte; UCP1; White adipocyte
Categories
Funding
- Novo Scholarship
- EU FP7 project DIABAT [HEALTH-F2-2011-278373]
- Danish Medical Research Council
- Novo Nordisk Foundation
- Carlsberg Foundation
- Aase and Ejnar Danielsen Foundation
- Augustinus Foundation
- Hartmann Brothers' Foundation
- Beckett Foundation
- Fonden til Laegevidenskabens Fremme
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Background: Increased adipose thermogenesis is being considered as a strategy aimed at preventing or reversing obesity. Thus, regulation of the uncoupling protein 1 (UCP1) gene in human adipocytes is of significant interest. Retinoic acid (RA), the carboxylic acid form of vitamin A, displays agonist activity toward several nuclear hormone receptors, including RA receptors (RARs) and peroxisome proliferator-activated receptor delta (PPAR delta). Moreover, RA is a potent positive regulator of UCP1 expression in mouse adipocytes. Results: The effects of all-trans RA (ATRA) on UCP1 gene expression in models of mouse and human adipocyte differentiation were investigated. ATRA induced UCP1 expression in all mouse white and brown adipocytes, but inhibited or had no effect on UCP1 expression in human adipocyte cell lines and primary human white adipocytes. Experiments with various RAR agonists and a RAR antagonist in mouse cells demonstrated that the stimulatory effect of ATRA on UCP1 gene expression was indeed mediated by RARs. Consistently, a PPAR delta agonist was without effect. Moreover, the ATRA-mediated induction of UCP1 expression in mouse adipocytes was independent of PPAR gamma coactivator-1 alpha. Conclusions: UCP1 expression is differently affected by ATRA in mouse and human adipocytes. ATRA induces UCP1 expression in mouse adipocytes through activation of RARs, whereas expression of UCP1 in human adipocytes is not increased by exposure to ATRA.
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