期刊
FEBS LETTERS
卷 582, 期 1, 页码 32-38出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2007.11.081
关键词
retinoid; retinaldehyde; PPARs; adipogenesis; obesity; apocarotenal
资金
- PHS HHS [R01 071745] Funding Source: Medline
Retinoids, naturally-occurring vitamin A derivatives, regulate metabolism by activating specific nuclear receptors, including the retinoic acid receptor (RAR) and the retinoid X receptor (RXR). RXR, an obligate heterodimeric partner for other nuclear receptors, including peroxisome proliferator-activated receptors (PPARs), helps coordinate energy balance. Recently, many groups have identified new connections between retinoid metabolism and PPAR responses. We found that retinaldehyde (Rald), a molecule that can yield RA through the action of retinaldehyde dehydrogenases (Raldh), is present in fat in vivo and can inhibit PPAR gamma-induced adipogenesis. In vitro, Rald inhibits RXR and PPAR gamma activation. Raldh1-deficient mice have increased Raid levels in fat, higher metabolic rates and body temperatures, and are protected against diet-induced obesity and insulin resistance. Interestingly, one specific asymmetric beta-carotene cleavage product, apo-14'-carotenal, can also inhibit PPAR gamma and PPAR alpha responses. These data highlight how pathways of beta-carotene metabolism and specific retinoid metabolites may have direct distinct metabolic effects. Crown Copyright (C) 2007 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies. All rights reserved.
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