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Article
Nature Medicine 13, 695 - 702 (2007)
Published online: 27 May 2007 | doi:10.1038/nm1587
Retinaldehyde represses adipogenesis and diet-induced obesity
Ouliana Ziouzenkova1, Gabriela Orasanu1, Molly Sharlach1, Taro E Akiyama2, Joel P Berger2, Jason Viereck3, James A Hamilton3, Guangwen Tang4, Gregory G Dolnikowski4, Silke Vogel5, Gregg Duester6 & Jorge Plutzky1
Abstract
The metabolism of vitamin A and the diverse effects of its metabolites are tightly controlled by distinct retinoid-generating enzymes, retinoid-binding proteins and retinoid-activated nuclear receptors. Retinoic acid regulates differentiation and metabolism by activating the retinoic acid receptor and retinoid X receptor (RXR), indirectly influencing RXR heterodimeric partners. Retinoic acid is formed solely from retinaldehyde (Rald), which in turn is derived from vitamin A. Rald currently has no defined biologic role outside the eye. Here we show that Rald is present in rodent fat, binds retinol-binding proteins (CRBP1, RBP4), inhibits adipogenesis and suppresses peroxisome proliferator-activated receptor-
and RXR responses. In vivo, mice lacking the Rald-catabolizing enzyme retinaldehyde dehydrogenase 1 (Raldh1) resisted diet-induced obesity and insulin resistance and showed increased energy dissipation. In ob/ob mice, administrating Rald or a Raldh inhibitor reduced fat and increased insulin sensitivity. These results identify Rald as a distinct transcriptional regulator of the metabolic responses to a high-fat diet.
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