Journal
ADIPOCYTE
Volume 2, Issue 3, Pages 184-187Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/adip.23489
Keywords
retinoic acid; adipogenesis; nuclear receptors; fatty acid-binding protein; cellular retinoic acid-binding protein; RAR; PPAR
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Funding
- NIH [RO1-DK60684]
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The vitamin A metabolite retinoic acid (RA) regulates gene transcription by activating the nuclear receptors RAR and PPAR beta/delta and their cognate lipid binding proteins CRABP-II, which delivers RA to RAR, and FABP5, which shuttles the hormone to PPAR beta/delta. In preadipocytes, RA signals predominantly through CRABP-II and the RAR isotype RAR. to induce the expression of hallmark markers of preadipocytes Pref-1, Sox9, and KLF2. RA thus maintains the preadipocyte phenotype and inhibits adipogenesis. In mature adipocytes, RA activates both of its receptors to upregulate expression of genes that enhance lipid oxidation, energy dissipation, and insulin responses. Consequently, RA potently protects mice from diet-induced obesity and insulin resistance by two distinct mechanisms: by counteracting adipogenesis, thereby moderating the formation of new fat cells, and by promoting energy expenditure, thereby preventing adipocyte hypertrophy.
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