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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #218639

Title: Vitamin D and Adipogenesis: New Molecular Insights

Author
item Wood, Richard

Submitted to: Nutrition Reviews
Publication Type: Review Article
Publication Acceptance Date: 11/15/2007
Publication Date: 1/1/2008
Citation: Wood, R. 2008. Vitamin D and Adipogenesis: New Molecular Insights. Nutrition Reviews. 66:40-46.

Interpretive Summary: The focus of the current review is to highlight some new insights into the molecular mechanism by which vitamin D, a potentially nutritionally modulated factor, influences the formation of new fat cells. Recent studies using cell culture have shown that the role of vitamin D in inhibiting the production of new fat cells from in the progenitor cells is mediated at the molecular level through hormone binding proteins in the precursor cell from which mature fat cells derive and a disruption of the ability of one of these hormone receptors to signal properly. These findings may be relevant to understand the nutritionally modifiable factors that can influence the development of obesity, a major public health problem. The next important step is to investigate the influence of vitamin D status on weight management in experimental animals and people.

Technical Abstract: The focus of the current review is to highlight some new insights into the molecular mechanism by which vitamin D, a potentially nutritionally modulated factor, influences adipogenesis. Recent studies, predominantly using the mouse 3T3-L1 pre-adipocyte cell culture model, have shown that the role of vitamin D in inhibiting adipogenesis is mediated at the molecular level through a vitamin D receptor (VDR)-dependent inhibition of CCAAT enhancer binding protein-alpha (C/EBPa) and peroxisome proliferator-activated receptor-gamma (PPARy) expression and a decrease in PPARy transactivating activity in the pre-adipocyte. The latter action may reflect a vitamin D-induced decrease in endogenous PPARy ligand availability and a competition between VDR and PPARy for a limiting amount of retinoid X receptor (RXR), a common heterodimeric binding partner of both nuclear receptors.