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Publication : Targeted expression of human vitamin D receptor in adipocytes decreases energy expenditure and induces obesity in mice.

First Author  Wong KE Year  2011
Journal  J Biol Chem Volume  286
Issue  39 Pages  33804-10
PubMed ID  21840998 Mgi Jnum  J:176720
Mgi Id  MGI:5292575 Doi  10.1074/jbc.M111.257568
Citation  Wong KE, et al. (2011) Targeted expression of human vitamin d receptor in adipocytes decreases energy expenditure and induces obesity in mice. J Biol Chem 286(39):33804-10
abstractText  Our previous studies demonstrated a high fat diet-resistant lean phenotype of vitamin D receptor (VDR)-null mutant mice mainly due to increased energy expenditure, suggesting an involvement of the VDR in energy metabolism. Here, we took a transgenic approach to further define the role of VDR in adipocyte biology. We used the aP2 gene promoter to target the expression of the human (h) VDR in adipocytes in mice. In contrast to the VDR-null mice, the aP2-hVDR Tg mice developed obesity compared with the wild-type counterparts without changes in food intake. The increase in fat mass was mainly due to markedly reduced energy expenditure, which was correlated with decreased locomotive activity and reduced fatty acid beta-oxidation and lipolysis in the adipose tissue in the transgenic mice. Consistently, the expression of genes involved in the regulation of fatty acid transport, thermogenesis, and lipolysis were suppressed in the transgenic mice. Taken together, these data confirm an important role of the VDR in the regulation of energy metabolism.
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