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1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the active metabolite of vitaminD, was found to have anti-adipogenic activity, however, its mechanism of actionhas not been fully elucidated. In this study, 3T3-L1 preadipocytes were differentiatedin the presence and absence of 1,25(OH)2D3, and the expression of the genes andproteins of the wingless-type MMTV integration site (WNT)/β-catenin pathway wereanalyzed. While the expression of the members of the WNT/β-catenin pathway weresignificantly downregulated during the adipogenesis of untreated 3T3-L1 cells,1,25(OH)2D3 treatment was found to maintain the WNT/β-catenin pathway. Among themembers of the WNT/β-catenin pathway, the levels of WNT10B and disheveled (DVL)2as well as the phosphorylation of glycogen synthase kinase (GSK)3β were maintainedby 1,25(OH)2D3 treatment. The levels of nuclear β-catenin, which were downregulatedduring adipogenesis, were also maintained by 1,25(OH)2D3 treatment. The resultsof this study suggested that the anti-adipogenic effect of 1,25(OH)2D3 was mediatedby the maintenance of the WNT/β-catenin pathway, which was normally downregulatedduring adipogenesis.

Anti-adipogenic effects of 1,25-dihydroxyvitamin D3 are mediated by the maintenance of the wingless-type MMTV integration site/β-catenin pathway