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• W2035483673 abstract "The present study was undertaken to investigate the mechanism by which 1α, 25-dihydroxy-cholecalciferol [1α,25-(OH)2-VD3] modulates the differentiation of mouse 3T3-L1 preadipocytes into mature adipocytes. Treatment with 1α,25-(OH)2-VD3 in the presence of insulin, dexamethasone and 3-isobutyl-1-methyl-xanthine significantly inhibited the triacylglycerol accumulation, and mRNA expressions of adipocytokines (adiponectin and tumor necrosis factor-α) and plasminogen activator inhibitor-1 in the pico-nanomolar concentration range, indicating that 1α,25-(OH)2-VD3 under physiological conditions inhibits the differentiation of 3T3-L1 cells. 1α,25-(OH)2-VD3 potently reduced the mRNA and/or protein expressions of CCAAT-enhancer binding protein α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), and the nuclear translocation of PPARγ. Furthermore, it inhibited the mRNA expression and phosphorylation of extracellular signal-regulated kinase (ERK), one of mitogen-activated protein kinases. These results indicate that 1α,25-(OH)2-VD3 can be an inhibitor of adipocyte differentiation, and suggest, in addition to C/EBPα and PPARγ, an important role of ERK in mediating 1α,25-(OH)2-VD3-induced alteration in adipocyte differentiation." @default.
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• W2035483673 date "2012-01-01" @default.
• W2035483673 modified "2023-10-18" @default.
• W2035483673 title "The Involvement of Mitogen-Activated Protein Kinases in the 1^|^alpha;,25-Dihydroxy-Cholecalciferol-Induced Inhibition of Adipocyte Differentiation In Vitro" @default.
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• W2035483673 doi "https://doi.org/10.3177/jnsv.58.1" @default.
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