The Involvement of Mitogen-Activated Protein Kinases in the 1α,25-Dihydroxy-Cholecalciferol-Induced Inhibition of Adipocyte Differentiation In Vitro

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-meth...

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Published in:Journal of Nutritional Science and Vitaminology 2012, Vol.58(1), pp.1-8
Main Authors: SAKUMA, Satoru, FUJISAWA, Junji, SUMIDA, Maki, TANIGAWA, Mami, INODA, Rie, SUJIHERA, Takuya, KOHDA, Tetsuya, FUJIMOTO, Yohko
Format: Article
Language:English
Subjects:
1α,25-dihydroxy-cholecalciferol
3T3-L1 cells
adipocyte differentiation
Adipocytes
Biological and medical sciences
Feeding. Feeding behavior
Fundamental and applied biological sciences. Psychology
mitogen-activated protein kinases
Vertebrates: anatomy and physiology, studies on body, several organs or systems
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Summary: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.
ISSN:0301-4800
1881-7742
DOI:10.3177/jnsv.58.1