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Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Tocotrienol Suppresses Adipocyte Differentiation and Akt Phosphorylation in 3T3-L1 Preadipocytes^1–3,

⁴ Internal Medicine 1, National Defense Medical College, Tokorozawa-shi, Saitama 359-8513, Japan; ⁵ Faculty of Education, Utsunomiya University, Utsunomiya-shi, Tochigi 321-8505, Japan; ⁶ Department of Applied Bioscience, Kanagawa Institute of Technology, Atsugi-shi, Kanagawa 243-0292, Japan; ⁷ Institute of Environmental Science for Human Life, Ochanomizu University, Bunkyo-ku, Tokyo 112-8610, Japan; ⁸ Department of Education, Hirosaki University, Hirosaki-shi, Aomori 036-8560, Japan; and ⁹ Department of Life Science, Ibaraki Christian University, Hitachi, Ibaraki 319-1295, Japan

In vivo studies show that -tocotrienol and -tocotrienol accumulate in adipose tissue. Furthermore, a recent study reports that the oral administration of -tocotrienol from a tocotrienol-rich fraction from palm oil (TRF) decreases body fat levels in rats. The objective of this study was to evaluate the effect of TRF and its components on adipocyte differentiation in 3T3-L1 preadipocytes, which differentiated into adipocytes in the presence of 1.8 µmol/L insulin. TRF suppressed the insulin-induced mRNA expression of adipocyte-specific genes such as PPAR, adipocyte fatty acid-binding protein (aP2), and CCAAT/enhancer-binding protein- (C/EBP) compared with the differentiation of 3T3-L1 preadipocytes into adipocytes only in the presence of insulin. To confirm the suppressive effect of TRF, the major components of TRF, such as -tocotrienol, -tocotrienol, and -tocopherol, were investigated. -Tocotrienol and -tocotrienol decreased the insulin-induced PPAR mRNA expression by 55 and 90%, respectively, compared with insulin, whereas -tocopherol increased the mRNA expression. In addition, -tocotrienol suppressed the insulin-induced aP2 and C/EBP mRNA expression, triglyceride accumulation, and PPAR protein levels compared with insulin. The current results also revealed that -tocotrienol inhibited the insulin-stimulated phosphorylation of Akt but not extracellular signal-regulated kinase (ERK)1/2 in the insulin signaling pathway of 3T3-L1 preadipocytes. Thus, the antiadipogenic effect of TRF depends on -tocotrienol and -tocotrienol, and -tocotrienol may be a more potent inhibitor of adipogenesis than -tocotrienol. Therefore, the results of this study suggest that tocotrienol suppresses insulin-induced differentiation and Akt phosphorylation in 3T3-L1 preadipocytes. Furthermore, tocotrienol could act as an antiadipogenic vitamin in the nutrient-mediated regulation of body fat through its effects on differentiation.

^* To whom correspondence should be addressed. E-mail: kondo.kazuo{at}ocha.ac.jp.

Manuscript received 15 July 2008. Initial review completed 12 August 2008. Revision accepted 22 October 2008.

Published online 3 December 2008.