MARIOS DIMOPOULOS

MARIOS DIMOPOULOS
Marios Dimopoulos Clinical Nutritionist, Author, Fellow of the American Council of the Applied Clinical Nutrition

Κυριακή, 9 Φεβρουαρίου 2014

Tocotrienols stop new fat cells from forming

One of the great problems involved with being overweight is the extreme ease with which new fat cells form.  A new study shows that alpha and gamma tocotrienol can help prevent baby fat cells from turning into adult fat cells. 
It should be rather obvious to anyone that if you overeat you will expand your fat cell population, regardless of what nutrients you may also consume, because your body must have some place to store all the extra calories.
However, one of the frustrating points regarding weight management is the ease with which fat cells are willing to multiply, even if you are mostly being good.  Just a few days of overeating and you can pack on five quick pounds – frustrating to say the least.
Once your fat cells have “learned” how to store weight in excess, it appears that this is a ‘lesson” not easily forgotten.  All you have to do is get your insulin too high, by eating a meal that is too large or by snacking between meals, and presto – new fat cells start forming.
It is known that the fat soluble forms of tocotrienol vitamin E accumulate in your fat cells.  The new study showed that once they are there they dramatically help change the way insulin is communicating within fat cells, towards the objective of not causing baby fat cells to turn into full-fledged fat-storing adults.
Tocotrienols are the superior form of vitamin E for cardiovascular health.  This study shows they are one more tool that helps in the battle to maintain your weight at the correct level.

Source
Uto-Kondo H, Ohmori R, Kiyose C, Kishimoto Y, Saito H, Igarashi O, Kondo K. Tocotrienol suppresses adipocyte differentiation and Akt phosphorylation in 3T3-L1 preadipocytes. J Nutr.   2009 January  139(1):51-7.
Internal Medicine 1, National Defense Medical College, Tokorozawa-shi, Saitama 359-8513, Japan.

Study Abstract:

In vivo studies show that alpha-tocotrienol and gamma-tocotrienol accumulate in adipose tissue. Furthermore, a recent study reports that the oral administration of gamma-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 micromol/L insulin. TRF suppressed the insulin-induced mRNA expression of adipocyte-specific genes such as PPARgamma, adipocyte fatty acid-binding protein (aP2), and CCAAT/enhancer-binding protein-alpha (C/EBPalpha) 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 alpha-tocotrienol, gamma-tocotrienol, and alpha-tocopherol, were investigated. Alpha-tocotrienol and gamma-tocotrienol decreased the insulin-induced PPARgamma mRNA expression by 55 and 90%, respectively, compared with insulin, whereas alpha-tocopherol increased the mRNA expression. In addition, gamma-tocotrienol suppressed the insulin-induced aP2 and C/EBPalpha mRNA expression, triglyceride accumulation, and PPARgamma protein levels compared with insulin. The current results also revealed that gamma-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 alpha-tocotrienol and gamma-tocotrienol, and gamma-tocotrienol may be a more potent inhibitor of adipogenesis than alpha-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.

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