Study on the Effect and Mechanism of Theaflavins on White Adipocyte Browning Transformation

碩士 === 國立嘉義大學 === 食品科學系研究所 === 106 === Prevention of obesity and related chronic diseases is the main nutritional health issue worldwide. Recent studies have proposed that promoting brown-like transformation of white adipocytes is the novel strategy for the treatment of obesity and related metabolic...

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Bibliographic Details
Main Author: 曹昌玉
Other Authors: 林淑美
Format: Others
Language:zh-TW
Published: 2018
Online Access:http://ndltd.ncl.edu.tw/handle/d9gfxt
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Summary:碩士 === 國立嘉義大學 === 食品科學系研究所 === 106 === Prevention of obesity and related chronic diseases is the main nutritional health issue worldwide. Recent studies have proposed that promoting brown-like transformation of white adipocytes is the novel strategy for the treatment of obesity and related metabolic diseases. The white adipocytes transform into brown adipocyte-like cells called beige adipocytes. Brown adipocytes are thermogenic that may increase systemic energy expenditure and prevent obesity. Black tea polyphenols are known to have a variety of health benefits. The purpose of this study is to further evaluate the polyphenolic compounds of the black tea, theaflavins, including theaflavin (TF1), theaflavin-3'-gallate (TF2) and theaflavin-3,3'-digallate (TF3) on adipose tissue browning and to elucidate the underlying mechanism of action. Mature 3T3-L1 adipocytes, 8 days after the adipogenic differentiation, were treated with or without 25 or 50 μM of TF1, TF2 or TF3 for 2 days, and isoproterenol (ISO; an adipocyte browning inducer)-treated cells served as a positive control group. The results showed that theaflavins or ISO treatment did not reduce the total lipid content in the mature adipocyte cells, but significantly reduced the intracellular oil droplet size and significantly reduced the cell mitochondrial membrane potential. The results of staining with nonylacridine orange (NAO) indicated that higher dose (50 μM) of theaflavins reduced the mitochondrial mass of the adipocytes, which was accompanied by the inhibition of mitochondrial biogenesis regulators, including PGC-1α (peroxisome proliferator-activated receptor-α coactivator), NRF-1 (nuclear respiratory factor-1), and mtTFA (mitochondrial transcription factor A). Low doses of theaflavins and Iso have no effect on the expression of these genes. Furthermore, theaflavins significantly reduced UCP1 (uncoupling protein1) and Cidea (cell death inducing DNA fragmentation factor -like effector A) in mouse adipocytes, Cited1 (Cbp/p300-inteacting transactivator with Glu-Asp-rich carboxyl-terminal domain 1), Ear2 and Slc27al gene expression, while ISO treatment does not have any effect on these gene expression. Based on the results of this study, the mechanism of the prevention of obesity by theaflavins is different from that of ISO, which may be through the regulation of the function, morphology and biosynthesis of mitochondria.