Rabbit Anti-Human TMEM26 (a.a. 84-188) Polyclonal antibody

To elucidate effects of catechins and caffeine on lipid metabolism in adipocytes and identify the mechanism of action, differentiated 3T3-L1 adipocytes were incubated in culture media containing catechins at 1, 2.5, 5, and 10 mu g/mL and caffeine at 50 and 100 mu g/mL, singly or in combination, for 8 days. Intracellular lipid accumulation and glycerol-3-phosphate dehydrogenase activity were strongly suppressed by catechins and caffeine combination treatment. The mRNA expression of PPAR & x264;, GLUT4, HSL, UCP-1, and TMEM26 were significantly increased in the combined groups. These findings suggest that the combined treatment inhibited lipid synthesis and improved lipid metabolism in adipocytes. Moreover, it was indicated that the differentiated 3T3-L1 adipocytes could be transformed from white adipocytes to beige-like adipocytes by catechins and caffeine, and accordingly that this transformation could promote calorigenic action. Practical Application In this study, we revealed that the combined treatment of catechins and caffeine inhibited lipid synthesis and improved lipid metabolism in adipocytes. Moreover, the treatment may contribute to the transforming from white adipocytes to beige-like adipocytes, which could strongly promote calorigenic action.

White adipose tissue (WAT) can differentiate into beige adipose tissue by the browning process. Some polyphenols, including isoflavones, particularly genistein, are suggested to increase the expression of browning markers. There is evidence that consumption of genistein can attenuate body weight gain and improve glucose tolerance and blood lipid levels. The aim of the present study was to investigate the potential mechanisms of stimulation by which genistein activates the browning of WAT. We studied the stimulation of the expression of browning markers in the following models: mice fed genistein; preadipocytes from 3 T3-L1 cells; and the stromal vascular fraction (SVF) from the inguinal adipose tissue of mice. The results indicated that genistein can stimulate the browning process by at least two mechanisms. An indirect mechanism was involved in the induction of PGC-1 alpha/FNDC5 in skeletal muscle leading to an increase in the myokine irisin. In preadipocytes, irisin was able to increase the expression of Ucpl and Tmem26, markers of browning, to increase energy expenditure. Interestingly, genistein was also able to activate browning by a direct mechanism. Incubation of preadipocytes with genistein increased UCP1 expression as well as some biomarkers of browning in a concentration-dependent manner, possibly via phosphorylation of AMPK. The effect of genistein was accompanied by an increase in the number of mitochondria as well as in the maximum respiration rate of the adipocytes. In conclusion, this study indicated that genistein can increase energy expenditure by stimulating the browning process directly in preadipocytes and indirectly by increasing the circulating levels of irisin. (C) 2019 Elsevier Inc. All rights reserved.