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Background : Non-alcoholic fatty liver disease (NAFLD) is caused by obesity, type 2 diabetes mellitus, dyslipidemia, and genetic factors. Also, hyperinsulinemia directly promotes fat accumulation in hepatocytes. Therefore, it is very important to suppress the most common risks of NAFLD, such as obesity and insulin resistance. In this context, we evaluated for the effects of black ginseng (BG) extract on lipid accumulation inhibition and degradation in hepatocytes.
Methods and Results : The aim of this study is to figure out the potential anti-lipogenic effects and the underlying mechanism of BG extract in a cellular-, type 2 diabetes mellitus (T2DM) animal model associated with NAFLD. T2DM animal used C57BL/KsJ db/db mouse (M. 6 wk, n = 56), treated with extract of BG and Red ginseng (RG) (each 100 and 900 ㎎/ ㎏/day, p.o) for 6 weeks. BG markedly reduced palmitate-induced intracellular lipid accumulation in HepG2 cells. On histology of liver tissues of T2DM animal, macrovesicular lipid droplets in cytoplasm of hepatocytes were decreased both RG and BG-treated groups. In liver tissue, BG-treated groups suppressed CCAAT/enhancer binding protein-α (C/EBP-α), sterol regulatory element-binding protein-1c (SREBP-1c) expression, and SREBP-1c mediated induction of acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) proteins related to the induction of adipose differentiation. Futhermore, adenosine monophosphate (AMP)-activated protein kinase (AMPK) activity was significantly increased in BG-treated groups compared to RG-treated groups. It is also found that peroxisome proliferator-activated receptor-α (PPAR-α) highly expressed in BG-treated groups.
Conclusion : Our results suggest that black ginseng extract has an anti-adipogenic and anti-lipogenic effects in the liver when administered as a food supplement and has potential as a therapeutic agent for obesity and T2DM induced NAFLD.
