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Curcumin Attenuates Diet‐Induced Hepatic Steatosis by Activating AMP ‐Activated Protein Kinase
Author(s) -
Um Min Young,
Hwang Kwang Hyun,
Ahn Jiyun,
Ha Tae Youl
Publication year - 2013
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.12076
Subject(s) - curcumin , steatosis , endocrinology , medicine , ampk , amp activated protein kinase , chemistry , fatty acid synthase , lipid metabolism , fatty liver , adipose tissue , protein kinase a , kinase , biochemistry , disease
Abstract Curcumin is a well‐known component of traditional turmeric ( C urcuma longa ), which has been reported to prevent obesity and diabetes. However, the effect of curcumin on hepatic lipid metabolism remains unclear. The aim of this study was to examine the effects of curcumin on hepatic steatosis in high‐fat/cholesterol diet ( HFD )‐induced obese mice. Male C57 BL /6J mice were fed a normal diet ( ND ), HFD or HFD with 0.15% curcumin ( HFD +C) for 11 weeks. We found that curcumin significantly lowered the body‐weight and adipose tissue weight of mice in the HFD +C group compared with the findings for the HFD group ( p < 0.05). The levels of total cholesterol, fasting glucose and insulin in serum were decreased, and HFD ‐induced impairment of insulin sensitivity was improved by curcumin supplementation ( p < 0.05). Curcumin protected against the development of hepatic steatosis by reducing hepatic fat accumulation. Moreover, curcumin activated AMP ‐activated protein kinase ( AMPK ) and elevated the gene expression of peroxisome proliferator‐activated receptor alpha. By contrast, curcumin suppressed the HFD ‐mediated increases in sterol regulatory element‐binding protein‐1, acetyl‐CoA carboxylase 1, fatty acid synthase and cluster of differentiation 36 expression. Taken together, these findings indicate that curcumin attenuates HFD ‐induced hepatic steatosis by regulating hepatic lipid metabolism via AMPK activation, suggesting its use as a therapeutic for hepatic steatosis.