Effects and Mechanism of Bisdemethoxycurcumin on Glucose and Lipid Metabolism in Obese Mice

OBJECTIVE To study the effects of bisdemethoxycurcumin(BDMC) on insulin resistance and disorders of glucose and lipid metabolism in high glucose/high fat diet-induced obese mice, and to explore its mechanism. METHODS Forty C57BL/6 mice were randomly divided into the normal group(10 mice) and the high-sugar and high-fat diet group(30 mice). The mice in the normal group were given conventional feed, and the other mice were fed high-sugar and high-fat diet to induce obesity for 8 weeks. After successful modeling, mice in the high-sugar and high-fat diet group were randomly divided into model group, BDMC low-dose group(20 mg·kg^-1), and BDMC high-dose group(40 mg·kg^-1), with 10 mice in each group. They were administered by gavage once a day, 5 times a week for 8 consecutive weeks. At the end of experiment, body weight, liver and adipose weight, the pathological changes and lipid accumulation in the liver of mice, biochemical indexes including blood glucose, blood lipid, serum insulin and others were monitored. The effects of BDMC on TRPV1, AMPK, the downstream insulin signal and glucose and lipid metabolism pathway were investigated. RESULTS Compared with the normal group, the body weight and organ index of mice in the model group were increased, the liver showed obvious pathological changes, the lipid accumulation was serious, the serum insulin, blood glucose and blood lipid parameters(TC, TG, LDL-C) were significantly increased, and HDL-C was significantly decreased; liver injury(ALT, AST) aggravated; the expression of TRPV1, SREBP and FAS in liver tissue was significantly increased, and the expression of p-IRS1, p-AMPK, GLUT4 and p-ACC was significantly decreased. Compared with the model group, after treatment with BDMC, liver lipid accumulation was reduced, histopathological changes were restored, blood glucose, serum insulin, TC, TG, LDL-C, ALT, AST were significantly decreased(P<0.05), HDL-C was significantly increased, p-IRS1, p-AMPK, GLUT4, p-ACC expression in liver was increased, TRPV1, SREBP, FAS expression was significantly decreased(P<0.05). CONCLUSION BDMC can improve insulin resistance and regulate metabolism disorders of glucose and lipid to treat high-sugar and high-fat diet induced obesity, and which may be related to the regulation of TRPV1 and AMPK.