?-Mangostin ameliorates hepatic steatosis and insulin resistance by inhibition C-C chemokine receptor 2.

ABSTRACT: Obesity induces various metabolic diseases such as dyslipidemia, nonalcoholic fatty liver disease (NAFLD), and type 2 diabetes. Fat expansion in adipose tissue induces adipose tissue dysfunction and inflammation, insulin resistance, and other metabolic syndromes. ?-Mangostin (?-MG) has been previously studied for its anti-cancer, anti-inflammatory, and antioxidant activities. In this study, we investigated the effects of ?-MG on adipose tissue inflammation and hepatic steatosis. We categorized study animals into four groups: regular diet control mice, RD mice treated with ?-MG, high fat diet-induced obese mice, and HFD mice treated with ?-MG. ?-MG treatment significantly reduced not only the body, liver, and fat weights, but also plasma glucose, insulin, and triglyceride levels in HFD mice. Additionally, adiponectin levels of ?-MG-treated mice were significantly higher than those of control HFD mice. Immunohistochemistry of liver and adipose tissue showed that CD11c expression was reduced in ?-MG fed obese mice. ?-MG treatment of HFD mice down-regulated the adipose-associated inflammatory cytokines and CCR2 in both liver and adipose tissue. Moreover, glucose tolerance and insulin sensitivity were significantly improved in ?-MG fed obese mice. ?-Mangostin ameliorates adipose inflammation and hepatic steatosis in HFD-induced obese mice.

SUBMITTER: Kim HM 

PROVIDER: S-EPMC5466328 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature