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PLoS One. 2017 Jun 9;12(6):e0179204. doi: 10.1371/journal.pone.0179204. eCollection 2017.

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

Author information

1
Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea.
2
Laboratory of Microbiology and Immunology, College of Pharmacy, Kangwon National University, Chuncheon, Korea.

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. α-Mangostin (α-MG) has been previously studied for its anti-cancer, anti-inflammatory, and antioxidant activities. In this study, we investigated the effects of α-MG on adipose tissue inflammation and hepatic steatosis. We categorized study animals into four groups: regular diet control mice, RD mice treated with α-MG, high fat diet-induced obese mice, and HFD mice treated with α-MG. α-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 α-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 α-MG fed obese mice. α-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 α-MG fed obese mice. α-Mangostin ameliorates adipose inflammation and hepatic steatosis in HFD-induced obese mice.

PMID:
28598982
PMCID:
PMC5466328
DOI:
10.1371/journal.pone.0179204
[Indexed for MEDLINE]
Free PMC Article

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