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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 PLoS+One
2017 ; 12
(6
): e0179204
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?-Mangostin ameliorates hepatic steatosis and insulin resistance by inhibition
C-C chemokine receptor 2
#MMPMID28598982
Kim HM
; Kim YM
; Huh JH
; Lee ES
; Kwon MH
; Lee BR
; Ko HJ
; Chung CH
PLoS One
2017[]; 12
(6
): e0179204
PMID28598982
show ga
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.