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Open Access Research article

The relationship between hepatic resistin overexpression and inflammation in patients with nonalcoholic steatohepatitis

Chuan Shen1, Cai-Yan Zhao1*, Wei Wang1, Ya-Dong Wang1, Hui Sun1, Wei Cao1, Wei-Yan Yu1, Li Zhang1, Ru Ji1, Meng Li2 and Jian Gao3

Author Affiliations

1 Department of Infectious Disease, The Third Affiliated Hospital of Hebei Medical University, 139 Ziqiang Road, Shijiazhuang 050051, China

2 Department of Endocrinology and Metabolism, The Third Affiliated Hospital of Hebei Medical University, 139 Ziqiang Road, Shijiazhuang 050051, China

3 Department of Hepatobiliary Surgery, The Third Affiliated Hospital of Hebei Medical University, 139 Ziqiang Road, Shijiazhuang 050051, China

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BMC Gastroenterology 2014, 14:39  doi:10.1186/1471-230X-14-39

Published: 23 February 2014

Abstract

Background

The relationship between resistin and non-alcoholic steatohepatitis (NASH) is not clear, some studies claimed that serum resistin levels were associated with neither the presence of NASH nor its severity, others declared that serum resistin was related with inflammation and fibrosis in NASH. Our animal study verified that the distribution of resistin in the liver is correlated with inflammation in NASH. However, there is no pertinent study in humans.

Methods

Thirty patients with NASH, 28 simple steatosis, and 43 controls were recruited. Blood was collected for resistin, liver chemistries, fasting insulin and some metabolic parameters. Liver histology was scored according to NAFLD activity scoring system. Hepatic resistin expression was examined by real-time polymerase chain reaction, immunohistochemistry. Resistin protein expression was confirmed by western blotting in 13 patients with concomitant NAFLD and gallstone.

Results

Serum resistin was significantly elevated in both NASH and simple steatotic subjects compared with controls (all P < 0.05). Hepatic resistin was significantly increased in NASH patients in both mRNA and protein levels than those in simple steatosis and control subjects (all P < 0.05). Both serum and hepatic resistin had a correlation with obesity, but not with insulin resistance. The distribution of resistin positive cells was predominantly in perisinusoidal cells (such as Kupffer cells and hepatic stellate cells) in human NASH. Multivariate analysis revealed that waist-hip ratio, higher serum triglyceride, and hyperresistinemia were independent factors related to higher grade of steatosis; whereas hepatic resistin and serum cytokeratin predict NASH and severity of liver fibrosis.

Conclusions

Hepatic resistin overexpression in NASH patients is associated with the severity of liver inflammation and fibrosis. Liver-derived resistin may be involved in the pathogenesis of human NASH.

Keywords:
Resistin; Nonalcoholic steatohepatitis; Nonalcoholic fatty liver disease; Inflammation; Adipokine