Chronic stress induces steatohepatitis while decreases visceral fat mass in mice
1 Laboratory of Stress Medicine, Faculty of Psychology and Mental Health, Second Military Medical University, Shanghai, PR of China
2 Department of Nautical Medicine, Second Military Medical University, Shanghai, PR of China
3 Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai, PR of China
4 Department of Endocrinology and Metabolism, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, PR of China
BMC Gastroenterology 2014, 14:106 doi:10.1186/1471-230X-14-106Published: 10 June 2014
Prolonged stress leads over time to allostatic load on the body and is likely to exacerbate a disease process. Long-term of stress exposure is one of a risk factor for metabolism-related diseases such as obesity and type 2 diabetes. However, the relationship between chronic stress and non-alcoholic fatty liver disease (NAFLD) remain unknown.
To address the hypothesis that chronic stress associate to NAFLD development, we subjected C57bl/6 mice to electric foot shock and restraint stress for 12 weeks to set up chronic stress model. Then the serum and hepatic triglyceride (TG), total cholesterol (TC) were measured. Hepatic HE and Oil red O staining were used to specify the state of the NAFLD. To investigate whether inflammation takes part in the stress-induced NAFLD process, related visceral fat, serum and hepatic inflammatory factors were measured.
We observed that chronic stress led to an overall increase of hepatic triglyceride and cholesterol while decreasing body weight and visceral fat mass. Microvesicular steatosis, lobular inflammation and ballooning degeneration were seen in stress liver section. This effect was correlated with elevated hepatic and serum inflammatory factors. Although the amount of visceral fat was decreased in stress group, various adipocytokines were elevated.
We showed that chronic stress is associated to NAFLD and chronic inflammation in visceral fat, though food intake and visceral fat mass were decreased. These results may contribute to better understanding of the mechanism from steatosis to steatohepatitis, and propose a novel insight into the prevention and treatment of NAFLD.