Intermittent restraint-induced sympathetic activation attenuates hepatic steatosis and inflammation in a high fat-diet fed-mouse model.

08:00 EDT 11th October 2019 | BioPortfolio

Summary of "Intermittent restraint-induced sympathetic activation attenuates hepatic steatosis and inflammation in a high fat-diet fed-mouse model."

NAFLD is very prevalent worldwide, and is associated with insulin resistance and metabolic syndrome. Stress is physiological and biological response to maintain homeostasis of body against stressors while severe stress response is an important contributor to various illnesses including metabolic syndrome and brain disorders. We have evaluated the effects of intermittent restraint stress on NAFLD in a HFD-fed mouse model. C57/BL6 mice had free access to a 60% HFD for 8 weeks, with or without intermittent restraint stress (3 h) conducted 3 times a week. HFD administration increased fat accumulation in liver tissues. Unlike the stressed standard diet group, the levels of hepatic total cholesterol and triglycerides were significantly ameliorated in the HFD with stress group compared to the HFD alone group. These beneficial results were in accordance with serum levels of liver enzymes (AST, ALT) and hepatic levels of TNF-α and oxidative stress parameters (ROS, NO, and malondialdehyde). The intermittent restraint stress significantly attenuated the HFD-derived alterations in serum insulin levels, hepatic protein kinase B (AKT) activity and gene expression especially related to lipogenesis. This intermittent restraint stress also elevated the serum epinephrine concentration and activated the adrenergic receptor β2 or β 3 in livers or WAT. The activations of energy expenditure markers (UCP1, PGC1α) in brown adipose tissue and the browning of WAT were also observed in the HFD with stress group. Taken together, our findings showed the beneficial effects of sympathetic activation by intermittent restraint stress on HFD-induced hepatic steatosis and partial inflammation.


Journal Details

This article was published in the following journal.

Name: American journal of physiology. Gastrointestinal and liver physiology
ISSN: 1522-1547


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