Liver Fibrosis-Fighting Hormones Found

Insulin-like growth factor-I has been shown to reduce fatty deposits, inflammation and fibrosis in mice with symptoms of non-alcoholic liver disease.

AsianScientist (Oct. 20, 2016) – A Japanese research team has identified and clarified the mechanism for a hormone that limits the fibrosis associated with NASH and cirrhosis. These findings were published in Scientific Reports.

Non-alcoholic steatohepatitis (NASH) has been emerging worldwide, and effective treatment is essential for improving the prognosis. NASH is a progression of non-alcoholic fatty liver disease (NAFLD) in the context of obesity and diabetes, resulting in fatty deposits, inflammation and fibrosis.

NAFLD is closely associated with metabolic syndrome, and cases of NASH are increasing along with obesity and diabetes. Furthermore, liver fibrosis (including its manifestation in liver cirrhosis) is strongly associated with increased mortality. However, current medicines only have limited effectiveness.

The prevalence of fatty liver and NASH are very high in patients with growth hormone (GH) deficiency. The research group, led by Associate Professor Takahashi Yutaka and medical research fellow Dr. Nishizawa Hitoshi from Kobe University, has demonstrated that this was caused by a lack of insulin-like growth factor-I (IGF-I), which is mainly induced by growth hormones.

The research group further proved that administering growth hormone alleviated the NASH conditions caused by adult growth hormones deficiency, and treatments of GH and IGF-I were effective when applied to model animals with growth hormone deficiency.

They also discovered that IGF-I improved the characteristics of NASH, especially fibrosis. When mice suffering from obesity-related NASH were given IGF-I, they showed drastic reductions in the hallmarks of NASH: fatty deposits, inflammation and fibrosis. This positive outcome was found to be due to the effect of IGF-I on hepatic stellate cells, which play a key role in the development of fibrosis. IGF-I was found to suppress the activation of these cells by causing cellular senescence and consequently preventing fibrosis.

These findings suggest that IGF-I can be used to prevent the development of fibrosis, and thus improve prognosis and alleviate complications for sufferers of NASH and cirrhosis.

The article can be found at: Nishizawa et al. (2016) IGF-I Induces Senescence of Hepatic Stellate Cells and Limits Fibrosis in a p53-Dependent Manner.


Source: Kobe University; Photo: Shutterstock.
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