Alterations in the production and function of growth hormone and insulin-like growth factor 1 are associated with obesity and the development and progression of nonalcoholic fatty liver disease.
Targeting the GH/IGF1 axis represents a potential novel therapeutic approach for the treatment of NAFLD and NASH.
Patients with obesity have a high prevalence of nonalcoholic fatty liver disease (NAFLD), representing a spectrum of simple steatosis to nonalcoholic steatohepatitis (NASH), without and with fibrosis. Understanding the etiology of NAFLD is clinically relevant since NAFLD is an independent risk factor for diabetes and cardiovascular disease. In addition, NASH predisposes patients to the development of cirrhosis and hepatocellular carcinoma, and NASH cirrhosis represents the fastest growing indication for liver transplantation in the United States. It is appreciated that multiple factors are involved in the development and progression of NAFLD. Growth hormone (GH) and insulin-like growth factor 1 (IGF1) regulate metabolic, immune, and hepatic stellate cell function, and alterations in the production and function of GH is associated with obesity and NAFLD/NASH. Therefore, this review will focus on the potential role of GH and IGF1 in the regulation of hepatic steatosis, inflammation, and fibrosis.
Dichtel et al. (Wed,) conducted a review in Nonalcoholic Fatty Liver Disease (NAFLD) and Nonalcoholic Steatohepatitis (NASH). Growth Hormone (GH) and Insulin-like Growth Factor 1 (IGF1) was evaluated. Alterations in the production and function of growth hormone and insulin-like growth factor 1 are associated with obesity and the development and progression of nonalcoholic fatty liver disease.