Non-alcoholic fatty liver disease (NAFLD) including hepatic steatosis, non-alcoholic steatohepatitis (NASH), and progressive liver fibrosis is now common in western countries. 

Overweight people are at increased risk of Fatty liver and liver fat being directly linked with hepatic insulin resistance. Hepatic steatosis is considered a benign stage of NAFLD which may advance to NASH in some patients.

Liver biopsy remains the only diagnostic tool to identify patients with NASH and it still sees a lack of effective treatment. 

Visceral obesity remains the prime risk factor for NAFLD and improper storage of triglycerides in adipocytes and elevated concentrations of free fatty acids may further increase hepatic lipid storage, insulin resistance, and progressive liver damage. 

Obesity increases the majority of adipose tissue-derived proteins which may contribute to systemic inflammation and liver damage. Notably, Adiponectin is highly abundant in human serum but obesity reduces its level. It lowers even more in patients with hepatic steatosis or NASH. Adiponectin distresses excess lipid storage in the liver and protects it from inflammation and fibrosis. Thus is famed as a protective adipokine in insulin resistance and obesity-related liver diseases. 

Drugs that tend to elevate the levels of systemic adiponectin may serve as therapeutics for NAFLD. There still lacks investigations and reports regarding Adiponectin receptor signalling pathways and potential hepatic adiponectin resistance in NASH. Recognizing molecules downstream of AdipoR1/2 and methods that enhance adiponectin receptor activity will prove reassuring for the treatment of NAFLD.

Source: World J Gastroenterol. 2011;17(23):2801-2811. doi:10.3748/wjg.v17.i23.2801