Study of visfatin level in patients with non-alcoholic fatty liver disease and its role in progression to non-alcoholic steatohepatitis

Abstract

Nonalcoholic fatty liver disease (NAFLD) includes a wide range of liver clinicpathological conditions, starting from pure fatty steatosis (fatty infiltration in more than 5% of hepatocytes) which is a benign condition up to nonalcoholic steatohepatitis (NASH), which may develop to cirrhosis, liver failure and hepatocellular carcinoma (Noureddin et al., 2015).NAFLD has become by far the commonest chronic liver disease (CLD) in the United States, accounting for a steadily increasing percentage of CLD cases over the last quarter century. NAFLD accounted for 46.8% of CLD cases from 1988 to 1994; 62.8% from 1994 to 2004 and 75.1% from 2005 to 2008 (Younossi et al., 2011).

Visfatin was identified first as PreB cell Colony Enhancing Factor (PBEF). Recently, PBEF was identified by Fukuhara et al, as visfatin a novel adipokine (Fukuhara A et al., 2005).Visfatin is inflammatory cytokine that is produced and released by the adipose tissue derived macrophages. It promotes B-cell maturation, inhibits neutrophil apoptosis, enhances activation of leukocytes, synthesis of adhesion molecules and production of proinflammatory cytokines (DahL T et al., 2011). Visfatin is also suggested to be expressed in hepatocytes and inhibit apoptosis of hepatocytes in vitro, downregulation of visfatin in advanced inflammatory processes as NASH suggests a hepatoprotective role for visfatin(Jia SH et al., 2004). The role of Visfatin in non-alcoholic fatty liver disease is unclear.