Possible genetic involvement in non - alcoholic fatty liver disease

The most common condition affecting the liver is non-alcoholic liver disease (NAFLD). It is well known that the majority of people who suffer from nonalcoholic fatty liver disease (NAFLD) have one or more of the recently identified metabolic syndrome symptoms, including central obesity, impaired glucose tolerance, hypertension, and dyslipidemia. NAFLD is a group of illnesses that ranges from simple steatosis, which is defined by hepatocyte damage, inflammation, and a fatty liver, to steatohepatitis, fibrosis, and cirrhosis. NAFLD is a complicated disease. Through the promotion of liver inflammation, cell necrosis and apoptosis, and the creation of fibrosis, Cytokines may have a direct role in the development of nonalcoholic fatty liver disease (NAFLD). Adiponectin levels rise in NASH patients receiving thiazolidinedione therapy, indicating improvement in hepatic steatosis, necroinflammation, and—most importantly—fibrosis.Obese patients who inherit both high TGF-1 and angiotensinogen -producing polymorphisms may be more susceptible to advanced fibrosis.There have been a number of candidate gene studies and a small number of GWAS (genome-wide association studies) in NAFLD populations as a result of the heritability and complexity of NAFLD.PNPLA3 was the first variant associated with NAFLD.Recent GWA studies have demonstrated a relationship between the SNP rs58542926 C>T in theTM6SF2 gene and the severity of NAFLD. Both raised serum triglyceride levels and an enhanced fibrosis risk in NAFLD patients are linked to the GCKR P446L variant.An increase in inflammation and hepatic fibrosis in NAFLD patients is linked to the MBOAT7 variant.