Overview of Genetics in Non Alcoholic Fatty Liver Disease: A Futuristic Cognizance

Abstract

Non Alcoholic Fatty Liver Disease (NAFLD) is an emerging epidemic worldwide. It comprehends simple steatosis to escalating steatosis with associated fibrosis, cirrhosis, and Hepatocellular Carcinoma (HCC). NAFLD patients are at increased risk of liver-related as well as cardiovascular mortality. It seems to have a robust interconnection with visceral adiposity, Insulin Resistance (IR), inflammation, and environmental factors. Although the pathogenesis of NAFLD is presumed to be linked to lifestyle patterns, nutritional factors, and genetics, the predictor of advancement of this disease spectrum caused by genetics stands imprecise. In the past decade, multiple genome-wide associations and large candidate gene studies have recognised the contribution of several genetic polymorphisms in regulating hepatic lipid metabolism, thus influencing NAFLD establishment and progression. Recent understanding of the genetic underpinning of NAFLD explains the involvement of several common naturally occurring variants in PNPLA3, TM6SF2, MBOAT7, GCKR, LYPLAL1 and PPP1R3B genes in the evolution of the disease. The genetic landscape may play a role to appraise the risk stratification and ascertaining the potential therapeutic target in NAFLD patients. The perspective of this review was to emphasise the genetic basis of the NAFLD spectrum, which modulates the severity and progression of the disease.