Published online Jul 18, 2016. doi: 10.4254/wjh.v8.i20.827
Peer-review started: April 1, 2016
First decision: April 18, 2016
Revised: May 4, 2016
Accepted: June 14, 2016
Article in press: June 16, 2016
Published online: July 18, 2016
Genetics plays an important role in determining the susceptibility of an individual to develop a disease. Complex, multi factorial diseases of modern day (diabetes, cardiovascular disease, hypertension and obesity) are a result of disparity between the type of food consumed and genes, suggesting that food which does not match the host genes is probably one of the major reasons for developing life style diseases. Non-alcoholic fatty liver is becoming a global epidemic leading to substantial morbidity. While various genotyping approaches such as whole exome sequencing using next generation sequencers and genome wide association studies have identified susceptibility loci for non-alcoholic fatty liver disease (NAFLD) including variants in patatin-like phospholipase domain containing 3 and transmembrane 6 superfamily member 2 genes apart from others; nutrient based studies emphasized on a combination of vitamin D, E and omega-3 fatty acids to manage fatty liver disease. However majority of the studies were conducted independent of each other and very few studies explored the interactions between the genetic susceptibility and nutrient interactions. Identifying such interactions will aid in optimizing the nutrition tailor made to an individual’s genetic makeup, thereby aiding in delaying the onset of the disease and its progression. The present topic focuses on studies that identified the genetic susceptibility for NAFLD, nutritional recommendations, and their interactions for better management of NAFLD.
Core tip: Various genome wide association and replication studies across ethnicities have consistently associated variants in patatin-like phospholipase domain containing 3 gene with a higher risk of non-alcoholic fatty liver disease (NAFLD). More recently a variant in transmembrane 6 superfamily member 2 gene was also associated with susceptibility to the disease. Functional studies have established the role of these genes in NAFLD. Gene and nutrient interactions should be the focus of future research in the management of NAFLD.