The TM6SF2 rs58542926 polymorphism (E167K) increases the risk of non-alcoholic fatty liver disease by causing disorders in hepatic triglyceride metabolism and lipid deposition.
Does the TM6SF2 rs58542926 polymorphism increase the risk of non-alcoholic fatty liver disease?
The TM6SF2 rs58542926 polymorphism plays an important role in the pathogenesis of NAFLD by causing triglyceride metabolism disorders in the liver.
INTRODUCTION: nonalcoholic fatty liver disease is a common liver disease with a global average prevalence of about 25%. In addition to the incidence of NAFLD being related to obesity, diabetes, hyperlipidemia, etc., genetic factors also have an important impact on the incidence of NAFLD. AREAS COVERED: Current experimental results and clinical studies show that the transmembrane 6 superfamily member 2 (TM6SF2) gene plays an important role in the pathogenesis of NAFLD. The research on genetic polymorphism of TM6SF2 gene mainly focuses on rs58542926 locus (rs58542926 c.449 C > T, p. Glu167Lys, E167K). The Mutations of this site might increase the risk of NAFLD in carriers. EXPERT OPINION: The mutation of this site causes the disorder of triglyceride metabolism in the liver, which leads to the deposition of a large amount of lipids in the liver, and further induces the incidence of NAFLD. With the study of the mechanism of TM6SF2 gene polymorphism in the pathogenesis of NAFLD, it is helpful to understand the molecular mechanism of the pathogenesis of NAFLD, which has a great value for the treatment of NAFLD.
Xue et al. (Fri,) conducted a review in non-alcoholic fatty liver disease. TM6SF2 rs58542926 polymorphism was evaluated on risk of NAFLD. The TM6SF2 rs58542926 polymorphism (E167K) increases the risk of non-alcoholic fatty liver disease by causing disorders in hepatic triglyceride metabolism and lipid deposition.