Polymorphisms of <i>HSD17B13</i>, <i>GCKR</i>, <i>HFE</i>, and <i>CP</i> as factors of the development of non-alcoholic fatty liver disease and comorbid diseases

Abstract

Currently, non-alcoholic fatty liver disease is one of the most common chronic liver diseases. In recent years, this condition has been considered as a hepatic manifestation of the metabolic syndrome, which is associated with overweight and impaired glucose and fat metabolism. Despite the obvious role of lifestyle in the development of this disease, it is increasingly being suggested that disorders in the metabolism of fats and carbohydrates have a genetic basis, which determines the tendency to develop NAFLD. Mutant polymorphisms of the HSD17B13, GCKR, HFE, and CP genes have been shown to affect the course of NAFLD, but these effects require further study. Therefore, the aim of this work was to analyze and systematize the available data from foreign articles over the past 10 years. In this study, 573 articles were analyzed, the most important 64 original research works were used here. Mutations in  the HSD17B13  gene are associated with a  milder course of  NAFLD, while GCKR gene polymorphisms, on the contrary, are associated with more severe histological manifestations of this disease, such as steatosis and fibrosis. The HFE and CP genes, although not directly related to macronutrient metabolism, nevertheless contribute to the development of more severe forms of NAFLD, which may be associated with the development of inflammation and oxidative stress caused by excessive accumulation of iron in hepatocytes.