Selenoprotein P and Non-alcoholic Fatty Liver Disease

Overview

The pathogenesis of nonalcoholic fatty liver disease has not been fully elucidated. The most widely supported theory implicates insulin resistance as the key mechanism leading to hepatic steatosis, and perhaps also to steatohepatitis. Selenoprotein P(SeP) is a secretory protein primarily produced by the liver. Previous studies demonstrated that SeP, a liver-derived secretory protein, causes insulin resistance. Therefore, the purpose of this study is to determine the different Sep levels between healthy normal group and NAFLD group.

Nonalcoholic fatty liver disease (NAFLD), a disease spectrum that includes simple steatosis, nonalcoholic steatohepatitis (NASH) and cirrhosis, has been increasingly recognized as the hepatic manifestation of metabolic syndrome. Both inflammation and insulin resistance are considered to be pivotal pathogenic mechanisms of NAFLD, as well as metabolic syndrome, type 2 diabetes, and atherosclerosis. There is mounting evidence implicating adipokines secreted from adipose tissue in the pathogenesis and progression of NAFLD, in addition to the development of insulin resistance and inflammation. Selenoprotein P (SeP) has recently been reported as a novel hepatokine that regulates insulin resistance and systemic energy metabolism in rodents and humans. Although previous studies have shown a close relationship among insulin resistance, inflammation, and NAFLD, as far as we know, there is no previous report evaluating the association between SeP and NAFLD. In the present study, we examined serum SeP levels in subjects with increased visceral fat area (VFA) or liver fat accumulation measured with computed tomography (CT). We evaluated the relationship between SeP levels and cardiometabolic risk factors.

Conditions

Eligibility

Locations (1)

Outcomes