Suppressing NLRP2 expression accelerates hepatic steatosis: A  mechanism involving inflammation and oxidative stress.

Suppressing NLRP2 expression accelerates hepatic steatosis: A mechanism involving inflammation and oxidative stress. Biochem Biophys Res Commun. 2018 Nov 16;: Authors: Li C, Liu Q, Xie L Abstract Nonalcoholic fatty liver disease (NAFLD) is characterized by lipid accumulation and inflammation in the liver, contributing to a broad spectrum of severe pathologies, such as metabolic syndrome and hepatocellular carcinoma. Presently, the pathogenesis that attributes to NAFLD has not been fully understood. NLRP2 has been shown to inhibit the NF-κB signaling, and thus may contribute to regulate the inflammatory response. However, its role in NAFLD is largely unclear. In the study, we found that NLRP2 was markedly decreased in liver tissues of individuals with severe steatosis, or in a genetic deficiency (ob/ob) mice. High fat diet (HFD) feeding also led to a significant reduction of NLRP2 in liver of mice. Then, the wild type (WT) and NLRP2 knockout (KO) mice were used to further explore the role of NLRP2 in the NAFLD progression. NLRP2 knockout mice exhibited severer metabolic syndrome and hepatic steatosis after HFD administration, as evidenced by the increased body weight, liver histological changes and lipid accumulation. Moreover, HFD feeding-induced inflammation was significantly accelerated by the loss of NLRP2, as evidenced by the increased expression of pro-inflammatory cytokines and activation of nuclear factor κB (NF-κB) pathwa...
Source: Biochemical and Biophysical Research communications - Category: Biochemistry Authors: Tags: Biochem Biophys Res Commun Source Type: research