Depletion of B cell-activating factor attenuates hepatic fat accumulation in a murine model of nonalcoholic fatty liver disease.

ABSTRACT: Obesity-induced adipose-tissue dysfunction is a critical contributor to the pathogenesis of nonalcoholic fatty liver disease (NAFLD). B cell-activating factor (BAFF) is an adipokine related to impaired insulin sensitivity, and the serum BAFF concentration is associated with NAFLD severity. In this study, we aimed to determine the direct in vivo role of BAFF in the development of insulin resistance, adipocyte dysfunction, and hepatic steatosis using BAFF^-/- mice fed a high-fat diet (HFD). HFD-fed BAFF^-/- mice exhibited significantly improved insulin sensitivity despite their increased weight gain and adiposity relative to HFD-fed wild-type mice. Moreover, inflammation, especially the accumulation of CD11c⁺ adipose-tissue macrophages, and fibrosis of epididym

SUBMITTER: Nakamura Y 

PROVIDER: S-EPMC6353938 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature