IκBζ regulates the development of nonalcoholic fatty liver disease through the attenuation of hepatic steatosis in mice.

ABSTRACT: IκBζ is a transcriptional regulator that augments inflammatory responses from the Toll-like receptor or interleukin signaling. These innate immune responses contribute to the progression of nonalcoholic fatty liver disease (NAFLD); however, the role of IκBζ in the pathogenesis of NAFLD remains elusive. We investigated whether IκBζ was involved in the progression of NAFLD in mice. We generated hepatocyte-specific IκBζ-deficient mice (Alb-Cre; Nfkbiz^fl/fl) by crossing Nfkbiz^fl/fl mice with Alb-Cre transgenic mice. NAFLD was induced by feeding the mice a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD). CDAHFD-induced IκBζ expression in the liver was observed in Nfkbiz^fl/fl mice, but not in Alb-Cre; Nfkbiz^fl/fl mice. Contrary to our i

SUBMITTER: Ishikawa H 

PROVIDER: S-EPMC9270369 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature