Lgals9 deficiency ameliorates obesity by modulating redox state of PRDX2.

ABSTRACT: The adipose tissue is regarded as an endocrine organ and secretes bioactive adipokines modulating chronic inflammation and oxidative stress in obesity. Gal-9 is secreted out upon cell injuries, interacts with T-cell immunoglobulin-3 (Tim-3) and induces apoptosis in activated Th1 cells. Gal-9 also binds to protein disulfide isomerase (PDI), maintains PDI on surface of T cells, and increases free thiols in the disulfide/thiol cycles. To explore the molecular mechanism of obesity, we investigated Gal-9^-/- and Gal-9^wt/wt C57BL/6J mice fed with high fat-high sucrose (HFHS) chow. Gal-9^-/- mice were resistant to diet-induced obesity associated with reduction of epididymal and mesenteric fat tissues and improved glucose tolerance compared with Gal-9^wt/wt

SUBMITTER: Nunoue T 

PROVIDER: S-EPMC7966757 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature