Macrophage JAK2 deficiency protects against high-fat diet-induced inflammation.

ABSTRACT: During obesity, macrophages can infiltrate metabolic tissues, and contribute to chronic low-grade inflammation, and mediate insulin resistance and diabetes. Recent studies have elucidated the metabolic role of JAK2, a key mediator downstream of various cytokines and growth factors. Our study addresses the essential role of macrophage JAK2 in the pathogenesis to obesity-associated inflammation and insulin resistance. During high-fat diet (HFD) feeding, macrophage-specific JAK2 knockout (M-JAK2^-/-) mice gained less body weight compared to wildtype littermate control (M-JAK2^+/+) mice and were protected from HFD-induced systemic insulin resistance. Histological analysis revealed smaller adipocytes and qPCR analysis showed upregulated expression of some adipogenesis marker

SUBMITTER: Desai HR 

PROVIDER: S-EPMC5550513 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature