Macrophage deletion of SOCS1 increases sensitivity to LPS and palmitic acid and results in systemic inflammation and hepatic insulin resistance.

ABSTRACT:

Objective

Macrophage secretion of proinflammatory cytokines contributes to the pathogenesis of obesity-related insulin resistance. An important regulator of inflammation is the suppressor of cytokine signaling-1 (SOCS1), which inhibits the JAK-STAT and toll-like receptor-4 (TLR4) pathways. Despite the reported role of SOCS1 in inhibiting insulin signaling, it is surprising that a SOCS1 polymorphism that increases SOCS1 promoter activity is associated with enhanced insulin sensitivity despite obesity. In the current study, we investigated the physiological role of myeloid and lymphoid cell SOCS1 in regulating inflammation and insulin sensitivity.

Research design and methods

We used mice generated by crossing SOCS1 floxed mice with mice expressing Cre recombinase under the con

SUBMITTER: Sachithanandan N 

PROVIDER: S-EPMC3142066 | biostudies-literature | 2011 Aug

REPOSITORIES: biostudies-literature