CGI-58/ABHD5-Derived Signaling Lipids Regulate Systemic Inflammation and Insulin Action

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FIG. 2.
FIG. 2.

CGI-58 KD alters HFD-induced inflammation: Evidence of hepatic cytokine resistance. C57BL/6N mice were fed either a standard chow or HFD in conjunction with biweekly injections of either a nontargeting control ASO (□) or ASO targeting KD of CGI-58 (CGI-58 ASO; ■) for 10 weeks. A: Plasma levels of proinflammatory cytokines, including IL-6 and IL-12p40; monocyte chemoattractant protein-1 (MCP-1); macrophage inflammatory protein-2 (MIP-2); CXCL1 (KC); and regulated upon activation, normal T-cell expressed, and RANTES. Data represent the mean ± SEM from five mice per group, and values not sharing a common superscript letter differ significantly (P < 0.05). ND, levels below limit of detection. B and C: HFD-induced stress kinase activation. Representative immunoblots from liver (B) or epididymal adipose tissue (C) are shown for phospho-IκB kinase α/β (p-IKKα/β; Ser176/180), phospho-mTOR (p-mTOR; Ser2448), and phospho-S6 ribosomal protein (p-S6; Ser235/236). Membranes were probed for β-actin and CGI-58 to serve as loading controls; data from four representative animals are shown for each group.

This Article

  1. Diabetes vol. 61 no. 2 355-363