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

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FIG. 1.
FIG. 1.

CGI-58 KD dissociates hepatic steatosis from insulin resistance. A: Photographs depicting hepatic steatosis and adiposity in C57BL/6N mice fed either a chow or HFD for 10 weeks in conjunction with biweekly injections (25 mg/kg) of either a nontargeting control ASO or ASO targeting KD of CGI-58 (CGI-58 ASO). B–G: Despite hepatic lipid insult, KD of CGI-58 enhances insulin signaling. Mice were fed either a chow or HFD and treated with ASOs for 8 weeks. Mice were fasted for 10 h before saline or insulin injection into the portal vein. Exactly 5 min later, tissues were excised and immediately snap-frozen in liquid nitrogen. Protein extracts from the liver (B), skeletal muscle (C), and adipose tissue (D) were analyzed by Western blotting for total Akt, phospho (p)-Akt (Ser473 and Thr308), and phospho (p)-FoxO1 (Ser256); three representative animals are shown for each group. E–G: Densitometric analyses of insulin signaling: Phospho-Akt protein levels were normalized to total Akt in liver (E), skeletal muscle (F), and adipose tissue (G). □, control ASO; ■, CGI-58 ASO. Data represent the mean ± SEM from three mice per group, and values not sharing a common superscript letter differ significantly (P < 0.05). AU, arbitrary unit. (A high-quality digital representation of this figure is available in the online issue.)

This Article

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