Fig 1: Improved glucose tolerance and insulin sensitivity in SgkLtko mice(A) SGK2 and SGK3 western blot 2 h following refeeding after an overnight 16 h fast.(B) Hepatic knockout of Sgk1, Sgk2, and Sgk3 validated by western blotting.(C) Insulin-stimulated Akt phosphorylation by western blotting in control and SgkLtko primary hepatocytes.(D) I.p. glucose tolerance test in control (n = 11) and SgkLtko (n = 13) mice fed a HFD.(E) AMPK phosphorylation in sgk-1 mutant C. elegans under fed conditions at the young adult stage, quantified in the right panel versus actin (n = 3 biological replicates per group).(F) Extended starvation survival of sgk-1 mutant worms is dependent on the AMPKα catalytic subunit aak-2 (n = 60–90 animals per group per time point). Corrected p < 0.005 sgk-1(vector RNAi) versus wild-type(vector RNAi); corrected p < 0.005 sgk-1(vector RNAi) versus sgk-1(aak-2 RNAi); and non-significant sgk-1(aak-2 RNAi) versus wild-type(aak-2 RNAi) for mean lifespan by nonlinear regression analysis.See also Figure S6 and Table S1 for information on mouse sex, age, n, and replication. *p < 0.05 by t test (D and E) and p value as indicated by two-way ANOVA for effect by genotype (D, left panel). All bars indicate mean and SEM.