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. 2017 Mar 14;18:128–138. doi: 10.1016/j.ebiom.2017.03.019

Fig. 5.

Fig. 5

SRT1720 does not improve glucose homeostasis in AMPKα2 KO mice.

Body weight of WT (A) and AMPKα2 KO (B) mice fed HFD (± SRT1720) (n = 5–7 per treatment group). All values are expressed as mean ± s.e.m. *p < 0.05; **p < 0.01; ***p < 0.001 (C) Food intake for WT and AMPK α2KO mice treated either vehicle or SRT1720 (n = 5–7 per each genotype). All values are expressed as mean ± s.e.m. (D) Relative locomotor activity for WT and AMPK α2KO mice fed either vehicle or SRT1720 (n = 5–7 per each genotype). All values are expressed as mean ± s.e.m. (E) Glucose tolerance of WT and AMPK α2KO mice on HFD (SRT1720) for 17 weeks are shown (n = 5–7 per treatment group). All values are given as mean ± s.e.m. **p < 0.01; ***p < 0.001. (F) Area under the curve (AUC) data for glucose tolerance of WT and AMPK α2KO mice on HFD (SRT1720) for 17 weeks are shown (n = 5–7 per treatment group). All values are given as mean ± s.e.m. **p < 0.01. (G) Insulin sensitivity of WT and AMPK α2KO mice on HFD (SRT1720) for 17 weeks are shown (n = 5–7 per treatment group). All values are given as mean ± s.e.m. *p < 0.05. (H) Area under the curve (AUC) data for insulin sensitivity of WT and AMPK α2KO mice on HFD (SRT1720) for 17 weeks are shown (n = 5–7 per treatment group). All values are given as mean ± s.e.m.