Fig. 3

Deficiency of CRP decreases susceptibility to DHEA and HFD-induced insulin resistance. Four-week-old of placebo or dehydroepiandrosterone (DHEA)-treated female WT and CRP KO rats were fed a ND or HFD for 3 month. (a, e) Blood glucose levels during the glucose tolerance test (GTT). (b, f) Area under curve (AUC) during the GTT. (c, g) Blood glucose levels during the insulin tolerance test (ITT). (d, h) AUC during the ITT.(^*P < 0.05, ^**P < 0.01vs WT group; ^#P < 0.05, ^##P < 0.01 DHEA-WT group) (i) Experimental procedure and EHC protocol. (j) Glucose infusion rate (GIR) time course. (k) Cumulative GIR (l). Hepatic glucose production (HGP). (m) Percentage of suppression of HGP. (n) Glucose disappearance rates (GRD). (o) RT-PCR assays of hepatic PEPCK mRNA (p) Immunoblotting assays of hepatic expression of PEPCK protein, phosphorylation of InsR and Akt and densitometric quantification (^*P < 0.05, ^**P < 0.01vs ND-DHEA-WT group; ^#P < 0.05, ^##P < 0.01 HFD-DHEA-WT group). Data are expressed as the mean ± SEM (n = 6 rats for each group)