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. 2017 Oct 25;159(1):272–284. doi: 10.1210/en.2017-00850

Figure 5.

Figure 5.

Fatty acid and glucose metabolism is impaired in ΔCtnnb1 mice. (A–E) Serum analysis of (A) triglycerides, (B) cholesterol, (C) β-hydroxybutyrate, (D) free fatty acids, and (E) glycerol in random-fed control and ΔCtnnb1 mice. (F) Blood glucose levels in random-fed and overnight-fasted control and ΔCtnnb1 mice. (G) Serum insulin levels in random-fed mice. (H) Glucose tolerance testing (GTT). (I) Insulin tolerance testing (ITT). (J) Area under the curve (AUC) analysis for GTT and ITT studies. (K) Representative histological images of β-cell islets immunostained for insulin (original magnification ×10). (L) Quantification of islet area. (M) Representative immunoblots of phospho-AKT (Ser473) and total AKT in gWAT and the liver of control and ΔCtnnb1 mice at baseline (NT) and after insulin administration. (N) Quantification of the fold increase in AKT phosphorylation in liver and gonadal white adipose tissue (gWAT). (O and P) qPCR analysis of insulin-responsive genes in the (O) liver and (P) gWAT of control and ΔCtnnb1 mice. (Q) Serum undercarboxylated (Glu) osteocalcin. Data are expressed as mean ± standard error of the mean; n = 5 to 10 mice per group. *P < 0.05.