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. 2021 Mar 2;24(4):102260. doi: 10.1016/j.isci.2021.102260

Figure 4.

Figure 4

Gpr52 accelerates fat accumulation in liver and induces insulin resistance in response to excessive fat intake

(A) Changes in body weight of Gpr52−/− and WT mice in HFD (n = 6–12).

(B) Plasma glucose (left) and insulin (right) concentrations of Gpr52−/− and WT mice in fed (n = 8–9) and fasted (n = 26–39) conditions at age 17–18 weeks.

(C) OGTT (2 g/kg) on 17- to 18-week-old Gpr52−/− and WT mice. Plasma glucose and insulin concentrations are plotted at the indicated time points (n = 26–39).

(D) Liver weight (left) and hepatic triglyceride content (right) of Gpr52−/− and WT mice aged 16–23 weeks under normal diet (ND) (n = 4–6) or 17-week HFD (n = 15–21).

(E) Hepatic gene expressions involved in fatty acid biosynthesis in Gpr52−/− and WT mice fed ND (n = 5) and HFD (n = 9) at age 21–23 weeks under fed condition. The average Ct value of WT mice fed ND was 22.5, 26.7, 29.0, 27.7, 32.1, and 31.5 for Scd1, Elovl6, Acc1, Acc2, Srebp1c, and Pparg2, respectively, when cDNAs synthesized from 20 ng total RNA were used for each qPCR.

Data are means ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, between the animal groups by one-way or two-way analysis of variance (ANOVA) followed by the Tukey-Kramer post-hoc test.