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. 2021 Jan 26;47:101172. doi: 10.1016/j.molmet.2021.101172

Figure 5.

Figure 5

Ptc deletion in Glast+cells prevented HFD-induced obesity and alteration of glucose response. (A) Diagram representing the course of the experiments: high-fat diet (HFD) was started 11 weeks after the end of tamoxifen treatment (Tx) and lasted for 12 weeks. Glucose-tolerance tests (GTTs) were performed 10 and 20 weeks after Tx and insulin-tolerance tests (ITTs) 22 weeks after Tx. The mice were euthanized and tissue samples taken 23 weeks after Tx. (B) Representative images of the YFP-Ptc+/+ and YFP-Ptc−/− mice after 12 weeks of the HFD. (C) Time course of body weights. Data are represented as mean ± SEM. n = 8–11 mice/group. ∗∗p < 0.01 and ∗∗∗p < 0.001 by Student's t test. (D–E) Dissected livers (D) and ratio of total organ to body weights (E) at the end of the HFD challenge. Masses of SAT, VAT, and BAT were reduced in the YFP-Ptc−/− mice, whereas the liver, spleen, kidney, and heart mass did not differ significantly between the two cohorts. Data are represented as mean ± SEM from n = 4–6 mice/group. ∗∗p < 0.01 and ∗∗∗p < 0.001 by Student's t test. (F–H) Blood glucose levels measured during glucose- (F and G) and (H) insulin-tolerance tests on the fasted YFP-Ptc+/+ and YFP-Ptc−/− mice. Insets represent the area under the curve (AUC) of the associated graphs. Data are represented as mean ± SEM. n = 6 mice/group, ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 by Student's t test. GTT, glucose-tolerance test; ITT, insulin-tolerance test; SAT, subcutaneous adipose tissue; VAT, visceral adipose tissue; BAT, brown adipose tissue.