Fig. 3: P-PTEN KO mice are protected against HFD-induced obesity and glucose intolerance. | Nature Communications

Fig. 3: P-PTEN KO mice are protected against HFD-induced obesity and glucose intolerance.

From: PTEN regulates vagal-insulin signaling to optimize autonomic output determining peripheral inflammatory and metabolic homeostasis

Fig. 3: P-PTEN KO mice are protected against HFD-induced obesity and glucose intolerance.

A, B Body and organ weights normalized to total body weights of P-PTEN WT and P-PTEN KO male mice fed HFD for 3 months (Body weights: n = 14 for P-PTEN WT mice and n = 11 for P-PTEN KO mice; Organ weights: n = 22 for P-PTEN WT mice and n = 10 for P-PTEN KO mice). CG Daily non-normalized metabolic caging data for the mice fed HFD for 3 months, including: (C) energy expenditure, (D) oxygen consumption (VO2), (E) carbon dioxide production (VCO2), (F) respiratory exchange ratio, and (G) locomotion. Dark and light refer to the 12 h on/off light cycle (Energy Expenditure/RER/VO2/VCO2: n = 7 for both groups of mice; Locomotion: n = 8 for both groups of mice). H, I (H) Glucose and (I) insulin tolerance tests (and (J) fasting serum insulin of mice fed a HFD for 3 months (A, B) (GTT: n = 13 for P-PTEN WT mice and n = 12 for P-PTEN KO mice; ITT: n = 14 for P-PTEN WT and n = 12 for P-PTEN KO mice, n = 8-10 per group; baseline insulin: n = 8 for P-PTEN WT mice and n = 10 for P-PTEN KO mice). Data are the mean ± SEM. p-values for (J) were determined by an unpaired, two-tailed Student’s t test. Unadjusted p-values are shown for (BI) in the figure for clarity; multiple comparisons were applied with the Holm-Sidak method, and adjusted p-values are provided in the data source file.

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