Fig. 2: SAPS3 deletion in mice reverses HFD induced detrimental effects.
a Schematic strategy of ppp6r3 knockout. WT: ppp6r3+/+; FF: ppp6r3 fl/fl; HE: ppp6r3+/-; KO: ppp6r3-/-. Colored arrows indicated the positions of primers designed to determine the genotype of wildtype (WT) and SAPS3 knockout (KO) mice. PCR analysis showed a complete loss of SAPS3 expression. The results are representative of at least three independent experiments. b Indicated tissues were collected from SAPS3 KO mice. Tissue lysates were analyzed by Western blotting. n = 3 mice per group. c 8 weeks old male WT and KO mice were fed with HFD (45 kcal% fat) for 16 weeks. Bodyweight was measured (CD, ctrl diet; HFD, high-fat diet). Mean ± s.d., n = 8 mice per group analyzed by one-way ANOVA, ****p < 0.0001. d Fat mass and lean mass composition of mice were measured by echo-MRI. Mean ± s.d., n = 7 mice per group analyzed by two-tailed t-test. Fat mass ***p = 0.0005, lean mass ***p = 0.0004; n.s., not significant. e Glucose tolerance test and insulin tolerance test were performed at the endpoint. Mean ± s.d., CD, n = 7 mice per group; HFD, n = 8 mice per group analyzed by one-way ANOVA, ****p < 0.0001. f Representative pictures of WT and KO mice and their livers. Liver weight was measured and shown in g. Mean ± s.d., n = 7 mice per group analyzed by two-tailed t-test, **p = 0.002; n.s., not significant. h Representative images of H&E staining of the liver, epididymal white adipose tissue (eWAT), and muscle. Scale bar, 100 µm. i The quantification of fat percentages from the H&E staining images shown in h. Mean ± s.d., CD, n = 4 mice per group; HFD, n = 6 per group analyzed by two-tailed t-test, ***p = 3.06E-06; n.s., not significant. j Liver samples were collected from WT and SAPS3 KO mice under CD and HFD. Tissue lysates were analyzed by Western blotting. The results are representative of two independent experiments.
