Skip to main content
. 2018 Jul 24;293(36):13974–13988. doi: 10.1074/jbc.RA118.003541

Figure 6.

Figure 6.

Plin1−/− mice show insulin resistance through lipid dysregulation. A and B, Plin1+/+ and Plin1−/− mice were fasted for 15 h. Fasting serum glucose (A) and ad libitum insulin (B) were measured in Plin1+/+ and Plin1−/− mice. *, p < 0.05; **, p < 0.01 versus Plin1+/+ group by Student's t test. Intraperitoneal GTT (C) and ITT (D) were performed on Plin1+/+ and Plin1−/− mice. *, p < 0.05; **, p < 0.01 versus Plin1+/+ group by repeated-measures ANOVA (RM-ANOVA) followed by Bonferroni's post hoc test. E, homeostatic model assessment-insulin resistance (HOMA-IR) was measured in Plin1+/+ and Plin1−/− mice. **, p < 0.01 versus Plin1+/+ group by Student's t test. F, ITT was performed after treatment with NS398 (10 mg/kg body weight) for 7 days. *, p < 0.05 versus Plin1+/+, vehicle group; #, p < 0.05 versus Plin1−/−, vehicle group by RM-ANOVA followed by Bonferroni's post hoc test. G–I, Plin1+/+ and Plin1−/− mice were injected with saline or insulin (0.75 units/kg body weight). Insulin signaling in eWAT (G), skeletal muscle (H), and liver (I) was assessed by immunoblot analysis using antibodies against pAKT (S473), AKT, PLIN1, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Levels of TG and FFAs in skeletal muscle (J) or in liver (K) were measured. p value versus Plin1+/+ mice by Student's t test. All data represent the mean ± S.E.