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. Author manuscript; available in PMC: 2024 Aug 1.
Published in final edited form as: Metabolism. 2023 May 23;145:155591. doi: 10.1016/j.metabol.2023.155591

Figure 6. ER stress, but not lipogenesis, improves following T-KHK knockdown in lipodystrophic mice.

Figure 6.

Weight gain A) in 2-month-old, male, wild type, insulin receptor (IR) Lox/Lox, Adiponectin Cre negative (WT-lox/lox) littermates, as well as lipodystrophic, IR Lox/Lox, Adiponectin Cre positive, luciferase control injected (FIRKO-siCont) or KHK siRNA injected (FIRKO-siKHK) mice for four weeks, n=6–8 mice per group. B) Liver weight, hepatic C) triglycerides (TG) and cholesterol levels in these mice. Random fed D) blood glucose obtained at sacrifice, n=6–8 mice per group. E) Glucose tolerance test (GTT) in overnight fasted mice performed after 2 weeks following siRNA injection and F) area under curve (AUC) from GTT analysis. Serum G) TG and H) aspartate aminotransferase (AST) at sacrifice. Hepatic mRNA expression of I) genes regulating endogenous fructose production (Akr1b1, Sord). Western blot quantification of KHK in the liver and proteins mediating J)de novo lipogenesis (ACLY, ACC1, FASN, SCD1) and K) ER stress (KHK-C, XBP1, PERK, CHOP) pathways. Sample number for WB is n=4 and for mRNA n=6 mice. Statistically significant results are marked with # using one-way ANOVA analysis, with Dunnett’s multiple comparisons test to the Chow group, # p<0.05; ## p<0.01; ### p<0.001; #### p<0.0001, while * represents a post-hoc analysis between the groups under the line, *p <0.05; ** p<0.01, *** p<0.001, **** p<0.0001. All data are presented as mean ± S.E.M.