Skip to main content
. 2016 Nov 14;126(12):4659–4673. doi: 10.1172/JCI86905

Figure 6. Sirt6 deficiency upregulates levels of glycolytic metabolism intermediates.

Figure 6

(A) Immunoblotting for regulators of glycolytic metabolism in the retinae of treated and untreated mice at P21 revealed increased levels of HIF1A and HIF2A; GLUT1 and GLUT2; and MYC in Sirt6–/–Pde6bH620Q/H620Q mice. There was a corresponding decrease in VHL protein and p-LDHA. No difference was detected for LDHA between the groups. β-Actin (ACTIN) was used as a loading control. (B) Protein expression was quantified to assess changes between Sirt6–/–Pde6bH620Q/H620Q and Sirt6loxP/loxPPde6bH620Q/H620Q mice, and a paired t test was used to determine statistical significance. HIF1A, HIF2A, GLUT1, GLUT2, and MYC were found to be increased in the Sirt6–/–Pde6bH620Q/H620Q mice compared with controls. SIRT6, VHL, and p-LDHA were found to be decreased in the Sirt6–/–Pde6bH620Q/H620Q group. No difference between groups was found for LDHA. SIRT6 P < 0.001, HIF1A P = 0.02, HIF2A P = 0.01, GLUT1 P = 0.04, GLUT2 P = 0.048, LDHA P = 0.68, p-LDHA P = 0.04, VHL P = 0.02, MYC P < 0.001. n = 4 for both groups. *P < 0.05, **P < 0.01, and ***P < 0.001.