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. Author manuscript; available in PMC: 2017 Apr 19.
Published in final edited form as: Cell Rep. 2017 Apr 4;19(1):1–9. doi: 10.1016/j.celrep.2017.03.026

Figure 4. SIRT1 mediates the effects of ATGL on autophagy/lipophagy.

Figure 4

(A) The ATGL-mediated increase in autophagy gene expression was abolished in the absence of SIRT1. SIRT1flox/flox or L-SIRT1−/− mice were treated with Ad-Null or Ad-ATGL viruses for 7 days prior to sacrifice (n=6); *P<0.05 vs. Ad-Null and #P<0.05 vs. SIRT1+/+. (B) Protein expression of autophagy genes in response to ATGL overexpression and/or SIRT1 ablation; a representative Western blot and densitometry analysis from 4 mice is shown. (C-D) Primary mouse hepatocytes were treated with dual adenoviruses and TAG turnover and FA oxidation during the chase period were measured (n=5); *P<0.05 vs. Ad-Null and #P<0.05 vs. shSCR. (E) L-SIRT1−/− mice treated with Ad-ATGL had lower β-hydroxybutyrate compared to the floxed controls (n=6); *P<0.05 vs. Ad-Null and #P<0.05 vs. SIRT1+/+. (F–G) Confocal imaging revealed that Ad-ATGL enhanced LC3-LD and lysosome-LD co-localization, which was lost with 10 mM EX527, a SIRT1 inhibitor (n=2).