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. Author manuscript; available in PMC: 2021 Jul 2.
Published in final edited form as: Mol Cell. 2020 May 29;79(1):30–42.e4. doi: 10.1016/j.molcel.2020.05.007

Figure 5. Increasing acetyl-CoA levels restores mTORC1 activation, inhibits autophagy and elevates triglyceride levels in Acox1-LKO mice.

Figure 5.

A) Schematic illustrating the role of dichloroacetic acid (DCA) in acetyl-CoA production through pyruvate dehydrogenase (PDH) activation. B) Liver acetyl-CoA levels in 8–10 weeks old female mice i.p. treated with 250 mg/kg DCA or vehicle for 3 consecutive days; n = 5–7, *p < 0.05 (unpaired t-test). C-D) Endogenous Raptor was immunoprecipitated from liver homogenates using an anti-Raptor antibody, followed by Western blot analysis using antibodies against acetylated-lysine (AcK), Raptor or actin; n = 3, *p < 0.05 (unpaired t-test). E-F) DCA restores lysosomal localization of mTOR in Acox1-LKO liver. n = 13–16, *p < 0.05 (unpaired t-test). G) Western blot analysis of mTORC1 activation and autophagy inhibition in the livers of mice treated with or without DCA as indicated (n=3/group). H-I) DCA inhibits lysosomal localization of PLIN2 in Acox1-LKO liver; n=12, *p < 0.05 (unpaired t-test). J) Liver TG content in female mice treated with or without DCA; n = 8, *p <0.05 (unpaired t-test). Data represent mean ± SEM. See also Figure S5.