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. Author manuscript; available in PMC: 2018 Jul 23.
Published in final edited form as: Cell Rep. 2018 Jul 3;24(1):47–55. doi: 10.1016/j.celrep.2018.06.008

Figure 2. Controlled-Release Mitochondrial Protonophore Slows MC38 Tumor Growth and Limits Tumor Glucose Uptake and Oxidation due to Reversal of Hyperinsulinemia.

Figure 2

(A) Tumor size.

(B) In vitro proliferation of cells incubated in media containing DNP. Data are the mean ± SEM of 6 replicate wells for each condition, each counted in duplicate. The two conditions were compared by the two-tailed unpaired Student’s t test.

(C and D) Tumor glucose uptake (C) and oxidation (VPDH/VCS) (D).

(E and F) Plasma acetate concentrations (E) and whole-body acetate turnover (F).

(G) Ratio of tumor to plasma acetate enrichment in mice infused with [1-13C] acetate.

(H) Ratio of tumor TCA cycle intermediate enrichment to plasma acetate enrichment in mice infused with [1-13C] acetate.

In (A) and (C)–(H), n = 7 HFD mice and 8 in all other groups. In all panels, data are the mean ± SEM with comparisons by ANOVA with Bonferroni’s multiple comparisons test unless otherwise stated.