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. 2018 Aug 23;3(16):e120794. doi: 10.1172/jci.insight.120794

Figure 6. Hepatic PPARγ is required for Aloxe3 to induce hepatic energetic inefficiency.

Figure 6

(A) RNA-seq analysis of the top 5 downregulated molecular processes in hepatocytes overexpressing Aloxe3. Highlighted are ATPase-related and mitochondrial coupling processes. Graphed is logFC relative to cultures expressing β galactosidase. n = 3 from a single RNA sequencing run performed once. (B and C) Seahorse XF96 analysis of proton leak, basal OCR, ATP production, coupling efficiency, and nonmitochondrial oxygen consumption in AML12 cells overexpressing Aloxe3 with or without GW9662 (PPARγ inhibitor) treatment. n = 8 independent cultures combined from 2 distinct experimental runs. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001 by 2-tailed t testing with Bonferroni-Dunn post hoc correction versus the bracketed comparison group as indicated.