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. 2022 May 16;132(10):e145889. doi: 10.1172/JCI145889

Figure 11. Kisspeptin increases fatty acid oxidation in isolated primary mouse hepatocytes.

Figure 11

(A–D) Oxygen consumption rate (OCR) in hepatocytes treated with 100 μM palmitate (PA) or BSA with or without kisspeptin agonist (KPA) (3 nM) or etomoxir (ETO), an CPT1 inhibitor. Representative OCR trace using Seahorse analyzer, following sequential treatment with 2.5 μM oligomycin (Oligo); 3 μM carbonyl cyanide-4 (trifluoromethoxy) phenylhydrazone (FCCP), an uncoupler of mitochondrial oxidative phosphorylation; and 2.5 μM rotenone and antimycin A (R +A), complex I and III inhibitors. (E) Representative Western blot showing expression of indicated protein in primary hepatocytes isolated from control (CTRL) and hepatic Kiss1r-knockout (LKO) livers. Quantification is shown in Supplemental Figure 12, G and H. (F) Representative Western blot showing expression of indicated proteins in KPA-treated HFD-fed mouse livers. Quantification is shown in Supplemental Figure 12, I and J. (G) Schematic showing proposed signaling pathways by which KISS1R activation suppresses hepatic lipogenesis and NASH progression.*P < 0.05 versus controls; 1-way ANOVA followed by Dunnett’s post hoc test.