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. Author manuscript; available in PMC: 2021 Aug 18.
Published in final edited form as: Cell Rep. 2021 Aug 3;36(5):109487. doi: 10.1016/j.celrep.2021.109487

Figure 6. Model of Kbhb under ketogenic conditions.

Figure 6.

In ketogenic liver, as the concentration of β-OHB rises, so does the concentration of its activated CoA form β-OHB-CoA, which serves as the substrate for Kbhb. β-OHB-CoA may be generated by mitochondrial enzymes that participate in fatty acid β-oxidation or by ACSS2, a nucleo-cytoplasmic enzyme that generates other short-chain acyl-CoA species. Kbhb has the potential to feed back on the hepatic proteome and impact metabolism—as demonstrated for AHCY and the methionine cycle—as well as alter gene expression through modification of histones.