As the primary source of acetyl CoA shifts from glycolysis to [beta]-oxidation and ketolysis, this ratio increases, more than doubling for [beta]-oxidation of longerchain fatty acids.
These effects were prevented by inhibition of complex II with 3-nitropropionic acid or malonate, indicating that BHB primarily influences mitochondrial respiration at complex II [112], which is consistent with ketolysis increasing formation of succinate and [FADH.sub.2].