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Probably, the sharp increase in ALAS1 activity during AIP crises consumes most of the available succinyl-CoA in the mitochondria, hindering the TCA cycles ability to generate essential redox factors, NADH/H+and FADH2, that are transferred to ETC to produce energy.27 Collectively, these observations support the previously noted cataplerosis of the TCA cycle observed in the mouse AIP model during phenobarbital-induced AIP crises.27 28 Notably, hepatic succinate and malate levels, substrates for FADH2 and NADH/H+, respectively, were recovered to normal levels following MD administration of hPBGD mRNA

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