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Claxton, A

Serum metabolomics reveals irreversible Inhibition of fatty acid beta-oxidation through the suppression of PPARalpha activation as a contributing mechanism of acetaminophen-induced hepatotoxicity

Since cell physiology must not be compromised under the production conditions, metabolic alterations should be controlled in order to enable a proper functioning of the metabolic networks involved

If the induction of anaplerosis through pyruvate carboxylation is a compensatory mechanism to maintain Krebs cycle moieties, 17 early supplementation with an anaplerotic substrate may allow pyruvate to be oxidized by PDH