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Alteration of several metabolic enzymes and pathways that affect KG abundance and KGDD activity have been reported in cancer, such as mutations of IDH1 and IDH2, changes in glutaminolysis that deplete KG, or alterations in fumarate hydratase (FH) and succinate dehydrogenase (SDH) that inhibit KGDD activity (Losman et al., 2020)

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In line with this observation, 2-hydroxybutyrate is increasingly recognized as a biomarker of metabolic disturbances, particularly in insulin resistance and glucose intolerance 27