Abstract
Unripe fruit of the Jamaican ackee tree, Blighia sapida, contains hypoglycin, l-(methylenecyclopropyl)alanine), a hypoglycaemic toxin which has caused an estimated 5000 deaths. Methylenecyclopropylacetyl-CoA, a metabolite of hypoglycin, inactivates several, but not all, flavoprotein acyl-CoA dehydrogenases causing widespread disturbances of the oxidation of fatty acids and several amino acids leading to secondary inhibition of gluconeogenesis. Despite intensive study for three decades the mechanism of hypoglycin poisoning is still only partly understood. H. S. A. Sherratt reviews these complex effects which have implications for toxicology and the study of metabolic regulation and of many inborn errors of metabolism.
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