Abstract
Rats deficient in pantothenic acid have diminished acetylating powers due to a lack of coenzyme A, and they develop hypersecretion of gastric acid and duodenal ulcers. Human beings are genetically constituted as either rapid or slow acetylators due to a polymorphism of the enzyme acetyl transferase. A population of duodenal ulcer subjects studied has a normal incidence of slow acetylators, suggesting that this phenotype is not more liable to develop the disease. Other possible ways in which the acetylation polymorphism might be related to duodenal ulcer are discussed.