Animal study demonstrates that central prolactin increases gastric acid secretion and ulcer severity in rats, indicating a proulcerogenic role driven by gastric hypersecretion.
The effect of centrally administered prolactin on gastric acid secretion and experimentally-induced gastric and duodenal ulcers was studied. The acute gastric ulcer models used were pylorus ligation, indomethacin-induced and ethanol-induced gastric ulcers. Chronic gastric ulcers were induced using acetic acid and duodenal ulcers by cysteamine hydrochloride. In pylorus ligated rats, prolactin (1 microg/kg icv) produced 45% increase in gastric content volume, significant increase in free acidity (P < 0.001), total acidity (P < 0.001) and ulcer index (P < 0.001). It did not show any significant effect on ethanol-induced and indomethacin-induced gastric ulcers. Prolactin increased the ulcer index (P < 0.001) and ulcer score (P < 0.05) in acetic acid-induced chronic gastric ulcers. It also increased ulcer area (P < 0.05) in cysteamine-induced duodenal ulcers. Therefore, the proulcerogenic activity of prolactin was due to its gastric hypersecretory effect.
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Asad et al. (2001) studied this question.
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