{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T21:12:06Z","timestamp":1761513126294},"reference-count":52,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2012,7,1]]},"abstract":"<jats:p> The cause of lower prevalence of duodenal ulcer in young women compared with men is largely unknown. We recently found that sex difference in duodenal mucosal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion existed in humans and mice, but the mechanisms are not clear. Prostaglandin E<jats:sub>2<\/jats:sub> (PGE<jats:sub>2<\/jats:sub>) is an important endogenous mediator that plays an important role in the regulation of duodenal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion. Therefore, in the present study, we investigated the effect of estrogen on PGE<jats:sub>2<\/jats:sub>-stimulated duodenal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion and the underlying mechanisms. The results showed that 17\u03b2-estradiol at the physiological concentration (1 nM) had no significant effects on duodenal mucosal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion or short-circuit current ( I<jats:sub>sc<\/jats:sub>) in mice. However, the pretreatment of 17\u03b2-estradiol (1 nM) markedly potentiated PGE<jats:sub>2<\/jats:sub>-stimulated duodenal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion and I<jats:sub>sc <\/jats:sub>( P &lt; 0.01 and P &lt; 0.05). Global estrogen receptor (ER) antagonist ICI-182,780 and ER\u03b1-specific antagonist MPP, but not the ER\u03b2-specific antagonist PHTPP, abolished estrogen-potentiated PGE<jats:sub>2<\/jats:sub>-stimulated duodenal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion and I<jats:sub>sc<\/jats:sub>. 17\u03b2-Estradiol and PGE<jats:sub>2<\/jats:sub> additively increased phosphatidylinositol 3-kinase (PI3K) activity and Akt phosphorylation. Wortmannin, a specific PI3K inhibitor, inhibited estrogen-potentiated PGE<jats:sub>2<\/jats:sub>-stimulated duodenal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion and I<jats:sub>sc<\/jats:sub>. In conclusion, estrogen at the physiological concentration potentiates PGE<jats:sub>2<\/jats:sub>-stimulated duodenal mucosal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion through the activation of ER\u03b1 and the PI3K-dependent mechanism, which may contribute to the sex difference in duodenal mucosal HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup> secretion and the lower prevalence of duodenal ulcer in young women. <\/jats:p>","DOI":"10.1152\/ajpendo.00575.2011","type":"journal-article","created":{"date-parts":[[2012,4,25]],"date-time":"2012-04-25T20:25:53Z","timestamp":1335385553000},"page":"E111-E121","source":"Crossref","is-referenced-by-count":17,"title":["Estrogen potentiates prostaglandin E<sub>2<\/sub>-stimulated duodenal mucosal HCO<sub>3<\/sub><sup>\u2212<\/sup> secretion in mice"],"prefix":"10.1152","volume":"303","author":[{"given":"Biguang","family":"Tuo","sequence":"first","affiliation":[{"name":"Department of Gastroenterology, Affiliated 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