{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T11:03:11Z","timestamp":1787655791429,"version":"build-2736575974"},"reference-count":42,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2015,6,18]],"date-time":"2015-06-18T00:00:00Z","timestamp":1434585600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2015,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Functional dyspepsia (<jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content>) is one of the most common disorders of gastrointestinal (<jats:styled-content style=\"fixed-case\">GI<\/jats:styled-content>) diseases. However, no curable treatment is available for <jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content> because the detailed mechanism of <jats:styled-content style=\"fixed-case\">GI<\/jats:styled-content> dysfunction in stressed conditions remains unclear. We aimed to clarify the association between endogenous acylated ghrelin signaling and gastric motor dysfunction and explore the possibility of a drug with ghrelin signal\u2010enhancing action for <jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content> treatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Solid gastric emptying (<jats:styled-content style=\"fixed-case\">GE<\/jats:styled-content>) and plasma acylated ghrelin levels were evaluated in an urocortin1 (<jats:styled-content style=\"fixed-case\">UCN<\/jats:styled-content>1) \u2010induced stress model. To clarify the role of acylated ghrelin on <jats:styled-content style=\"fixed-case\">GI<\/jats:styled-content> dysfunction in the model, exogenous acylated ghrelin, an endogenous ghrelin enhancer, rikkunshito, or an <jats:italic>\u03b1<\/jats:italic><jats:sub>2<\/jats:sub>\u2010adrenergic receptor (<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content>) antagonist was administered. Postprandial motor function was investigated using a strain gauge force transducer in a free\u2010moving condition.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>Exogenous acylated ghrelin supplementation restored <jats:styled-content style=\"fixed-case\">UCN<\/jats:styled-content>1\u2010induced delayed <jats:styled-content style=\"fixed-case\">GE<\/jats:styled-content>. Alpha<jats:sub>2<\/jats:sub>\u2010<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content> antagonist and rikkunshito inhibited the reduction in plasma acylated ghrelin and <jats:styled-content style=\"fixed-case\">GE<\/jats:styled-content> in the stress model. The action of rikkunshito on delayed <jats:styled-content style=\"fixed-case\">GE<\/jats:styled-content> was blocked by co\u2010administration of the ghrelin receptor antagonist. <jats:styled-content style=\"fixed-case\">UCN<\/jats:styled-content>1 decreased the amplitude of contraction in the antrum while increasing it in the duodenum. The motility index of the antrum but not the duodenum was significantly reduced by <jats:styled-content style=\"fixed-case\">UCN<\/jats:styled-content>1 treatment, which was improved by acylated ghrelin or rikkunshito.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions &amp; Inferences<\/jats:title><jats:p>The <jats:styled-content style=\"fixed-case\">UCN<\/jats:styled-content>1\u2010induced gastric motility dysfunction was mediated by abnormal acylated ghrelin dynamics. Supplementation of exogenous acylated ghrelin or enhancement of endogenous acylated ghrelin secretion by rikkunshito may be effective in treating functional <jats:styled-content style=\"fixed-case\">GI<\/jats:styled-content> disorders.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nmo.12588","type":"journal-article","created":{"date-parts":[[2015,6,19]],"date-time":"2015-06-19T02:44:55Z","timestamp":1434681895000},"page":"1089-1097","source":"Crossref","is-referenced-by-count":14,"title":["Ghrelin enhancer, rikkunshito, improves postprandial gastric motor dysfunction in an experimental stress model"],"prefix":"10.1111","volume":"27","author":[{"given":"Y.","family":"Harada","sequence":"first","affiliation":[{"name":"Tsumura Research Laboratories Tsumura &amp; Co. Ibaraki Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Ro","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology Saitama Medical Center Saitama Medical University Saitama Japan"},{"name":"Central Research Laboratories Teikyo University Chiba Medical Center Chiba Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Ochiai","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology Saitama Medical Center Saitama Medical University Saitama Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.","family":"Hayashi","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology Saitama Medical Center Saitama Medical University Saitama Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E.","family":"Hosomi","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology Saitama Medical Center Saitama Medical University Saitama Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N.","family":"Fujitsuka","sequence":"additional","affiliation":[{"name":"Tsumura Research Laboratories Tsumura &amp; Co. 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