{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T16:26:08Z","timestamp":1792167968613,"version":"4.4.0"},"reference-count":0,"publisher":"American Diabetes Association","issue":"7","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1975,7,1]]},"abstract":"<jats:p>We assayed glucose tolerance and insulin secretion in ten patients with metastatic carcinoid tumors and the carcinoid syndrome (\u201cactive tumors\u201d) and in seven patients with metastatic carcinoid tumors without the carcinoid syndrome (\u201cinactive tumors\u201d). The patients with \u201cactive tumors\u201d had elevated serum serotonin levels while the patients with \u201cinactive tumors\u201d had normal serum serotonin levels. Of the ten patients with \u201cactive tumors\u201d, five had diabetic and three had borderline intravenous glucose disposal rate constants (KG = 0.88 \u00b1 0.07, M. \u00b1 S.E.M.). Their KG was significantly lower (p&amp;lt;0.01) than a group of agematched normals. AH of the patients with \u201cinactive tumors\u201d had normal KG values (KG = 1.67 \u00b1 0.24). Their KG did not differ from that of age-matched normal subjects. Both groups of carcinoid patients had a comparable decrease in their insulinogenic index. Two days' administration of the serotonin antagonist cyproheptadine (Cypro) to eight of the patients with \u201cactive tumors\u201d resulted in a significant increase in the \u201cinsulinogenic index\u201d (50 per cent) but a nonsignificant increase in the KG (12 per cent). Administration of p-chlorophenylalanine, a compound that blocks serotonin synthesis, resulted in an increase in both the KG (60 per cent) and the \u201cinsulinogenic index\u201d (55 per cent). The insulin half-life (\u00bd) of patients with \u201cactive tumors\u201d (6.1 \u00b1 0.4 min.) did not differ from the t\u00bd of normal subjects (6.6 \u00b1 0.4 min.), suggesting that the decreased plasma insulin levels following intravenous glucose were due to impaired insulin secretion rather than accelerated insulin destruction. Seven of the patients received treatment with the antitumor agent streptozotocin (Strepto). The patients received cumulative doses of from 70 to 300 mg. of Strepto per kilogram body weight with no impairment in glucose tolerance or insulin secretion. We conclude that there is high incidence of glucose intolerance (80 per cent) and impaired insulin secretion in patients with the carcinoid syndrome and that serotonin plays a role in producing these alterations.<\/jats:p>","DOI":"10.2337\/diab.24.7.664","type":"journal-article","created":{"date-parts":[[2013,9,19]],"date-time":"2013-09-19T17:13:09Z","timestamp":1379610789000},"page":"664-671","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":19,"title":["Glucose Intolerance in the Carcinoid Syndrome"],"prefix":"10.2337","volume":"24","author":[{"given":"Jerome M","family":"Feldman","sequence":"first","affiliation":[{"name":"Durham Veterans Administration Hospital and Division of Endocrinology, Department of Medicine, Duke University Medical Center\u2008Durham, North Carolina, 27710"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James W","family":"Plonk","sequence":"additional","affiliation":[{"name":"Durham Veterans Administration Hospital and Division of Endocrinology, Department of Medicine, Duke University Medical Center\u2008Durham, North Carolina, 27710"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carl H","family":"Bivens","sequence":"additional","affiliation":[{"name":"Durham Veterans Administration Hospital and Division of Endocrinology, Department of Medicine, Duke University Medical Center\u2008Durham, North Carolina, 27710"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harold E","family":"Lebovitz","sequence":"additional","affiliation":[{"name":"Durham Veterans Administration Hospital and Division of Endocrinology, Department of Medicine, Duke University Medical Center\u2008Durham, North Carolina, 27710"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1167","container-title":["Diabetes"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.org\/diabetes\/diabetes\/article-pdf\/24\/7\/664\/348332\/24-7-664.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/diabetesjournals.org\/diabetes\/article-pdf\/24\/7\/664\/348332\/24-7-664.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,11,2]],"date-time":"2022-11-02T16:25:49Z","timestamp":1667406349000},"score":1,"resource":{"primary":{"URL":"https:\/\/diabetesjournals.org\/diabetes\/article\/24\/7\/664\/4138\/Glucose-Intolerance-in-the-Carcinoid-Syndrome"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1975,7,1]]},"references-count":0,"journal-issue":{"issue":"7","published-print":{"date-parts":[[1975,7,1]]}},"URL":"https:\/\/doi.org\/10.2337\/diab.24.7.664","relation":{},"ISSN":["0012-1797","1939-327X"],"issn-type":[{"value":"0012-1797","type":"print"},{"value":"1939-327X","type":"electronic"}],"subject":[],"published":{"date-parts":[[1975,7,1]]}}}