{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T07:36:32Z","timestamp":1761896192333,"version":"build-2065373602"},"reference-count":48,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,1,13]],"date-time":"2016-01-13T00:00:00Z","timestamp":1452643200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2016,3]]},"abstract":"<jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>\n                      To investigate the effect of infusion of the glucagon\u2010like peptide\u20101 (\n                      <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n                      \u20101) receptor agonist exenatide on exocrine pancreatic function.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      This was a randomized, placebo\u2010controlled, double\u2010blind, crossover study in 12 male patients with type 2 diabetes, treated with oral glucose\u2010lowering agents. On two separate occasions, exenatide or placebo (saline 0.9%) were administered intravenously, in randomized order. Exocrine pancreatic function was measured using secretin\u2010enhanced magnetic resonance cholangiopancreatography. The primary outcome measure was defined as secretin\u2010stimulated pancreatic excretion volume. Secondary outcome measures were maximum secretion speed and the time to reach this maximum. In addition, changes in pancreatic duct (\n                      <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                      ) diameter were measured.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Exenatide did not change secretin\u2010stimulated pancreatic excretion volume, as compared with placebo (mean\u2009\u00b1\u2009standard error of the mean 142.2\u2009\u00b1\u200915.6\u2009ml vs 142.6\u2009\u00b1\u20098.5\u2009ml, respectively; p\u2009=\u20090.590). Also, exenatide did not change the maximum secretion speed (33.1\u2009\u00b1\u20091.4 vs 36.9\u2009\u00b1\u20092.2; p\u2009=\u20090.221), nor the time to reach this maximum (both 4\u2009min 30\u2009s). No differences in\n                      <jats:styled-content style=\"fixed-case\">PD<\/jats:styled-content>\n                      diameter were observed between the two groups.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Infusion of exenatide did not directly influence\n                      <jats:styled-content style=\"fixed-case\">MRI<\/jats:styled-content>\n                      \u2010measured exocrine pancreatic excretion in patients with type 2 diabetes. Although long\u2010term studies are warranted, these findings suggest that potential adverse pancreatic effects of\n                      <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n                      \u20101 receptor agonists are not mediated by changes in exocrine pancreatic secretion.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/dom.12612","type":"journal-article","created":{"date-parts":[[2015,12,6]],"date-time":"2015-12-06T23:49:13Z","timestamp":1449445753000},"page":"281-288","source":"Crossref","is-referenced-by-count":5,"title":["Glucagon\u2010like peptide\u20101 receptor agonist exenatide has no acute effect on\n                    <scp>MRI<\/scp>\n                    \u2010measured exocrine pancreatic function in patients with type 2 diabetes: a randomized trial"],"prefix":"10.1111","volume":"18","author":[{"given":"M. M.","family":"Smits","sequence":"first","affiliation":[{"name":"Diabetes Centre, Department of Internal Medicine VU University Medical Centre  Amsterdam The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.","family":"Tonneijck","sequence":"additional","affiliation":[{"name":"Diabetes Centre, Department of Internal Medicine VU University Medical Centre  Amsterdam The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. H. A.","family":"Muskiet","sequence":"additional","affiliation":[{"name":"Diabetes Centre, Department of Internal Medicine VU University Medical Centre  Amsterdam The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. H. H.","family":"Kramer","sequence":"additional","affiliation":[{"name":"Diabetes Centre, Department of Internal Medicine VU University Medical Centre  Amsterdam The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Diamant","sequence":"additional","affiliation":[{"name":"Diabetes Centre, Department of Internal Medicine VU University Medical Centre  Amsterdam The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"I. C.","family":"Pieters\u2010van den Bos","sequence":"additional","affiliation":[{"name":"Department of Radiology and Nuclear Medicine VU University Medical Centre  Amsterdam The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D. H.","family":"van Raalte","sequence":"additional","affiliation":[{"name":"Diabetes Centre, Department of Internal Medicine VU University Medical Centre  Amsterdam The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D. L.","family":"Cahen","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology and Hepatology Erasmus University Medical Centre  Rotterdam The 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