{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T16:54:19Z","timestamp":1791910459782,"version":"4.3.4"},"reference-count":30,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2016,8,30]],"date-time":"2016-08-30T00:00:00Z","timestamp":1472515200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004963","name":"Seventh Framework Programme","doi-asserted-by":"publisher","award":["FP7\/2007\u20102013"],"award-info":[{"award-number":["FP7\/2007\u20102013"]}],"id":[{"id":"10.13039\/501100004963","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004963","name":"Seventh Framework Programme","doi-asserted-by":"publisher","award":["n\u00b0 282521"],"award-info":[{"award-number":["n\u00b0 282521"]}],"id":[{"id":"10.13039\/501100004963","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100004325","name":"AstraZeneca","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004325","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008349","name":"Boehringer Ingelheim","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008349","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004191","name":"Novo Nordisk","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004191","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100004339","name":"Sanofi","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004339","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2016,12]]},"abstract":"<jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>\n                      Treatment with glucagon\u2010like peptide (\n                      <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n                      )\u20101 receptor agonists or dipeptidyl peptidase (\n                      <jats:styled-content style=\"fixed-case\">DPP<\/jats:styled-content>\n                      )\u20104 inhibitors might increase gallstone formation; however, the mechanisms involved are unknown. We aimed to assess the effects of these drugs on gallbladder volume and bile acid profile.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods<\/jats:title>\n                    <jats:p>\n                      A total of 57 type 2 diabetes patients (mean\u2009\u00b1\u2009\n                      <jats:styled-content style=\"fixed-case\">SD<\/jats:styled-content>\n                      age, 62.8\u2009\u00b1\u20096.9\u2009years;\n                      <jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content>\n                      , 31.8\u2009\u00b1\u20094.1\u2009kg\/m\n                      <jats:sup>2<\/jats:sup>\n                      ;\n                      <jats:styled-content style=\"fixed-case\">HbA1c<\/jats:styled-content>\n                      , 7.3%\u2009\u00b1\u20090.6%), treated with metformin and\/or sulfonylureas, were included in this 12\u2010week randomized, placebo\u2010controlled, double\u2010blind, single\u2010centre trial between\n                      <jats:styled-content style=\"fixed-case\">J<\/jats:styled-content>\n                      uly 2013 and\n                      <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                      ugust 2015 at the\n                      <jats:styled-content style=\"fixed-case\">VU U<\/jats:styled-content>\n                      niversity\n                      <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>\n                      edical\n                      <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>\n                      enter, the\n                      <jats:styled-content style=\"fixed-case\">N<\/jats:styled-content>\n                      etherlands. Patients received the\n                      <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n                      \u20101 receptor agonist liraglutide, the\n                      <jats:styled-content style=\"fixed-case\">DPP<\/jats:styled-content>\n                      \u20104 inhibitor sitagliptin or matching placebo for 12\u2009weeks. Gallbladder fasting volume and ejection fraction were measured using ultrasonography after a high\u2010fat meal. Serum bile acids were measured in the fasting and postprandial state and in faecal samples. The trial was registered at\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/ClinicalTrials.gov\">ClinicalTrials.gov<\/jats:ext-link>\n                      (\n                      <jats:styled-content style=\"fixed-case\">NCT01744236<\/jats:styled-content>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Neither liraglutide nor sitagliptin had an effect on gallbladder fasting volume and ejection fraction (p\u2009&gt;\u2009.05). Liraglutide increased serum levels of deoxycholic acid in the fasting state [0.20\u2009\u00b5mol\/\n                      <jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>\n                      (95%\n                      <jats:styled-content style=\"fixed-case\">CI<\/jats:styled-content>\n                      0.027\u20100.376), p\u2009\n                      <jats:italic>=<\/jats:italic>\n                      \u20090.024] and postprandial state [\n                      <jats:styled-content style=\"fixed-case\">AUC<\/jats:styled-content>\n                      40.71 (13.22\u201068.21), p\u2009=\u20090.005] and in faeces [ratio 1.5 (1.03\u20102.19); p\u2009=\u20090.035]. Sitagliptin had no effect on serum bile acids, but increased faecal levels of chenodeoxycholic acid [ratio 3.42 (1.33\u20108.79), p\u2009=\u20090.012], cholic acid [ratio 3.32 (1.26\u20108.87), p\u2009=\u20090.017] and ursodeoxycholic acid [ratio 3.81 (1.44\u201010.14), p\u2009=\u20090.008].\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Neither liraglutide nor sitagliptin has an effect on gallbladder volume. Observed changes in bile acids with liraglutide suggest alterations in the intestinal microbiome, while sitagliptin appears to increase hepatic bile acid production.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/dom.12748","type":"journal-article","created":{"date-parts":[[2016,7,23]],"date-time":"2016-07-23T04:16:45Z","timestamp":1469247405000},"page":"1217-1225","source":"Crossref","is-referenced-by-count":52,"title":["Biliary effects of liraglutide and sitagliptin, a 12\u2010week randomized placebo\u2010controlled trial in type 2 diabetes patients"],"prefix":"10.1111","volume":"18","author":[{"given":"Mark M.","family":"Smits","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Diabetes Center VU University Medical Center  Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lennart","family":"Tonneijck","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Diabetes Center VU 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