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The aim of this study is to test the hypothesis that treatment with a dipeptidyl peptidase\u20104 inhibitor initiated soon after a coronary event improves beta\u2010cell function.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Acute coronary syndrome<jats:styled-content style=\"fixed-case\">ACS<\/jats:styled-content> patients with <jats:styled-content style=\"fixed-case\">IGT<\/jats:styled-content> or T2<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> (<jats:italic>n\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>71), screened by oral glucose tolerance test (<jats:styled-content style=\"fixed-case\">OGTT<\/jats:styled-content>) 4\u201323\u00a0days (median 6\u00a0days) after hospital admission, were randomly assigned to sitagliptin 100\u00a0mg (<jats:italic>n\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>34) or placebo (<jats:italic>n\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>37) and treated for a duration of 12\u00a0weeks. All patients received lifestyle advice but no glucose\u2010lowering agents other than the study drug. The study end\u2010point was beta\u2010cell function assessed using the insulinogenic index (<jats:styled-content style=\"fixed-case\">IGI<\/jats:styled-content>\u00a0=\u00a0\u0394Insulin<jats:sub>30<\/jats:sub>\/\u0394Glucose<jats:sub>30<\/jats:sub>), derived from an <jats:styled-content style=\"fixed-case\">OGTT<\/jats:styled-content>, and acute insulin response to glucose (<jats:styled-content style=\"fixed-case\">AIR<\/jats:styled-content>g) assessed by a frequently sampled intravenous glucose tolerance test.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The <jats:styled-content style=\"fixed-case\">IGI<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">AIR<\/jats:styled-content>g did not differ at baseline between the sitagliptin and placebo groups (69.9 vs. 66.4\u00a0pmol\u00a0mmol<jats:sup>\u22121<\/jats:sup> and 1394 vs. 1106\u00a0pmol L<jats:sup>\u22121<\/jats:sup>\u00a0min<jats:sup>\u22121<\/jats:sup> respectively). After 12\u00a0weeks, the <jats:styled-content style=\"fixed-case\">IGI<\/jats:styled-content> was 85.0 in the sitagliptin and 58.1\u00a0pmol\/mmol in the placebo group (<jats:italic>P\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>0.013) and <jats:styled-content style=\"fixed-case\">AIR<\/jats:styled-content>g was 1909 and 1043\u00a0pmol\u00a0L<jats:sup>\u22121<\/jats:sup>\u00a0min<jats:sup>\u22121<\/jats:sup> (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.0001) in the sitagliptin and placebo groups respectively. Fasting glucose at baseline was 6.1\u00a0mmol\u00a0L<jats:sup>\u22121<\/jats:sup> in sitagliptin\u2010treated patients and 6.0\u00a0mmol\u00a0L<jats:sup>\u22121<\/jats:sup> in those who received placebo compared with 5.8 and 5.9\u00a0mmol\u00a0L<jats:sup>\u22121<\/jats:sup> respectively, after 12\u00a0weeks of treatment. Post load glucose metabolism improved in significantly more sitagliptin\u2010treated patients compared with the placebo group (<jats:italic>P\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>0.003). Sitagliptin was well tolerated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Sitagliptin improved beta\u2010cell function and glucose perturbations in patients with <jats:styled-content style=\"fixed-case\">ACS<\/jats:styled-content> and newly diagnosed glucose disturbances.<\/jats:p><\/jats:sec>","DOI":"10.1111\/joim.12032","type":"journal-article","created":{"date-parts":[[2013,4,12]],"date-time":"2013-04-12T13:35:19Z","timestamp":1365773719000},"page":"410-421","source":"Crossref","is-referenced-by-count":20,"title":["Sitagliptin improves beta\u2010cell function in patients with acute coronary syndromes and newly diagnosed glucose abnormalities\u2013the <scp>BEGAMI<\/scp> study"],"prefix":"10.1111","volume":"273","author":[{"given":"C.","family":"Hage","sequence":"first","affiliation":[{"name":"Cardiology Unit Department of Medicine Karolinska Institutet Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.","family":"Brismar","sequence":"additional","affiliation":[{"name":"Endocrine and Diabetes Unit Department of Molecular Medicine and Surgery Karolinska Institutet Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S.","family":"Efendic","sequence":"additional","affiliation":[{"name":"Endocrine and Diabetes Unit Department of Molecular Medicine and Surgery Karolinska Institutet Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Lundman","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine Department of Clinical Sciences Karolinska Institutet Danderyd Hospital Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L.","family":"Ryd\u00e9n","sequence":"additional","affiliation":[{"name":"Cardiology Unit Department of Medicine Karolinska Institutet Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L.","family":"Mellbin","sequence":"additional","affiliation":[{"name":"Cardiology Unit Department of Medicine Karolinska Institutet Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,2,14]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(02)09089-X"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ehj.2004.07.027"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehl207"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.1253\/circj.71.834"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ehj.2004.09.021"},{"key":"e_1_2_10_7_1","doi-asserted-by":"publisher","DOI":"10.2337\/db09-9028"},{"key":"e_1_2_10_8_1","doi-asserted-by":"publisher","DOI":"10.1007\/s001250100580"},{"key":"e_1_2_10_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.mcna.2010.11.005"},{"key":"e_1_2_10_10_1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2011-0246"},{"key":"e_1_2_10_11_1","doi-asserted-by":"crossref","first-page":"1249","DOI":"10.2337\/diab.44.11.1249","article-title":"Overview of 6\u00a0years' therapy of type II diabetes: a progressive disease. 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