{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T09:53:55Z","timestamp":1770976435483,"version":"3.50.1"},"reference-count":40,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2014,4,11]],"date-time":"2014-04-11T00:00:00Z","timestamp":1397174400000},"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":[[2014,9]]},"abstract":"<jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>\n                      Glucagon\u2010like peptide\u20101 (\n                      <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n                      \u20101) receptor agonists improve islet function and delay gastric emptying in patients with type 2 diabetes mellitus (\n                      <jats:styled-content style=\"fixed-case\">T2DM<\/jats:styled-content>\n                      ). This meta\u2010analysis aimed to investigate the effects of the once\u2010daily prandial\n                      <jats:styled-content style=\"fixed-case\">GLP<\/jats:styled-content>\n                      \u20101 receptor agonist lixisenatide on postprandial plasma glucose (\n                      <jats:styled-content style=\"fixed-case\">PPG<\/jats:styled-content>\n                      ), glucagon and insulin levels.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Six randomized, placebo\u2010controlled studies of lixisenatide 20\u2009\u00b5g once daily were included in this analysis: lixisenatide as monotherapy (\n                      <jats:styled-content style=\"fixed-case\">GetGoal<\/jats:styled-content>\n                      \u2010Mono), as add\u2010on to oral antidiabetic drugs (\n                      <jats:styled-content style=\"fixed-case\">OADs<\/jats:styled-content>\n                      ;\n                      <jats:styled-content style=\"fixed-case\">GetGoal<\/jats:styled-content>\n                      \u2010M,\n                      <jats:styled-content style=\"fixed-case\">GetGoal<\/jats:styled-content>\n                      \u2010S) or in combination with basal insulin (\n                      <jats:styled-content style=\"fixed-case\">GetGoal<\/jats:styled-content>\n                      \u2010L,\n                      <jats:styled-content style=\"fixed-case\">GetGoal<\/jats:styled-content>\n                      \u2010Duo\u20101 and\n                      <jats:styled-content style=\"fixed-case\">GetGoal<\/jats:styled-content>\n                      \u2010L\u2010Asia). Change in 2\u2010h\n                      <jats:styled-content style=\"fixed-case\">PPG<\/jats:styled-content>\n                      and glucose excursion were evaluated across six studies. Change in 2\u2010h glucagon and postprandial insulin were evaluated across two studies. A meta\u2010analysis was performed on least square (\n                      <jats:styled-content style=\"fixed-case\">LS<\/jats:styled-content>\n                      ) mean estimates obtained from analysis of covariance (\n                      <jats:styled-content style=\"fixed-case\">ANCOVA<\/jats:styled-content>\n                      )\u2010based linear regression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Lixisenatide significantly reduced 2\u2010h\n                      <jats:styled-content style=\"fixed-case\">PPG<\/jats:styled-content>\n                      from baseline (\n                      <jats:styled-content style=\"fixed-case\">LS<\/jats:styled-content>\n                      mean difference vs. placebo: \u22124.9\u2009mmol\/l, p\u2009&lt;\u20090.001) and glucose excursion (\n                      <jats:styled-content style=\"fixed-case\">LS<\/jats:styled-content>\n                      mean difference vs. placebo: \u22124.5\u2009mmol\/l, p\u2009&lt;\u20090.001). As measured in two studies, lixisenatide also reduced postprandial glucagon (\n                      <jats:styled-content style=\"fixed-case\">LS<\/jats:styled-content>\n                      mean difference vs. placebo: \u221219.0\u2009ng\/l, p\u2009&lt;\u20090.001) and insulin (\n                      <jats:styled-content style=\"fixed-case\">LS<\/jats:styled-content>\n                      mean difference vs. placebo: \u221264.8 pmol\/l, p\u2009&lt;\u20090.001). There was a stronger correlation between 2\u2010h postprandial glucagon and 2\u2010h\n                      <jats:styled-content style=\"fixed-case\">PPG<\/jats:styled-content>\n                      with lixisenatide than with placebo.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Lixisenatide significantly reduced 2\u2010h\n                      <jats:styled-content style=\"fixed-case\">PPG<\/jats:styled-content>\n                      and glucose excursion together with a marked reduction in postprandial glucagon and insulin; thus, lixisenatide appears to have biological effects on blood glucose that are independent of increased insulin secretion. These effects may be, in part, attributed to reduced glucagon secretion.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/dom.12290","type":"journal-article","created":{"date-parts":[[2014,3,18]],"date-time":"2014-03-18T10:58:41Z","timestamp":1395140321000},"page":"861-868","source":"Crossref","is-referenced-by-count":25,"title":["Pronounced reduction of postprandial glucagon by lixisenatide: a meta\u2010analysis of randomized clinical trials"],"prefix":"10.1111","volume":"16","author":[{"given":"B.","family":"Ahr\u00e9n","sequence":"first","affiliation":[{"name":"Department of Clinical Sciences Lund University  Lund Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.\u2010F.","family":"Gautier","sequence":"additional","affiliation":[{"name":"Centre of Diabetes and its Complications Lariboisi\u00e8re Hospital  Paris France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R.","family":"Berria","sequence":"additional","affiliation":[{"name":"Global Medical Affairs Sanofi  Bridgewater NJ USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W.","family":"Stager","sequence":"additional","affiliation":[{"name":"Global Medical Affairs Sanofi  Bridgewater NJ USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R.","family":"Aronson","sequence":"additional","affiliation":[{"name":"LMC Diabetes and Endocrinology  Toronto Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C. 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