{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,31]],"date-time":"2025-12-31T06:37:52Z","timestamp":1767163072969,"version":"build-2238731810"},"reference-count":35,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2014,6,19]],"date-time":"2014-06-19T00:00:00Z","timestamp":1403136000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Diabet. Med."],"published-print":{"date-parts":[[2014,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>To compare the effects of vildagliptin with those of glimepiride on glycaemic control, fat tolerance and inflammatory markers in people with Type 2 diabetes mellitus receiving metformin treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      A total of 167 participants were randomized to vildagliptin 50\u00a0mg twice a day or glimepiride 2\u00a0mg three times a day, for 6\u00a0months. We evaluated the following variables:\n                      <jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content>\n                      ; glycaemic control; fasting plasma insulin; homeostatic model assessment of insulin resistance index; fasting plasma proinsulin; glucagon; lipid profile; adiponectin; high\u2010sensitivity C\u2010reactive protein; interleukin\u20106; and tumour necrosis factor\u2010\u03b1. A euglycaemic\u2010hyperinsulinaemic clamp procedure and an oral fat load test were also performed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Despite a similar decrease in HbA\n                      <jats:sub>1c<\/jats:sub>\n                      levels (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\n                      <jats:italic>\u00a0<\/jats:italic>\n                      0.009, and\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\n                      <jats:italic>\u00a0<\/jats:italic>\n                      0.008, respectively), body weight increased with glimepiride (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\n                      <jats:italic>\u00a0<\/jats:italic>\n                      0.048 vs baseline) and decreased with vildagliptin (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\n                      <jats:italic>\u00a0<\/jats:italic>\n                      0.041 vs baseline and vs glimepiride). Fasting plasma insulin and homeostatic model assessment of insulin resistance index were significantly lower with vildagliptin compared with glimepiride (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\n                      <jats:italic>\u00a0<\/jats:italic>\n                      0.035 and 0.047). M value, an index of insulin sensitivity, increased with vildagliptin, both compared with baseline and with glimepiride (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\n                      <jats:italic>\u00a0<\/jats:italic>\n                      0.028 and 0.039, respectively). Vildagliptin improved all post\u2010oral fat load peaks of lipid profile compared with glimepiride. Adiponectin levels were higher (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\n                      <jats:italic>\u00a0<\/jats:italic>\n                      0.035) and high\u2010sensitivity C\u2010reactive protein levels were lower (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\n                      <jats:italic>\u00a0<\/jats:italic>\n                      0.038) with vildagliptin vs glimepiride. During the oral fat load test, interleukin\u20106, high\u2010sensitivity C\u2010reactive protein and tumour necrosis factor\u2010\u03b1 peaks were lower and adiponectin peak was higher in the vildagliptin group than in the glimepiride group. There was a higher dropout rate as a result of hypoglycaemia in the glimepiride group than in the vildagliptin group.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Vildagliptin was more effective than glimepiride in reducing post\u2010oral fat load peaks of lipid\u2010trafficking adipocytokines and inflammatory markers.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/dme.12499","type":"journal-article","created":{"date-parts":[[2014,5,13]],"date-time":"2014-05-13T12:41:08Z","timestamp":1399984868000},"page":"1515-1523","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["<i>Retracted<\/i>\n                    : Comparison of vildagliptin and glimepiride: effects on glycaemic control, fat tolerance and inflammatory markers in people with Type 2 diabetes"],"prefix":"10.1111","volume":"31","author":[{"given":"G.","family":"Derosa","sequence":"first","affiliation":[{"name":"Department of Internal Medicine and Therapeutics University of Pavia and Fondazione IRCCS Policlinico S. Matteo"},{"name":"Centre for the Study of Endocrine\u2010Metabolic Pathophysiology and Clinical Research University of Pavia Pavia Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"Bonaventura","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Therapeutics University of Pavia and Fondazione IRCCS Policlinico S. Matteo"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.","family":"Bianchi","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Therapeutics University of Pavia and Fondazione IRCCS Policlinico S. Matteo"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D.","family":"Romano","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Therapeutics University of Pavia and Fondazione IRCCS Policlinico S. Matteo"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E.","family":"Fogari","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Therapeutics University of Pavia and Fondazione IRCCS Policlinico S. Matteo"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"D'Angelo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Therapeutics University of Pavia and Fondazione IRCCS Policlinico S. Matteo"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.","family":"Maffioli","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine and Therapeutics University of Pavia and Fondazione IRCCS Policlinico S. 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