{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T07:26:33Z","timestamp":1761895593348,"version":"build-2065373602"},"reference-count":39,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,2,7]],"date-time":"2013-02-07T00:00:00Z","timestamp":1360195200000},"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":[[2013,6]]},"abstract":"Abstract<\/jats:title>\n \n Aim<\/jats:title>\n Recent studies suggest that the incretin concept is not restricted to glucose ingestion but relevant also after non\u2010glucose macronutrient administration. We therefore hypothesized that raising incretin hormones reduces circulating glucose after both glucose and non\u2010glucose macronutrient ingestion in healthy subjects.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n Twelve healthy subjects received the dipeptidyl peptidase\u20104 inhibitor sitagliptin (100\u2009mg) or placebo before ingestion of glucose, fat (olive oil) or protein mix in equicaloric amounts (8 kcal\/kg) plus paracetamol (1.5\u2009g). The 120\u2010min areas under curve (\n AUC<\/jats:styled-content>\n ) of intact glucagon\u2010like peptide\u20101 (\n GLP<\/jats:styled-content>\n \u20101), glucose, insulin, C\u2010peptide, glucagon and paracetamol, and model\u2010derived insulin secretion rate (\n ISR<\/jats:styled-content>\n ), insulin sensitivity, insulin clearance and glucose absorption were measured.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n The increased plasma intact\n GLP<\/jats:styled-content>\n \u20101 levels after each macronutrient was augmented by sitagliptin. This was associated with a robust lowering of glucose: glucose excursion after oral glucose was diminished, and glucose fell below baseline after oral fat and protein. In spite of lower glucose,\n \n AUC\n C<\/jats:sub>\n <\/jats:styled-content>\n \u2010peptide<\/jats:sub>\n and\n ISR<\/jats:styled-content>\n did not differ significantly between sitagliptin and placebo after any macronutrient.\n \n AUC\n glucagon<\/jats:sub>\n <\/jats:styled-content>\n , insulin sensitivity and insulin clearance were also not different between sitagliptin and placebo. Glucose absorption after oral glucose was reduced by sitagliptin, whereas\n \n AUC\n paracetamol<\/jats:sub>\n <\/jats:styled-content>\n was not statistically different between sitagliptin and placebo.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Physiological elevation of intact\n GLP<\/jats:styled-content>\n \u20101 levels after ingestion of glucose and non\u2010glucose macronutrients is robustly glucose\u2010lowering in healthy subjects. Hence, the incretin concept is not restricted to glucose ingestion in normal physiology. The glucose\u2010lowering action of sitagliptin at these low glucose levels in healthy subjects may have complex mechanisms, involving both islet\u2010dependent and islet\u2010independent mechanisms.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/dom.12062","type":"journal-article","created":{"date-parts":[[2013,1,17]],"date-time":"2013-01-17T14:17:14Z","timestamp":1358432234000},"page":"531-537","source":"Crossref","is-referenced-by-count":27,"title":["Glucose\u2010lowering effect of the\n DPP<\/scp>\n \u20104 inhibitor sitagliptin after glucose and non\u2010glucose macronutrient ingestion in non\u2010diabetic subjects"],"prefix":"10.1111","volume":"15","author":[{"given":"L.","family":"Ohlsson","sequence":"first","affiliation":[{"name":"Department of Clinical Sciences Lund Lund University Lund Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W.","family":"Alsalim","sequence":"additional","affiliation":[{"name":"Department of Clinical Sciences Lund Lund University Lund Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. 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