{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T11:37:07Z","timestamp":1789213027796,"version":"build-2803163510"},"reference-count":31,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2013,11,14]],"date-time":"2013-11-14T00:00:00Z","timestamp":1384387200000},"content-version":"vor","delay-in-days":13,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Diabetes Metabolism Res"],"published-print":{"date-parts":[[2013,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Type 2 diabetes mellitus (T2DM) is associated with peripheral insulin resistance, impaired incretin effect, and increased plasma levels of tumour necrosis factor\u2010alpha (TNF\u2010<jats:italic>\u03b1<\/jats:italic>). Although TNF\u2010<jats:italic>\u03b1<\/jats:italic> infusion at a dose that induces systemic inflammation in healthy volunteers has been demonstrated to induce peripheral insulin resistance, the influence of this cytokine on the incretin effect is unknown.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We investigated whether systemic inflammation induced by TNF\u2010<jats:italic>\u03b1<\/jats:italic> infusion in healthy volunteers alters the incretin hormone response to oral and intravenous glucose loads in a crossover study design with ten healthy male volunteers (mean age 24\u2009years, mean body mass index 23.7\u2009kg\/m<jats:sup>2<\/jats:sup>).<\/jats:p><jats:p>The study consisted of four study days: days 1 and 2, 6\u2010h infusion of saline; days 3 and 4, 6\u2010h infusion of TNF\u2010<jats:italic>\u03b1<\/jats:italic>; days 1 and 3, 4\u2010h oral glucose tolerance test; and days 2 and 4, 4\u2010h corresponding intravenous isoglycaemic glucose tolerance test. Glucose tolerance tests were initiated after 2\u2009h of saline\/TNF\u2010<jats:italic>\u03b1<\/jats:italic> infusion. Plasma concentrations of TNF\u2010<jats:italic>\u03b1<\/jats:italic>, interleukin 6, glucose, incretin hormones, and cortisol, and serum concentrations of C\u2010peptide and insulin were measured throughout the study days. Insulin sensitivity was estimated by the Matsuda index and homeostasis model assessment of insulin resistance (HOMA\u2010IR). Prehepatic insulin secretion rates were calculated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>TNF\u2010<jats:italic>\u03b1<\/jats:italic> infusion induced symptoms of systemic inflammation; increased plasma levels of cortisol, TNF\u2010<jats:italic>\u03b1<\/jats:italic>, and interleukin 6; and increased the HOMA\u2010IR. The secretion of incretin hormones as well as the incretin effect remained unchanged.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>In healthy young male volunteers, acute systemic inflammation induced by infusion of TNF\u2010<jats:italic>\u03b1<\/jats:italic> is associated with insulin resistance with no change in the incretin effect. Copyright \u00a9 2013 John Wiley &amp; Sons, Ltd.<\/jats:p><\/jats:sec>","DOI":"10.1002\/dmrr.2441","type":"journal-article","created":{"date-parts":[[2013,7,31]],"date-time":"2013-07-31T13:32:29Z","timestamp":1375277549000},"page":"655-663","source":"Crossref","is-referenced-by-count":21,"title":["Tumour necrosis factor\u2010alpha infusion produced insulin resistance but no change in the incretin effect in healthy volunteers"],"prefix":"10.1002","volume":"29","author":[{"given":"Signe Tellerup","family":"Nielsen","sequence":"first","affiliation":[{"name":"Centre of Inflammation and Metabolism and CMRC, Section 7641 Rigshospitalet, Faculty of Health Sciences University of Copenhagen  Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Louise","family":"Lehrskov\u2010Schmidt","sequence":"additional","affiliation":[{"name":"Centre of Inflammation and Metabolism and CMRC, Section 7641 Rigshospitalet, Faculty of Health Sciences University of Copenhagen  Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rikke","family":"Krogh\u2010Madsen","sequence":"additional","affiliation":[{"name":"Centre of Inflammation and Metabolism and CMRC, Section 7641 Rigshospitalet, Faculty of Health Sciences University of Copenhagen  Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas P. 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