{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T13:25:45Z","timestamp":1773408345902,"version":"3.50.1"},"reference-count":34,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2015,6,4]],"date-time":"2015-06-04T00:00:00Z","timestamp":1433376000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Endocrinology"],"published-print":{"date-parts":[[2016,1]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Systemic oxidative stress has been causally related to insulin resistance and the subsequent development of type 2 diabetes mellitus (T2D). We investigated associations between circulating oxidative stress markers and different surrogate indexes of insulin sensitivity\/resistance.<\/jats:p><\/jats:sec><jats:sec><jats:title>Patients<\/jats:title><jats:p>Cross\u2013sectional data were obtained from 1183 subjects with normal glucose tolerance (<jats:styled-content style=\"fixed-case\">NGT<\/jats:styled-content>), 280 subjects with impaired glucose tolerance (<jats:styled-content style=\"fixed-case\">IGT<\/jats:styled-content>) and 69 newly detected T2D individuals entering the <jats:styled-content style=\"fixed-case\">PREDIAS<\/jats:styled-content> (prevention of diabetes) study.<\/jats:p><\/jats:sec><jats:sec><jats:title>Measurements<\/jats:title><jats:p>Following oral glucose tolerance test, five different insulin sensitivity\/resistance indices were estimated: homoeostasis model of insulin resistance (<jats:styled-content style=\"fixed-case\">HOMA<\/jats:styled-content>\u2013<jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content>), quantitative insulin sensitivity check index (<jats:styled-content style=\"fixed-case\">QUICKI<\/jats:styled-content>), early phase insulin release (<jats:styled-content style=\"fixed-case\">EPIR<\/jats:styled-content>), insulin sensitivity index (<jats:styled-content style=\"fixed-case\">ISI<\/jats:styled-content>) and disposition index (<jats:styled-content style=\"fixed-case\">DI<\/jats:styled-content>). Additionally, circulating phagocyte generation of reactive oxygen species (<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>) and plasma total antioxidant capacity (<jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content>) was measured.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>After adjustment for five covariates, <jats:styled-content style=\"fixed-case\">HOMA<\/jats:styled-content>\u2013<jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content> was significantly increased in <jats:styled-content style=\"fixed-case\">IGT<\/jats:styled-content> and T2D subjects when compared to <jats:styled-content style=\"fixed-case\">NGT<\/jats:styled-content> subjects (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7000). <jats:styled-content style=\"fixed-case\">QUICKI<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7000), <jats:styled-content style=\"fixed-case\">ISI<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7000), <jats:styled-content style=\"fixed-case\">EPIR<\/jats:styled-content> (0\u00b7005\/0\u00b7012) and <jats:styled-content style=\"fixed-case\">DI<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7000) were significantly attenuated in <jats:styled-content style=\"fixed-case\">IGT<\/jats:styled-content> and T2D. The prevalence of <jats:styled-content style=\"fixed-case\">IGT<\/jats:styled-content> and T2D individuals increased with increasing <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> generation and <jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content> tertiles. Increased systemic <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> generation was paralleled by increased <jats:styled-content style=\"fixed-case\">HOMA<\/jats:styled-content>\u2013<jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b7001, tertile 1\/T1\/<jats:italic>vs<\/jats:italic> tertile 3\/T3\/), decreased <jats:styled-content style=\"fixed-case\">QUICKI<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b7001, T1 <jats:italic>vs<\/jats:italic> T3) and decreased <jats:styled-content style=\"fixed-case\">ISI<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b705, T1 <jats:italic>vs<\/jats:italic> T3). A similar tendency for indices was observed when comparing <jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content> tertiles: increase in <jats:styled-content style=\"fixed-case\">HOMA<\/jats:styled-content>\u2013<jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content>, decrease in <jats:styled-content style=\"fixed-case\">QUICKI<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">ISI<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b7001, T1 <jats:italic>vs<\/jats:italic> T3 each). <jats:styled-content style=\"fixed-case\">EPIR<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">DI<\/jats:styled-content> did not differ significantly across <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> generation and <jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content> tertiles.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Systemic oxidative stress is associated with elevated insulin resistance index <jats:styled-content style=\"fixed-case\">HOMA<\/jats:styled-content>\u2013<jats:styled-content style=\"fixed-case\">IR<\/jats:styled-content>, and decreased insulin sensitivity surrogates <jats:styled-content style=\"fixed-case\">QUICKI<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">ISI<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cen.12811","type":"journal-article","created":{"date-parts":[[2015,5,4]],"date-time":"2015-05-04T13:34:09Z","timestamp":1430746449000},"page":"48-54","source":"Crossref","is-referenced-by-count":21,"title":["Association between systemic oxidative stress and insulin resistance\/sensitivity indices \u2013 the <scp>PREDIAS<\/scp> study"],"prefix":"10.1111","volume":"84","author":[{"given":"Steffi","family":"Kopprasch","sequence":"first","affiliation":[{"name":"Department of Internal Medicine 3 Technische Universit\u00e4t Dresden University Hospital Carl Gustav Carus Dresden Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dheban","family":"Srirangan","sequence":"additional","affiliation":[{"name":"Department of Medical Informatics and Biometry Technische Universit\u00e4t Dresden University Hospital Carl Gustav Carus Dresden Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sybille","family":"Bergmann","sequence":"additional","affiliation":[{"name":"Institute of Clinical Chemistry and Laboratory Medicine Technische Universit\u00e4t Dresden University Hospital Carl Gustav Carus Dresden Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Juergen","family":"Graessler","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 3 Technische Universit\u00e4t Dresden University Hospital Carl Gustav Carus Dresden Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter E.H.","family":"Schwarz","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 3 Technische Universit\u00e4t Dresden University Hospital Carl Gustav Carus Dresden Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefan R.","family":"Bornstein","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine 3 Technische Universit\u00e4t Dresden University Hospital Carl Gustav Carus Dresden Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2015,6,4]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1007\/s11883-014-0419-z"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/414813a"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2007.1595"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature04634"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.2337\/dc07-0817"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.52.2.463"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00645.2007"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00280883"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1210\/jcem.85.7.6661"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.2337\/diacare.23.3.295"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.2337\/dc08-1195"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0168-8227(99)00116-3"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI110398"},{"key":"e_1_2_7_15_1","first-page":"1663","article-title":"Quantification of the relationship between insulin sensitivity and beta\u2013cell function in human subjects","volume":"42","author":"Kahn S.E.","year":"1993","journal-title":"Evidence for a Hyperbolic Function. 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