{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T07:50:40Z","timestamp":1761897040991,"version":"3.40.5"},"reference-count":40,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2019,7,24]],"date-time":"2019-07-24T00:00:00Z","timestamp":1563926400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["T32 DK007271"],"award-info":[{"award-number":["T32 DK007271"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Diabetes"],"published-print":{"date-parts":[[2020,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>The determinants of type 2 diabetes (T2D) remission and\/or relapse after gastric bypass (RYGB) remain fully unknown. This study characterized \u03b2\u2010 and \u03b1\u2010cell function, in cretin hormone release and insulin sensitivity in individuals with (remitters) or without (non\u2010remitters) diabetes remission after RYGB.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>This is a cross\u2010sectional study of two distinct cohorts of individuals with or without diabetes remission at least 2\u2009years after RYGB. Each individual underwent\u2010either an oral glucose (remitters) or a mixed meal (non\u2010remitters) test; glucose, proinsulin, insulin, C\u2010peptide, glucagon, incretins and leptin were measured.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Compared to remitters (n = 23), non\u2010remitters (n = 31) were older (mean [\u00b1SD] age 56.1\u2009\u00b1\u20098.2 vs. 46.0\u2009\u00b1\u20098.9\u2009years, <jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001), had longer diabetes duration (13.1\u2009\u00b1\u200910.1 vs. 2.2\u2009\u00b1\u20092.4\u2009years, <jats:italic>P<\/jats:italic> &lt;\u20090.001), were further out from the surgery (5.6\u2009\u00b1\u20093.3 vs. 3.5\u2009\u00b1\u20091.7\u2009years, <jats:italic>P<\/jats:italic>\u2009&lt;\u20090.01), were more insulin resistant (HOMA\u2010IR 4.01\u2009\u00b1\u20093.65 vs. 2.08\u2009\u00b1\u20091.22, <jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001), but did not differ for body weight. As predicted, remitters had higher \u03b2\u2010cell glucose sensitivity (1.95\u2009\u00b1\u20091.23 vs. 0.86\u2009\u00b1\u20090.55\u2009pmol\/kg\/min\/mmol, <jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001) and disposition index (1.55\u2009\u00b1\u20091.75 vs 0.33\u2009\u00b1\u20090.27, <jats:italic>P<\/jats:italic> = 0.003), compared to non\u2010remitters, who showed non\u2010suppressibility of glucagon during the oral challenge (time\u2009\u00d7\u2009group <jats:italic>P<\/jats:italic> = 0.001). Higher proinsulin (16.55\u2009\u00b1\u200910.45 vs. 6.62\u2009\u00b1\u20093.50 PM, <jats:italic>P<\/jats:italic>\u2009&lt;\u20090.0001), and proinsulin: C\u2010peptide (40.83\u2009\u00b1\u200929.43 vs. 17.13\u2009\u00b1\u20097.16, <jats:italic>P<\/jats:italic> &lt;\u20090.001) were strongly associated with non\u2010remission status, while differences in incretins between remitters and non\u2010remitters were minimal.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Individual without diabetes remission after gastric bypass have poorer \u03b2\u2010cell response and lesser suppression of glucagon to an oral challenge; body weight and incretins differ minimally according to remission status.<\/jats:p><\/jats:sec>","DOI":"10.1111\/1753-0407.12964","type":"journal-article","created":{"date-parts":[[2019,6,27]],"date-time":"2019-06-27T10:28:00Z","timestamp":1561631280000},"page":"77-86","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Proinsulin associates with poor \u03b2\u2010cell function, glucose\u2010dependent insulinotropic peptide, and insulin resistance in persistent type 2 diabetes after Roux\u2010en\u2010Y gastric bypass in humans"],"prefix":"10.1111","volume":"12","author":[{"given":"Kapila","family":"Patel","sequence":"first","affiliation":[{"name":"New York Obesity Research Center Columbia University  New York New York"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kiarra","family":"Levesque","sequence":"additional","affiliation":[{"name":"New York Obesity Research Center Columbia University  New York New 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