{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,14]],"date-time":"2026-01-14T00:34:34Z","timestamp":1768350874692,"version":"3.49.0"},"reference-count":42,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2014,9,14]],"date-time":"2014-09-14T00:00:00Z","timestamp":1410652800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100009933","name":"Ethicon","doi-asserted-by":"crossref","award":["19900"],"award-info":[{"award-number":["19900"]}],"id":[{"id":"10.13039\/100009933","id-type":"DOI","asserted-by":"crossref"}]},{"name":"NIH","award":["NIH RO1-DK089547"],"award-info":[{"award-number":["NIH RO1-DK089547"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Diabetes Obesity Metabolism"],"published-print":{"date-parts":[[2014,12]]},"abstract":"\n Aim<\/jats:title>\n To identify the metabolic determinants of type 2 diabetes non\u2010remission status after bariatric surgery at 12 and 24 months.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n A total of 40 adults [mean \u00b1\n sd<\/jats:sc>\n body mass index 36 \u00b1 3 kg\/m\n 2<\/jats:sup>\n , age 48 \u00b1 9 years, glycated haemoglobin (\n HbA1c<\/jats:styled-content>\n ) 9.7 \u00b1 2%) undergoing bariatric surgery [Roux\u2010en\u2010Y gastric bypass (\n RYGB<\/jats:styled-content>\n ) or sleeve gastrectomy (\n SG<\/jats:styled-content>\n )] were enrolled in the present study, the Surgical Treatment and Medication Potentially Eradicate Diabetes Efficiently (\n STAMPEDE<\/jats:styled-content>\n ) trial. Type 2 diabetes remission was defined as\n HbA1c<\/jats:styled-content>\n <6.5% and fasting glucose <126 mg\/dl (i.e. <7 mmol\/l) without antidiabetic medication. Indices of insulin secretion and sensitivity were calculated from plasma glucose, insulin and C\u2010peptide values during a 120\u2010min mixed\u2010meal tolerance test. Body fat, incretins (glucagon\u2010like polypeptide\u20101, gastric inhibitory peptide, ghrelin) and adipokines [adiponectin, leptin, tumour necrosis factor\u2010\u03b1, high\u2010sensitivity C\u2010reactive protein (hs\u2010\n CRP<\/jats:styled-content>\n )] were also assessed.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n At 24 months, 37 patients had available follow\u2010up data (\n RYGB<\/jats:styled-content>\n , n = 18;\n SG<\/jats:styled-content>\n , n = 19). Bariatric surgery induced type 2 diabetes remission rates of 40 and 27% at 12 and 24 months, respectively. Total fat\/abdominal fat loss, insulin secretion, insulin sensitivity and \u03b2\u2010cell function (C\u2010peptide\n 0\u2013120<\/jats:sub>\n \/glucose\n 0\u2013120<\/jats:sub>\n \u00d7 Matsuda index) improved more in those with remission at 12 and 24 months than in those without remission. Incretin levels were unrelated to type 2 diabetes remission, but, compared with those without remission, hs\u2010\n CRP<\/jats:styled-content>\n decreased and adiponectin increased more in those with remission. Only baseline adiponectin level predicted lower\n HbA1c<\/jats:styled-content>\n levels at 12 and 24 months, and elevated adiponectin correlated with enhanced \u03b2\u2010cell function, lower triglyceride levels and fat loss.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n Smaller rises in adiponectin level, a mediator of insulin action and adipose mass, characterize type 2 diabetes non\u2010remission up to 2 years after bariatric surgery. Adjunctive strategies promoting greater fat loss and\/or raising adiponectin may be key to achieving higher type 2 diabetes remission rates after bariatric surgery.<\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/dom.12376","type":"journal-article","created":{"date-parts":[[2014,8,11]],"date-time":"2014-08-11T06:38:25Z","timestamp":1407739105000},"page":"1230-1238","source":"Crossref","is-referenced-by-count":53,"title":["Attenuated improvements in adiponectin and fat loss characterize type 2 diabetes non\u2010remission status after bariatric surgery"],"prefix":"10.1111","volume":"16","author":[{"given":"S. K.","family":"Malin","sequence":"first","affiliation":[{"name":"Department of Pathobiology Cleveland Clinic Cleveland OH USA"},{"name":"Department of Nutrition Case Western Reserve University Cleveland Clinic Cleveland OH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Bena","sequence":"additional","affiliation":[{"name":"Department of Quantitative Health Sciences Cleveland Clinic Cleveland OH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B.","family":"Abood","sequence":"additional","affiliation":[{"name":"Department of Endocrinology Diabetes and Metabolism, Cleveland Clinic Cleveland OH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C. E.","family":"Pothier","sequence":"additional","affiliation":[{"name":"Department of Bariatric and Metabolic Institute Cleveland Clinic Cleveland OH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D. L.","family":"Bhatt","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital and Harvard Medical School Boston MA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Nissen","sequence":"additional","affiliation":[{"name":"Department of Heart and Vascular Cleveland Clinic Cleveland OH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S. A.","family":"Brethauer","sequence":"additional","affiliation":[{"name":"Department of Bariatric and Metabolic Institute Cleveland Clinic Cleveland OH USA"},{"name":"Metabolic Translational Research Center Endocrine and Metabolism Institute, Cleveland Clinic Cleveland OH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. R.","family":"Schauer","sequence":"additional","affiliation":[{"name":"Department of Bariatric and Metabolic Institute Cleveland Clinic Cleveland OH USA"},{"name":"Metabolic Translational Research Center Endocrine and Metabolism Institute, Cleveland Clinic Cleveland OH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. P.","family":"Kirwan","sequence":"additional","affiliation":[{"name":"Department of Pathobiology Cleveland Clinic Cleveland OH USA"},{"name":"Department of Nutrition Case Western Reserve University Cleveland Clinic Cleveland OH USA"},{"name":"Metabolic Translational Research Center Endocrine and Metabolism Institute, Cleveland Clinic Cleveland OH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S. 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