{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,18]],"date-time":"2026-06-18T06:47:07Z","timestamp":1781765227749,"version":"3.54.5"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2016,3,9]]},"abstract":"\n Background<\/jats:title>\n \n Myocardial mechanics are altered in adults with obesity and type 2 diabetes (T2D); insulin resistance and adipokines have been implicated as important risk factors for cardiovascular disease, but these relationships are poorly described in adolescents. We hypothesized that obese adolescents and adolescents with T2D would have abnormal cardiac function compared to lean adolescents. In addition, we hypothesized that insulin sensitivity (\n IS<\/jats:styled-content>\n ), adiposity, and adipokines would be associated with altered cardiac strain and cardiopulmonary fitness in adolescents with T2D.\n <\/jats:p>\n <\/jats:sec>\n \n Methods and Results<\/jats:title>\n \n Adolescents (15\u00b12\u00a0years) with T2D (n=37), obesity without diabetes (n=41), and lean controls (n=31) of similar age and pubertal stage underwent echocardiography with speckle tracking, assessment of\n IS<\/jats:styled-content>\n by hyperinsulinemic\u2013euglycemic clamp, body composition by dual\u2010energy x\u2010ray absorptiometry, peak oxygen consumption (\n VO<\/jats:styled-content>\n 2<\/jats:sub>\n peak) by cycle ergometry, adiponectin, and leptin. Compared to lean and to obese controls, adolescents with T2D had significantly lower cardiac circumferential strain (\n CS<\/jats:styled-content>\n ) (\u221218.9\u00b14.6 [T2D] versus \u221221.5\u00b13.5 [obese] versus \u221222.0\u00b14.2% [lean],\n P<\/jats:italic>\n =0.04) and\n VO<\/jats:styled-content>\n 2<\/jats:sub>\n peak (37.6\u00b17.5 [T2D] versus 43.4\u00b18.2 [obese] versus 47.6\u00b18.6\u00a0\n mL<\/jats:styled-content>\n \/lean kg\/min [lean],\n P<\/jats:italic>\n <0.0001). In T2D youth,\n VO<\/jats:styled-content>\n 2<\/jats:sub>\n peak was associated with\n CS<\/jats:styled-content>\n , and the association remained significant after adjusting for age, sex, and\n IS<\/jats:styled-content>\n (\u03b2\u00b1\n SE<\/jats:styled-content>\n : \u22120.73\u00b10.26,\n P<\/jats:italic>\n =0.02). Among adolescents with T2D,\n CS<\/jats:styled-content>\n was also associated with adiponectin, longitudinal strain with leptin, and\n VO<\/jats:styled-content>\n 2<\/jats:sub>\n peak with adiponectin and\n IS<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Adolescents with T2D had abnormal\n CS<\/jats:styled-content>\n and reduced\n VO<\/jats:styled-content>\n 2<\/jats:sub>\n peak compared to obese and lean controls, which may represent the earliest evidence of cardiac functional impairment in T2D. Low adiponectin, rather than conventional risk factors and\n IS<\/jats:styled-content>\n , correlated with\n CS<\/jats:styled-content>\n , while both adiponectin and\n IS<\/jats:styled-content>\n related to cardiopulmonary fitness.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.115.002804","type":"journal-article","created":{"date-parts":[[2016,3,19]],"date-time":"2016-03-19T04:15:57Z","timestamp":1458360957000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":45,"title":["Cardiopulmonary Dysfunction and Adiponectin in Adolescents With Type 2 Diabetes"],"prefix":"10.1161","volume":"5","author":[{"given":"Petter","family":"Bjornstad","sequence":"first","affiliation":[{"name":"Department of Pediatric Endocrinology, University of Colorado School of Medicine, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Uyen","family":"Truong","sequence":"additional","affiliation":[{"name":"Division of Pediatric Cardiology, University of Colorado School of Medicine, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer L.","family":"Dorosz","sequence":"additional","affiliation":[{"name":"Division of Pediatric Cardiology, University of Colorado School of Medicine, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melanie","family":"Cree\u2010Green","sequence":"additional","affiliation":[{"name":"Department of Pediatric Endocrinology, University of Colorado School of Medicine, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy","family":"Baumgartner","sequence":"additional","affiliation":[{"name":"Department of Pediatric Endocrinology, University of Colorado School of Medicine, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory","family":"Coe","sequence":"additional","affiliation":[{"name":"Department of Pediatric Endocrinology, University of Colorado School of Medicine, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Pyle","sequence":"additional","affiliation":[{"name":"Department of Pediatric Endocrinology, University of Colorado School of Medicine, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Judith G.","family":"Regensteiner","sequence":"additional","affiliation":[{"name":"Divisions of General Internal Medicine and Cardiology, Center for Women's Health Research, University of Colorado School of Medicine, Aurora, CO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jane E. 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