caa a22 4500 445825820 CHVBK 20180317145258.0 cr unu---uuuuu 170323e20110601xx s 000 0 eng 10.1007/s00246-011-9952-5 doi (NATIONALLICENCE)springer-10.1007/s00246-011-9952-5 Cellular and RAS Changes in the Hearts of Young Obese Rats [Elektronische Daten] [Kee Ha, Kee Yoo, Hyung Yim, Gi Jang, In Bae, Young Hong, Joo Lee] Obesity during childhood increases the risk of cardiac disease, hypertension, and other complications in adulthood. We investigated the cellular and renin-angiotensin system changes of the heart in obese young rats. We used Sprague-Dawley rats and early obesity was induced by overfeeding through adjusting the number of male pups per dam during the first 28days of life. The body weight, heart weight, blood pressure, serum glucose, and blood pressure were assessed and we performed echocardiography, proliferating cell nuclear antigen (PCNA); assessment, apoptosis and Masson's trichrome staining, and Western blotting and the results were compared between the normal litter (NL, control) and the small litter (SL, obesity). There were no differences in blood pressure and serum glucose, but the body weight increased 61.2% and the interventricular septal thickness in diastole on the echocardiography was increased in the SL. There was hyperplasia of the PCNA cells and apoptotic cells without cellular hypertrophy or change of the amount of collagen in the SL. On Western blotting, rennin, and angiotensin II type 2 receptor (AT2R) were increased without a change of angiotensin II type 1 receptor (AT1R) in the SL. Early obesity caused echocardiographically detected septal hypertrophy and an increase of cellular turnover. Renin and AT2R were upregulated without a change of AT1R and the increase of AT2R was regarded as a cardioprotective effect against the pathologic conditions caused by the early obesity. Springer Science+Business Media, LLC, 2011 Apoptosis nationallicence PCNA nationallicence Hypertrophy nationallicence Obesity nationallicence Renin angiotensin system nationallicence Ha Kee Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut Yoo Kee Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut Yim Hyung Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut Jang Gi Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut Bae In Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut Hong Young Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut Lee Joo Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut Pediatric Cardiology Springer-Verlag 32/5(2011-06-01), 659-666 0172-0643 32:5<659 2011 32 246 https://doi.org/10.1007/s00246-011-9952-5 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00246-011-9952-5 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Ha Kee Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut NATIONALLICENCE 700 1- Yoo Kee Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut NATIONALLICENCE 700 1- Yim Hyung Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut NATIONALLICENCE 700 1- Jang Gi Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut NATIONALLICENCE 700 1- Bae In Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut NATIONALLICENCE 700 1- Hong Young Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut NATIONALLICENCE 700 1- Lee Joo Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea aut NATIONALLICENCE 773 0- Pediatric Cardiology Springer-Verlag 32/5(2011-06-01), 659-666 0172-0643 32:5<659 2011 32 246 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer