ArticlePediatric cardiology2011
Cellular and RAS changes in the hearts of young obese rats.
Article in Pediatric cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Early life obesity and chronic kidney disease in later life.Pediatric nephrology (Berlin, Germany) · 2015Review
- Effects of coronary ischemia-reperfusion in a rat model of early overnutrition. Role of angiotensin receptors.PloS one · 2013Article
- Angiotensin II type-2 receptor-specific effects on the cardiovascular system.Cardiovascular diagnosis and therapy · 2012Review
- Adaptive mechanisms to compensate for overnutrition-induced cardiovascular abnormalities.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 28 days 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.
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