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Cellular and RAS changes in the hearts of young obese rats
Kee Soo Ha1, Kee Hwan Yoo, Hyung Eun Yim
1Department of Pediatrics, College of Medicine, Korea University, Seoul, South Korea.
Insights
Childhood obesity in rats led to heart septal thickening and increased cell turnover. Renin and angiotensin II type 2 receptor (AT2R) levels rose, suggesting a protective effect against obesity-induced heart changes.
Area of Science:
- Cardiology
- Pediatric Obesity
- Renin-Angiotensin System
Background:
- Childhood obesity is a risk factor for adult cardiovascular diseases.
- Understanding early cardiac changes in obesity is crucial for prevention.
- The renin-angiotensin system's role in pediatric obesity-related cardiac dysfunction requires further investigation.
Purpose of the Study:
- To investigate the cellular and renin-angiotensin system alterations in the heart of young obese rats.
- To assess the impact of early-onset obesity on cardiac structure and function.
Main Methods:
- Sprague-Dawley rats were used, with early obesity induced by pup overfeeding.
- Assessments included body weight, heart weight, blood pressure, serum glucose, echocardiography, PCNA, apoptosis, Masson's trichrome staining, and Western blotting.
- Comparisons were made between normal litter (NL) and small litter (SL, obesity) groups.
Main Results:
- Obese rats (SL) showed a 61.2% increase in body weight and increased interventricular septal thickness.
- Hyperplasia of proliferating cell nuclear antigen (PCNA) positive cells and increased apoptosis were observed, without cellular hypertrophy or altered collagen.
- Western blotting revealed increased renin and angiotensin II type 2 receptor (AT2R), with no change in angiotensin II type 1 receptor (AT1R).
Conclusions:
- Early-onset obesity in rats induces echocardiographically detected septal hypertrophy and increased cellular turnover.
- Renin and AT2R are upregulated in the obese rat heart, while AT1R remains unchanged.
- The upregulation of AT2R may represent a cardioprotective mechanism against early obesity-induced cardiac pathology.
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.
