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Cardiovascular Function in a Rat Model of Diet-Induced Obesity
Abstract
The obesity-prone/obesity-resistant rat model has been used to study mechanisms responsible for obesity-related abnormalities in renal function and blood pressure, but whether this model exhibits cardiac dysfunction has not been determined. We tested the hypothesis that obesity-prone rats would display cardiovascular abnormalities seen in other diet-induced obese models (ie, hypertension, tachycardia, left ventricular hypertrophy, increased collagen deposition, reduced cardiac contractility, and increased end diastolic pressure). Male Sprague-Dawley rats were fed a control diet or a moderate fat diet containing 32% kcal as fat while hemodynamics were continuously monitored using telemetry. After 12 weeks, obesity-prone rats were significantly heavier and had greater body fat compared with obesity-resistant rats and controls, but daily (20 hours/d) averages and diurnal rhythms of blood pressure and heart rate did not differ among groups. Echocardiographic indices of cardiac structure and function, histological evidence of cardiac collagen, and directly measured heart weights did not differ among groups. Peak left ventricular pressure, end diastolic pressure, +dP/dt, and −dP/dt were also not significantly different among groups. Plasma cholesterol and hepatic cholesterol were significantly higher in obesity-prone rats compared with obesity-resistant rats and controls; hepatic triglycerides were higher in obesity-prone rats compared with controls ( P ≤0.05). Leptin was significantly higher in obesity-prone rats compared with controls and across all groups was significantly correlated with body fat ( P ≤0.05). These results suggest that 12 weeks of a moderate fat diet in the obesity-prone/obesity-resistant rat model induced lipid and endocrine abnormalities typical of obesity but was not sufficient to cause significant cardiac abnormalities.
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“In contrast, high-fat feeding that is associated with the development of insulin resistance and obesity is associated with development of LV dysfunction in many (269, 273, 296) but not all studies (40).”
From Cardiac remodeling in obesity (2008) · cites this paper as [40]
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“Likewise, high-fat feeding of Sprague-Dawley rats for up to 14 wk has not been associated with LVH despite the development of obesity (40, 299), whereas 7 wk of high-fat feeding in Wistar rats results in LVH (269).”
From Cardiac remodeling in obesity (2008) · cites this paper as [40]
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“Thus 12 wk of high-fat feeding of Sprague-Dawley rats revealed no changes in invasive LV hemodynamics, e.g., dP/dt, echocardiographic parameters, LV hypertrophy, or LV fibrosis despite significant obesity and dyslipidemia (40).”
From Cardiac remodeling in obesity (2008) · cites this paper as [40]
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Oxidative Stress in a Rat Model of Obesity-Induced Hypertension
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Abel, E. D., Litwin, S. E., & Sweeney, G. (2008) · Physiological Reviews · doi:10.1152/physrev.00017.2007 · Cited by 736
de Castro, U. G. M., Santos, R. A. S., Silva, M. E., de Lima, W. G., Campagnole‐Santos, M. J., & Alzamora, A. C. (2013) · Lipids in Health and Disease · doi:10.1186/1476-511x-12-136 · Cited by 151
Cardiac remodeling in a rat model of diet-induced obesity
Leopoldo, A. S., Sugizaki, M. M., Lima‐Leopoldo, A. P., do Nascimento, A. F., Luvizotto, R. D. A. M., de Campos, D. H. S., Okoshi, K., Dal‐Pai‐Silva, M., Padovani, C. R., & Cicogna, A. C. (2010) · Canadian Journal of Cardiology · doi:10.1016/s0828-282x(10)70440-2 · Cited by 129
Leptin induces cardiac fibrosis through galectin-3, mTOR and oxidative stress
Martínez‐Martínez, E., Jurado-López, R., Valero‐Muñoz, M., Bartolomé, M. V., Ballesteros, S., Luaces, M., Briones, A. M., López‐Andrés, N., Miana, M., & Cachofeiro, V. (2014) · Journal of Hypertension · doi:10.1097/hjh.0000000000000149 · Cited by 126
Adaptation and maladaptation of the heart in obesity
Harmancey, R., Wilson, C. R., & Taegtmeyer, H. (2008) · Hypertension · doi:10.1161/hypertensionaha.108.110031 · Cited by 121
Metadata
- Authors
- Carroll, J. F., Zenebe, W. J., & Strange, T. B.
- Affiliations
- University of North Texas Health Science Center (US)
- Venue
- Hypertension
- Published
- 2006-07
- Volume
- 48
- Issue
- 1
- Pages
- 65-72
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2101820852
- Cited by
- 129
- References
- 35
- Citations by year
- 2026: 3 · 2024: 3 · 2023: 4 · 2022: 4 · 2021: 10 · 2020: 7 · 2019: 8 · 2018: 6 · 2017: 8 · 2016: 8 · 2015: 9 · 2014: 12 · 2013: 7 · 2012: 6
- FWCI
- 3.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01hl064913-04, 5k02hl004297-05)
- National Heart, Lung, and Blood Institute (HL04297, HL64913)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- diet-induced obesity, cardiac function, left ventricular hypertrophy, heart rate, serum cholesterol, liver cholesterol, hepatic triglycerides, leptin, fat mass, cardiovascular anomalies
- MeSH terms
- Animals, Blood Glucose, Blood Pressure, Circadian Rhythm, Diet, Dietary Fats, Disease Models, Animal, Echocardiography, Heart, Heart Rate, Insulin, Lipids, Male, Myocardium, Obesity, Rats, Sprague-Dawley, Leptin, Peptide Hormones, Rats, Ghrelin
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