Cited by 129Cardiovascular Function and Risk FactorsCardiac Fibrosis and RemodelingCardiovascular Disease and Adiposity

The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.

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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  1. 10.1161/hyp.26.3.465 · DOI
  2. 10.1161/hyp.35.4.1009 · DOI
  3. 10.1161/hyp.37.2.554 · DOI
  4. 10.1161/hyp.33.3.811 · DOI
  5. 10.1161/hyp.33.1.548 · DOI

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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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