Cardiovascular function in a rat model of diet-induced obesity.
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< or =0.05). Leptin was significantly higher in obesity-prone rats compared with controls and across all groups was significantly correlated with body fat (P< or =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.
Carroll
Joan F
JF
Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth TX 76107, USA. jcarroll@hsc.unt.edu
Zenebe
Woineshet J
WJ
Strange
Taylor B
TB
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology*; D002940:Circadian Rhythm; D004032:Diet; D004041:Dietary Fats / Q000008:administration & dosage*; D004195:Disease Models, Animal; D004452:Echocardiography; D054439:Ghrelin; D006321:Heart / Q000033:anatomy & histology; D006339:Heart Rate / Q000502:physiology*; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000032:analysis / Q000097:blood; D008297:Male; D009206:Myocardium / Q000473:pathology*; D009765:Obesity / Q000097:blood / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D036361:Peptide Hormones / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley
D001786:Blood Glucose; D004041:Dietary Fats; D054439:Ghrelin; D007328:Insulin; D020738:Leptin; D008055:Lipids; D036361:Peptide Hormones