Carroll Joan F, Zenebe Woineshet J, Strange Taylor B
Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth TX 76107, USA.
Hypertension. 2006 Jul;48(1):65-72. doi: 10.1161/01.HYP.0000224147.01024.77. Epub 2006 May 15.
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.
肥胖倾向/肥胖抵抗大鼠模型已被用于研究与肥胖相关的肾功能和血压异常的机制，但该模型是否存在心脏功能障碍尚未确定。我们检验了这样一个假设，即肥胖倾向大鼠会出现其他饮食诱导肥胖模型中所见的心血管异常（即高血压、心动过速、左心室肥厚、胶原沉积增加、心脏收缩力降低和舒张末期压力升高）。雄性斯普拉格-道利大鼠喂食对照饮食或含32%千卡脂肪的中等脂肪饮食，同时使用遥测技术持续监测血流动力学。12周后，与肥胖抵抗大鼠和对照组相比，肥胖倾向大鼠体重显著增加，体脂更多，但各组间血压和心率的每日（20小时/天）平均值和昼夜节律并无差异。心脏结构和功能的超声心动图指标、心脏胶原的组织学证据以及直接测量的心脏重量在各组间并无差异。各组间左心室峰值压力、舒张末期压力、+dP/dt和-dP/dt也无显著差异。与肥胖抵抗大鼠和对照组相比，肥胖倾向大鼠的血浆胆固醇和肝脏胆固醇显著更高；与对照组相比，肥胖倾向大鼠的肝脏甘油三酯更高（P≤0.05）。与对照组相比，肥胖倾向大鼠的瘦素显著更高，且在所有组中瘦素与体脂均显著相关（P≤0.05）。这些结果表明，在肥胖倾向/肥胖抵抗大鼠模型中，12周的中等脂肪饮食可诱导典型的肥胖脂质和内分泌异常，但不足以导致明显的心脏异常。
