High-carbohydrate, High-fat Diet-induced Metabolic Syndrome and Cardiovascular Remodeling in Rats
High-carbohydrate, High-fat Diet-induced Metabolic Syndrome and Cardiovascular Remodeling in Rats
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DOI：
10.1097/fjc.0b013e3181feb90a
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发表时间：
2011-05-01
影响因子：
3
通讯作者：
Brown, Lindsay
中科院分区：
文献类型：
--
作者：
Panchal, Sunil K.;Poudyal, Hemant;Brown, Lindsay
包括中心性肥胖、胰岛素抵抗、糖耐量受损、高血压和血脂异常在内的代谢综合征的患病率正在增加。开发针对代谢综合征的适当疗法需要模拟人类疾病状态的动物模型。因此，我们表征了雄性 Wistar 大鼠（8-9 周龄）的代谢、心血管、肝脏、肾脏和胰腺的变化，这些大鼠喂食高碳水化合物、高脂肪饮食，包括炼乳 (39.5%)、牛脂 (20%) 和果糖 (17.5%) 以及饮用水中的 25% 果糖；对照组大鼠喂食玉米淀粉饮食。在采用这种饮食的 16 周内，大鼠的体重、能量摄入、腹部脂肪沉积和腹围逐渐增加，并伴有糖耐量受损、血脂异常、高胰岛素血症以及血浆瘦素和丙二醛浓度增加。心血管体征包括收缩压升高和内皮功能障碍，以及心脏左心室的炎症、纤维化、肥大、硬度增加和复极延迟。肝脏表现出湿重增加、脂肪沉积、炎症和纤维化，且血浆肝酶活性增加。肾脏显示炎症和纤维化，而胰腺显示胰岛大小增加。与其他糖尿病和肥胖模型相比，这种饮食诱导模型更接近地模拟了人类代谢综合征中观察到的变化。包括向心性肥胖、胰岛素抵抗、糖耐量受损、高血压和血脂异常在内的代谢综合征的患病率正在增加。开发针对代谢综合征的适当疗法需要模拟人类疾病状态的动物模型。因此，我们表征了雄性 Wistar 大鼠（8-9 周龄）的代谢、心血管、肝脏、肾脏和胰腺的变化，这些大鼠喂食高碳水化合物、高脂肪饮食，包括炼乳 (39.5%)、牛脂 (20%) 和果糖 (17.5%) 以及饮用水中的 25% 果糖；对照组大鼠喂食玉米淀粉饮食。在采用这种饮食的 16 周内，大鼠的体重、能量摄入、腹部脂肪沉积和腹围逐渐增加，并伴有糖耐量受损、血脂异常、高胰岛素血症以及血浆瘦素和丙二醛浓度增加。心血管体征包括收缩压升高和内皮功能障碍，以及心脏左心室的炎症、纤维化、肥大、硬度增加和复极延迟。肝脏表现出湿重增加、脂肪沉积、炎症和纤维化，且血浆肝酶活性增加。肾脏显示炎症和纤维化，而胰腺显示胰岛大小增加。与其他糖尿病和肥胖模型相比，这种饮食诱导的模型更接近地模拟了在人类代谢综合征中观察到的变化。
The prevalence of metabolic syndrome including central obesity, insulin resistance, impaired glucose tolerance, hypertension, and dyslipidemia is increasing. Development of adequate therapy for metabolic syndrome requires an animal model that mimics the human disease state. Therefore, we have characterized the metabolic, cardiovascular, hepatic, renal, and pancreatic changes in male Wistar rats (8-9 weeks old) fed on a high-carbohydrate, high-fat diet including condensed milk (39.5%), beef tallow (20%), and fructose (17.5%) together with 25% fructose in drinking water; control rats were fed a cornstarch diet. During 16 weeks on this diet, rats showed progressive increases in body weight, energy intake, abdominal fat deposition, and abdominal circumference along with impaired glucose tolerance, dyslipidemia, hyperinsulinemia, and increased plasma leptin and malondialdehyde concentrations. Cardiovascular signs included increased systolic blood pressure and endothelial dysfunction together with inflammation, fibrosis, hypertrophy, increased stiffness, and delayed repolarization in the left ventricle of the heart. The liver showed increased wet weight, fat deposition, inflammation, and fibrosis with increased plasma activity of liver enzymes. The kidneys showed inflammation and fibrosis, whereas the pancreas showed increased islet size. In comparison with other models of diabetes and obesity, this diet-induced model more closely mimics the changes observed in human metabolic syndrome.The prevalence of metabolic syndrome including central obesity, insulin resistance, impaired glucose tolerance, hypertension, and dyslipidemia is increasing. Development of adequate therapy for metabolic syndrome requires an animal model that mimics the human disease state. Therefore, we have characterized the metabolic, cardiovascular, hepatic, renal, and pancreatic changes in male Wistar rats (8-9 weeks old) fed on a high-carbohydrate, high-fat diet including condensed milk (39.5%), beef tallow (20%), and fructose (17.5%) together with 25% fructose in drinking water; control rats were fed a cornstarch diet. During 16 weeks on this diet, rats showed progressive increases in body weight, energy intake, abdominal fat deposition, and abdominal circumference along with impaired glucose tolerance, dyslipidemia, hyperinsulinemia, and increased plasma leptin and malondialdehyde concentrations. Cardiovascular signs included increased systolic blood pressure and endothelial dysfunction together with inflammation, fibrosis, hypertrophy, increased stiffness, and delayed repolarization in the left ventricle of the heart. The liver showed increased wet weight, fat deposition, inflammation, and fibrosis with increased plasma activity of liver enzymes. The kidneys showed inflammation and fibrosis, whereas the pancreas showed increased islet size. In comparison with other models of diabetes and obesity, this diet-induced model more closely mimics the changes observed in human metabolic syndrome.