Ginzinger D G, Wilson J E, Redenbach D, Lewis M E, Clee S M, Excoffon K J, Rogers Q R, Hayden M R, McManus B M
Department of Medical Genetics, University of British Columbia, Vancouver, Canada.
Lab Invest. 1997 Nov;77(5):409-19.
The domestic cat has not been used in studies of atherosclerosis, with the exception of a single study published in 1970. We have further evaluated the susceptibility of the domestic cat to diet-induced atherosclerosis, the ultimate intent being to discern the atherogenic risk due to lipoprotein lipase deficiency in an affected feline kindred with a phenotype very similar to that of the human form of this condition. We subjected a group of normal domestic cats to a moderately high-fat, cholesterol-enriched diet (30% fat and 3% cholesterol) for a period of 2 to 8 months. Plasma lipid levels were monitored monthly. At the time of killing, all organs and the entire vascular tree were removed, sectioned, processed, and stained with hematoxylin and eosin. The entire vascular tree was also stained with Movat's pentachrome and oil red O (ORO) and assessed semiquantitatively (0 to 5+/5+) and quantitatively (mean intimal area and ORO positivity, mm2). Both blood lipid measurements (total cholesterol, high-density lipoprotein-cholesterol, triglycerides, and low-density lipoprotein-cholesterol) and vessel wall lesion assessment (intimal area, mm2) were statistically elevated (p < 0.05) in the cholesterol-fed cats as compared to those on a normal diet. The highest correlations obtained between blood lipid components and vessel wall measures were the percent increase in triglyceride from base line versus the ORO measurement or foam cell grade (r = 0.86), and percent increase in triglycerides versus the intimal area in the lower abdominal aorta (r = 0.91). Similar relationships were found when the intimal area in the brachiocephalic/subclavian vessels was correlated with the absolute triglyceride values (r = 0.85) or with the percent increase in triglycerides (r = 0.83). Thus, we produced atherosclerotic lesions in the cat within 2 to 4 months on a cholesterol-enriched diet; blood lipid levels were highly correlated with lesional measurements in the vessel wall. This study will provide the basis for evaluation of the susceptibility of New Zealand lipoprotein lipase-deficient cats to diet-induced atherosclerosis.
除了1970年发表的一项研究外，家猫尚未用于动脉粥样硬化研究。我们进一步评估了家猫对饮食诱导的动脉粥样硬化的易感性，最终目的是在一种表型与人类这种疾病非常相似的受影响猫科家族中，识别脂蛋白脂肪酶缺乏导致的动脉粥样硬化风险。我们让一组正常家猫食用中度高脂肪、富含胆固醇的饮食（30%脂肪和3%胆固醇），持续2至8个月。每月监测血浆脂质水平。处死时，取出所有器官和整个血管系统，切片、处理，并用苏木精和伊红染色。整个血管系统还用莫瓦特五色染色法和油红O（ORO）染色，并进行半定量（0至5+/5+）和定量（平均内膜面积和ORO阳性，mm2）评估。与正常饮食的猫相比，喂食胆固醇的猫的血脂测量值（总胆固醇、高密度脂蛋白胆固醇、甘油三酯和低密度脂蛋白胆固醇）和血管壁病变评估值（内膜面积，mm2）在统计学上均升高（p < 0.05）。血脂成分与血管壁测量值之间的最高相关性是甘油三酯相对于基线的增加百分比与ORO测量值或泡沫细胞分级之间的相关性（r = 0.86），以及甘油三酯相对于腹主动脉下段内膜面积的增加百分比之间的相关性（r = 0.91）。当头臂/锁骨下血管的内膜面积与甘油三酯绝对值（r = 0.85）或甘油三酯增加百分比（r = 0.83）相关时，也发现了类似的关系。因此，我们在富含胆固醇的饮食下2至4个月内在猫身上产生了动脉粥样硬化病变；血脂水平与血管壁病变测量值高度相关。这项研究将为评估新西兰脂蛋白脂肪酶缺乏猫对饮食诱导的动脉粥样硬化的易感性提供基础。
