EXPERIMENTAL CANINE ATHEROSCLEROSIS AND ITS PREVENTION - DIETARY INDUCTION OF SEVERE CORONARY, CEREBRAL, AORTIC, AND ILIAC ATHEROSCLEROSIS AND ITS PREVENTION BY SAFFLOWER OIL

  • 1 January 1976
    • journal article
    • research article
    • Vol. 34  (4) , 394-405
Abstract
Severe atherosclerotic lesions were produced without thyroid suppression in 7 of 8 dogs by feeding semisynthetic diets containing 5% cholesterol and 16% hydrogenated coconut oil for 12-14 mo. Occlusive plaques were located in the coronary arteries and major cerebral arteries and in the aorta and iliac vessels. The lesions were characterized by an intense sclerotic reaction to areas of lipid deposition and foam cell accumulation in the intima. The diet induced a rapid elevation of plasma-free and esterified cholesterol, triglyceride and phospholipid, and the extent of aortic atherosclerosis was partially dependent on mean plasma cholesterol concentration. A 2nd group of 8 dogs were fed a diet identical with the 1st except for the replacement of 4% hydrogenated coconut oil by 4% safflower oil. Despite receiving the same amounts of dietary cholesterol and fat, this 2nd group of dogs was completely protected from the atherogenic process. Plasma lipids became only slightly elevated, and no induced atheroscherotic lesions were found at autopsy. Circulating thyroid hormone concentrations were similar between the 2 groups of dogs, and the thyroid glands had a normal morphology in both groups. The atherogenic diet was designed to contain only trace amounts of essential fatty acids, and essential fatty acid deficiency was demonstrated in the animals to which it was fed. The 2nd diet was intended to counteract this deficiency by providing 8% of diet calories as linoleic acid. In the absence of essential fatty acids the dog becomes intolerant of dietary cholesterol, resulting in reactive hyperlipoproteinemia and atherosclerosis. The addition of linoleic acid to the diet appears to restore the normal resistance of this species to hypercholesterolemia. The protective effect of linoleic acid on atherogenesis can therefore be explained on the basis of its role as a regulator of plasma lipemia.