Coronary heart disease rabbit

The work of Brown and Goldstein got serendipitous support from the discovery, a Japanese veterinarian had made at Kobe University. In 1973, Yoshio Watanabe (1927-2008) noticed incidentally that a rabbit from his colony showed a tenfold increased blood cholesterol level. By appropriate breeding, he managed to establish a strain of rabbits with this characteristic dysregulation. AH of them developed a coronary heart disease, closely resembling its human variant. Thus, suddenly there was an animal model available to investigate familial hypercholesterolemia much better than with the elaborate method of Brown and Goldstein, who had used tissue cultures of skin cells, in lack of sufficient access to human hepatocytes (fiver cells). [360]... 

Millon et al. monitored plaque inflammation in atherosclerotic rabbits using a combined PET/MR scanner. Proton magnetic resonance metabolomic characterization of ovarian serous carcinoma was performed by Vettukattil et for diagnostic purposes. Pan et using NMR lipidomic approach, noticed increased unsaturation of lipids in cytoplasmic lipid droplets in DAOY cancer cells in response to cisplatin treatment. Akoudad et examined formation of cerebral microbleeds associated with the progression of ischemic vascular lesions, while Kos-tara et followed the progression of coronary heart disease NMR-based lipidomic analysis of blood lipoproteins. 

Atherosclerosis can occur spontaneously in various animals for instance, in old hens (Weitzel, 1956) and in the parrot (Cohrs, 1957), and probably in other animals (fed by man ) too. The atheroma, easily induced by high-cholesterol diets in rabbits and chickens cannot be considered comparable to the spontaneous disease in man. Such experiments as that carried out by Fillios et al. (1956), who supplemented purified diets with cholesterol, sodium cholate, and thiouracil, should be left out of consideration because a low basal metabolic rate was induced. However, the rats developed a blood pattern like that present in the human patient, together with coronary and aortic lesions, and lesions in the heart valves. Because no similar data for toxemia in pregnancy have yet been found, only the results in mammals with a normal metabolic rate will be considered. Similarly, animal experiments in which cholate, cholic acid, or other surface-active agents are used cannot be considered here. 

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