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Diet-Induced
Atherosclerosis in the Domestic Cat |
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David G. Ginzinger,
Janet E. Wilson, Darlene Redenbach, M. E. Suzanne Lewis, Susanne M. Clee,
Katherine J. D. Ashbourne Excoffon, Quinton R. Rogers, Michael R. Hayden,
and Bruce M. McManus |
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Departments
of Medical Genetics (DGG, MESL, SMC, KJDAE, MRH) and Pathology and Laboratory
Medicine (JEW, DR, BMMcM), University of British Columbia, Vancouver, British
Columbia; and Department of Molecular Biological Sciences (QRR), University
of California at Davis, Davis, California |
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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 suscepibility of New Zealand lipoprotein
lipase-deficient cats to diet-induced atherosclerosis. |
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