Intimal Thickening in Normochoiesterolemic Rhesus Monkeys Fed Low Supplements of Dietary Cholesterol
Autor: | Mark L. Armstrong, E. D. Warner, Marjorie B. Megan |
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Rok vydání: | 1974 |
Předmět: |
Experimental atherosclerosis
medicine.medical_specialty Arteriosclerosis Physiology Lipoproteins Aortic Diseases Subclavian Artery Coronary Disease Biology Cholesterol Dietary Lesion chemistry.chemical_compound Plasma cholesterol medicine.artery Internal medicine medicine Animals Distribution (pharmacology) Aorta Cholesterol Haplorhini Lipid Metabolism Coronary Vessels Femoral Artery Carotid Arteries Endocrinology Liver chemistry Macaca lipids (amino acids peptides and proteins) Thickening medicine.symptom Cardiology and Cardiovascular Medicine Dietary Cholesterol |
Zdroj: | Circulation Research. 34:447-454 |
ISSN: | 1524-4571 0009-7330 |
DOI: | 10.1161/01.res.34.4.447 |
Popis: | Rhesus monkeys were fed a high-fat diet containing either 0, 43, or 129 µg/kcal of cholesterol for 18 months. In the monkeys on the cholesterol-supplemented diets, changes in plasma cholesterol remained within the range found in monkeys fed the cholesterol-free diet. Monkeys on the cholesterol-supplemented diets were compared with monkeys given no dietary cholesterol with range-matched plasma cholesterol; intimal thickness of the aorta and branch arteries, distribution of lipoprotein cholesterol, and tissue content of cholesterol in aorta and liver were considered. The monkeys on the cholesterol-supplemented diets showed intimal thickening with more sudanophilia and increased aortic cholesterol, a decrease in plasma high-density lipoprotein cholesterol, and an increase in low-density lipoprotein cholesterol, and the monkeys fed the higher amount of dietary cholesterol showed an increase in hepatic cholesterol. No null point for the effect of dietary cholesterol on arterial intima was found even at an intake level far below that conventionally used for the induction of experimental atherosclerosis in the nonhuman primate. The intimal changes found in response to very low cholesterol intake imply that subtle qualitative alterations in lipoproteins are of critical importance to our understanding of lesion induction. |
Databáze: | OpenAIRE |
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