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August 1, 1999Arteriosclerosis Thrombosis and Vascular BiologyOpen Access

Hyperlipidemia and Atherosclerotic Lesion Development in LDL Receptor–Deficient Mice Fed Defined Semipurified Diets With and Without Cholate

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Key Points

To determine whether sodium cholate is required for atherosclerotic lesion development in LDL receptor–deficient mice fed defined semipurified diets.
Randomized trial allocating LDLR(-/-) mice across 4 semipurified AIN-76A-based diets (n=6/diet): control (10% kcal lipid), high fat (40% kcal) with moderate cholesterol (0.5% wt/wt), high fat with high cholesterol (1.25% wt/wt), or high fat/high cholesterol supplemented with 0.5% (wt/wt) sodium cholate.
Fed diets for 6 or 12 weeks, followed by quantification of fasting serum cholesterol and aortic lesion area using oil red O staining.
Fasting serum cholesterol increased significantly across all cholesterol-supplemented diets compared to controls after 6 and 12 weeks of feeding (P<0.01).
Aortic lesion area ranged from 7.01% to 12.79% in the thoracic and abdominal aorta among cholesterol-supplemented groups at 12 weeks versus control mice (P<0.002 for each group versus control).
Histological features and lesion distribution were comparable between mice fed diets with sodium cholate and those fed diets without sodium cholate.

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Implication

Randomized trial reveals atherosclerotic lesion formation without sodium cholate in LDL receptor–deficient mice, indicating defined semipurified diets model human atherogenesis.

Cite This Study

Lichtman et al. (1999) studied this question.

synapsesocial.com/papers/6a20014ad4e6d3589704c92b https://doi.org/10.1161/01.atv.19.8.1938

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