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Oxidized cholesterol in the diet accelerates the development of atherosclerosis in LDL receptor- and apolipoprotein E-deficient mice.
Arterioscler Thromb Vasc Biol. 2000 Mar; 20(3):708-14.AT

Abstract

The aim of the current study was to determine whether oxidized cholesterol in the diet accelerates atherosclerosis in low density lipoprotein receptor- (LDLR) and apolipoprotein E- (apo E) deficient mice. Mice were fed either a control diet or a diet containing oxidized cholesterol. For LDLR-deficient mice, the control diet consisted of regular mouse chow to which 1.0% cholesterol was added. The oxidized diet was identical to the control diet except that 5% of the added cholesterol was oxidized. In apo E-deficient mice, the control diet contained 0.15% cholesterol, whereas in the oxidized diet, 5% of the added cholesterol was oxidized. LDLR-deficient and apo E-deficient mice were fed the experimental diets for 7 and 4 months, respectively. In mice fed the oxidized-cholesterol diets, the levels of oxidized cholesterol in sera were increased. At the end of the experiment, aortas were removed and atherosclerosis was assessed. We found that in LDLR-deficient mice, feeding of an oxidized-cholesterol diet resulted in a 32% increase in fatty streak lesions (15.93+/-1.59% versus 21.00+/-1.38%, P<0.03). Similarly, in apo E-deficient mice, feeding of an oxidized-cholesterol diet increased fatty streak lesions by 38% (15.01+/-0.92% versus 20. 70+/-0.86%, P<0.001). The results of the current study thus demonstrate that oxidized cholesterol in the diet accelerates fatty streak lesion formation in both LDLR- and apo E-deficient mice.

Authors+Show Affiliations

Department of Veterans Affairs Medical Center, University of California, San Francisco 94121, USA. stapan@itsa.ucsf.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

10712395

Citation

Staprans, I, et al. "Oxidized Cholesterol in the Diet Accelerates the Development of Atherosclerosis in LDL Receptor- and Apolipoprotein E-deficient Mice." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 20, no. 3, 2000, pp. 708-14.
Staprans I, Pan XM, Rapp JH, et al. Oxidized cholesterol in the diet accelerates the development of atherosclerosis in LDL receptor- and apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol. 2000;20(3):708-14.
Staprans, I., Pan, X. M., Rapp, J. H., Grunfeld, C., & Feingold, K. R. (2000). Oxidized cholesterol in the diet accelerates the development of atherosclerosis in LDL receptor- and apolipoprotein E-deficient mice. Arteriosclerosis, Thrombosis, and Vascular Biology, 20(3), 708-14.
Staprans I, et al. Oxidized Cholesterol in the Diet Accelerates the Development of Atherosclerosis in LDL Receptor- and Apolipoprotein E-deficient Mice. Arterioscler Thromb Vasc Biol. 2000;20(3):708-14. PubMed PMID: 10712395.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidized cholesterol in the diet accelerates the development of atherosclerosis in LDL receptor- and apolipoprotein E-deficient mice. AU - Staprans,I, AU - Pan,X M, AU - Rapp,J H, AU - Grunfeld,C, AU - Feingold,K R, PY - 2000/3/11/pubmed PY - 2000/5/20/medline PY - 2000/3/11/entrez SP - 708 EP - 14 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler Thromb Vasc Biol VL - 20 IS - 3 N2 - The aim of the current study was to determine whether oxidized cholesterol in the diet accelerates atherosclerosis in low density lipoprotein receptor- (LDLR) and apolipoprotein E- (apo E) deficient mice. Mice were fed either a control diet or a diet containing oxidized cholesterol. For LDLR-deficient mice, the control diet consisted of regular mouse chow to which 1.0% cholesterol was added. The oxidized diet was identical to the control diet except that 5% of the added cholesterol was oxidized. In apo E-deficient mice, the control diet contained 0.15% cholesterol, whereas in the oxidized diet, 5% of the added cholesterol was oxidized. LDLR-deficient and apo E-deficient mice were fed the experimental diets for 7 and 4 months, respectively. In mice fed the oxidized-cholesterol diets, the levels of oxidized cholesterol in sera were increased. At the end of the experiment, aortas were removed and atherosclerosis was assessed. We found that in LDLR-deficient mice, feeding of an oxidized-cholesterol diet resulted in a 32% increase in fatty streak lesions (15.93+/-1.59% versus 21.00+/-1.38%, P<0.03). Similarly, in apo E-deficient mice, feeding of an oxidized-cholesterol diet increased fatty streak lesions by 38% (15.01+/-0.92% versus 20. 70+/-0.86%, P<0.001). The results of the current study thus demonstrate that oxidized cholesterol in the diet accelerates fatty streak lesion formation in both LDLR- and apo E-deficient mice. SN - 1079-5642 UR - https://www.unboundmedicine.com/medline/citation/10712395/Oxidized_cholesterol_in_the_diet_accelerates_the_development_of_atherosclerosis_in_LDL_receptor__and_apolipoprotein_E_deficient_mice_ L2 - https://www.ahajournals.org/doi/10.1161/01.atv.20.3.708?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -