Dietary sodium chloride restriction enhances aortic wall lipid storage and raises plasma lipid concentration in LDL receptor knockout mice

被引:24
作者
Catanozi, S
Rocha, JC
Passarelli, M
Guzzo, ML
Alves, C
Furukawa, LNS
Nunes, VS
Nakandakare, ER
Heimann, JC
Quintao, ECR [1 ]
机构
[1] Univ Sao Paulo, Sch Med, Lipids Lab LIM 10, Sao Paulo, Brazil
[2] Univ Sao Paulo, Sch Med, Expt Hypertens Lab LIM 16, Sao Paulo, Brazil
[3] Univ Sao Paulo, Sch Med, Dept Rheumatol LIM 17, Sao Paulo, Brazil
[4] Univ Sao Paulo, Sch Med, Dept Dermatol, Sao Paulo, Brazil
关键词
salt restriction; triacylglycerol; hypertriglyceridemia; hyperlipidemia; atherosclerosis;
D O I
10.1194/jlr.M200330-JLR200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This study aimed at measuring the influence of a low salt diet on the development of experimental atherosclerosis in moderately hyperlipidemic mice. Experiments were carried out on LDL receptor (LDLR) knockout (KO) mice, or apolipoprotein E (apoE) KO mice on a low sodium chloride diet (LSD) as compared with a normal salt diet (NSD). On LSD, the rise of the plasma concentrations of TG and nonesterified fatty acid (NEFA) was, respectively, 19% and 34% in LDILR KO mice, and 21% and 35% in apoE KO mice, and that of plasma cholesterol was limited to the LDLR KO group alone (15%). Probably due to the apoE KO severe hypercholesterolemia, the arterial inner-wall fat storage was not influenced by the diet salt content and was far more abundant in the apoE KO than in the LDLR KO mice. However, in the less severe hypercholesterolemia of the LDILR KO mice, lipid deposits on the LSD were greater than on the NSD. Arterial fat storage correlated with NEFA concentrations in the LDLR KO mice alone (n = 14, P = 0.0065). M Thus, dietary sodium chloride restriction enhances aortic wall lipid storage in moderately hyperlipidemic mice.
引用
收藏
页码:727 / 732
页数:6
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