Abstract

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 LDLR 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 LDLR 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). Thus, dietary sodium chloride restriction enhances aortic wall lipid storage in moderately hyperlipidemic mice.

Highlights

  • This study aimed at measuring the influence of a low salt diet on the development of experimental atherosclerosis in moderately hyperlipidemic mice

  • Present experiments were carried out in mice models with a plasma LP profile closer to that found in Abbreviations: KO, knockout; LDL receptor (LDLR), low density lipoprotein receptor; LP, lipoprotein; LSD, low sodium chloride diet; normal salt diet (NSD), normal sodium chloride diet; TC, total cholesterol; UKV, urinary potassium; UNaV, urinary sodium

  • On NSD, the plasma concentration of nonesterified fatty acid (NEFA) was similar in LDL-receptor KO (LDLR KO) and apolipoprotein E (apoE) KO mice, whereas plasma TG was higher in LDLR KO than in apoE KO, and cholesterol was higher in apoE KO than in LDLR KO (Table 1)

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Summary

Introduction

This study aimed at measuring the influence of a low salt diet on the development of experimental atherosclerosis in moderately hyperlipidemic mice. Previous work from our laboratory showed that Wistar rats fed a low salt diet (LSD) developed higher plasma concentrations of nonesterified fatty acid (NEFA), TG, and cholesterol, as compared with controls either on a normal-salt or on a high-salt intake [14]. This fact has been explained by an impairment of the removal rate of TG-rich lipoproteins (LP) from plasma [14]. Present experiments were carried out in mice models with a plasma LP profile closer to that found in Abbreviations: KO, knockout; LDLR, low density lipoprotein receptor; LP, lipoprotein; LSD, low sodium chloride diet; NSD, normal sodium chloride diet; TC, total cholesterol; UKV, urinary potassium; UNaV, urinary sodium

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