Abstract
Background: A low-sodium (LS) diet reduces blood pressure, contributing to the prevention of cardiovascular diseases. However, intense dietary sodium restriction impairs insulin sensitivity and worsens lipid profile. Considering the benefits of aerobic exercise training (AET), the effect of LS diet and AET in hepatic lipid content and gene expression was investigated in LDL receptor knockout (LDLr-KO) mice. Methods: Twelve-week-old male LDLr-KO mice fed a normal sodium (NS) or LS diet were kept sedentary (S) or trained (T) for 90 days. Body mass, plasma lipids, insulin tolerance testing, hepatic triglyceride (TG) content, gene expression, and citrate synthase (CS) activity were determined. Results were compared by 2-way ANOVA and Tukey’s post-test. Results: Compared to NS, LS increased body mass and plasma TG, and impaired insulin sensitivity, which was prevented by AET. The LS-S group, but not the LS-T group, presented greater hepatic TG than the NS-S group. The LS diet increased the expression of genes related to insulin resistance (ApocIII, G6pc, Pck1) and reduced those involved in oxidative capacity (Prkaa1, Prkaa2, Ppara, Lipe) and lipoprotein assembly (Mttp). Conclusion: AET prevented the LS-diet-induced TG accumulation in the liver by improving insulin sensitivity and the expression of insulin-regulated genes and oxidative capacity.
Highlights
Dietary sodium restriction reduces blood pressure (BP) contributing to preventing cardiovascular diseases (CVD)
It was recently demonstrated that low-density lipoprotein (LDL) receptor knockout (LDLr-KO) mice chronically fed a low-sodium (LS) diet present many alterations in skeletal muscle lipidomics, namely glycerophospholipid and fatty acid species that relate to the reduced insulin sensitivity observed in those animals [4]
The present study investigated the effect of an intensive and chronically administered LS diet and aerobic exercise training (AET) in the modulation of lipid content and expression of genes related to lipid metabolism and insulin sensitivity in the liver of LDLr-KO mice
Summary
Dietary sodium restriction reduces blood pressure (BP) contributing to preventing cardiovascular diseases (CVD). Long-term intensive sodium restriction in the diet activates the renin-angiotensin-aldosterone system (RAAS), and the sympathetic nervous system favoring insulin resistance Those events contribute to the increase in plasma lipids, especially triglycerides (TG) and free fatty acids (FFA), enhanced lipid infiltration in the arterial wall, and glycoxidative stress [3]. It was recently demonstrated that LDL receptor knockout (LDLr-KO) mice chronically fed a low-sodium (LS) diet present many alterations in skeletal muscle lipidomics, namely glycerophospholipid and fatty acid species that relate to the reduced insulin sensitivity observed in those animals [4]. Results: Compared to NS, LS increased body mass and plasma TG, and impaired insulin sensitivity, which was prevented by AET. Conclusion: AET prevented the LS-diet-induced TG accumulation in the liver by improving insulin sensitivity and the expression of insulin-regulated genes and oxidative capacity
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