Aerobic Exercise Training Prevents Insulin Resistance and Hepatic Lipid Accumulation in LDL Receptor Knockout Mice Chronically Fed a Low-Sodium Diet

Nutrients. 2021 Jun 24;13(7):2174. doi: 10.3390/nu13072174.

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.

Keywords: aerobic exercise; dyslipidemia; insulin resistance; sodium restriction.

MeSH terms

  • Animals
  • Body Weight
  • Citrate (si)-Synthase / metabolism
  • Diet, Sodium-Restricted / adverse effects*
  • Gene Expression
  • Insulin Resistance / physiology*
  • Lipid Metabolism / physiology*
  • Lipids / blood
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Knockout
  • Physical Conditioning, Animal / physiology*
  • Receptors, LDL / deficiency*
  • Sodium, Dietary / metabolism
  • Triglycerides / metabolism

Substances

  • Lipids
  • Receptors, LDL
  • Sodium, Dietary
  • Triglycerides
  • Citrate (si)-Synthase