Aerobic Exercise Improves Cardiac Hypertrophy Through the RAF/MEK/ERK Complex Pathway in the Experimental Model of Obesity Induced by a High Fat/Fructose Diet in Rats

Abstract

Background: The association between obesity and cardiovascular diseases is well established. Objectives: This study aimed to evaluate the effects of aerobic exercise (EX) on cardiac hypertrophy in obese (OB) rats fed a high-fat/fructose diet by investigating gene expression in cardiac tissue. Methods: Twenty-four male Wistar rats were randomly assigned to three groups: Control, high-fat/fructose diet (OB), and obese with aerobic exercise (OB+EX). Cardiac Hypertrophy Index, biomarkers, and the expression levels of rapidly accelerated fibrosarcoma (RAF), mitogen-activated protein kinase (MEK), and extracellular signal-regulated kinase (ERK) genes in cardiac tissue were assessed at the experiment’s end. Data analysis was performed using SPSS software with the one-way ANOVA test. Results: The addition of fructose to a high-fat diet led to an increase in the ratio of heart weight to body weight and left ventricle weight to body weight, indicating cardiac hypertrophy. Elevated vascular endothelial growth factor (VEGF) and NAD-dependent deacetylase sirtuin-3 (SIRT3) were identified as biomarkers of cardiac hypertrophy. The expression levels of RAF, MEK, and ERK genes were significantly higher in the cardiac tissue of OB rats compared with the control group. However, eight weeks of aerobic EX significantly reduced cardiac hypertrophy indices and biomarker levels, which correlated with decreased expression of RAF and MEK genes. While the ERK gene expression level tended to decrease in the high-fat diet plus aerobic EX group compared to the OB group, this difference was not statistically significant. Conclusions: The current findings suggest that aerobic EX can modulate cardiac hypertrophy in OB subjects by regulating the RAF/MEK/ERK complex pathway.