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Dissecting the molecular landscape of exercise-mediated protection against fructose-induced cardiac dysfunction:

Mojca Stojiljkovic1, Snezana Tepavcevic1, Milan Kostic1

  • 1Laboratory for Molecular Biology and Endocrinology, Vinca Institute of Nuclear Sciences, National Institute of the Republic of Serbia, University of Belgrade, Serbia.

Progress in Biophysics and Molecular Biology
|July 11, 2026
PubMed
Summary

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Low-intensity exercise prevents cardiac inflammation through the NF-κB/TNFα pathway in insulin-resistant male rats.

Molecular and cellular biochemistry·2025

Regular physical exercise can protect the heart from damage caused by excessive fructose intake. Exercise improves fructose metabolism and cardiac function, offering a promising non-pharmacological strategy for cardiometabolic health.

Area of Science:

  • Cardiology and Exercise Physiology
  • Metabolic Disease Research

Background:

  • High fructose consumption and sedentary lifestyles drive global cardiometabolic disease increase.
  • The evolutionary balance of fructose intake and energy expenditure is disrupted, necessitating lifestyle interventions.

Purpose of the Study:

  • To review the cardioprotective effects of physical exercise in the context of high fructose intake.
  • To explore cellular and molecular mechanisms in animal models relevant to human cardiometabolic health.

Main Methods:

  • Analysis of 30 PubMed-identified animal studies on fructose intake and exercise.
  • Focus on cellular and molecular mechanisms of exercise's impact on fructose metabolism and cardiac function.

Main Results:

Keywords:
Animal modelExerciseFructose-rich dietHeartMolecular mechanisms

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  • Exercise reduces fructose absorption, increases hepatic oxidation, suppresses lipogenesis, and lowers uric acid.
  • Improvements observed in myocardial structure, diastolic function, electrical stability, and coronary blood flow.
  • Benefits linked to modulation of oxidative stress, inflammation, energy metabolism, insulin signaling, and nitric oxide synthesis.
  • Conclusions:

    • Exercise is a potent non-pharmacological strategy against fructose-induced cardiac dysfunction.
    • Low- to moderate-intensity aerobic exercise shows significant benefits; high-intensity interval training warrants consideration.
    • Further human studies are needed to confirm these findings for clinical application.