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The effects of low-intensity exercise on cardiac glycogenesis and glycolysis in male and ovariectomized female rats on a fructose-rich diet.

Jelena StanišićGoran KorićanacTijana ĆulafićSnjezana RomicMojca StojiljkovicMilan KosticTamara IvkovicSnežana Tepavčević
Published in: Journal of food biochemistry (2021)
We previously reported that low-intensity exercise prevented cardiac insulin resistance induced by a fructose-rich diet (FRD). To examine whether low-intensity exercise could prevent the disturbances of key molecules of cardiac glucose metabolism induced by FRD in male and ovariectomized (ovx) female rats, animals were exposed to 10% fructose solution (SF) or underwent both fructose diet and exercise (EF). Exercise prevented a decrease in cardiac GSK-3β phosphorylation induced by FRD in males (p < .001 vs. SF). It also prevented a decrease in PFK-2 phosphorylation in ovx females (p < .001 vs. SF) and increased the expression of PFK-2 in males (p < .05 vs. control). Exercise did not prevent a decrease in plasma membrane GLUT1 and GLUT4 levels in ovx females on FRD. The only effect of exercise on glucose transporters that could be indicated as beneficial is an augmented GLUT4 protein expression in males (p < .05 vs. control). Obtained results suggest that low-intensity exercise prevents harmful effects of FRD towards cardiac glycogenesis in males and glycolysis in ovx females. PRACTICAL APPLICATIONS: Low-intensity exercise, equivalent to brisk walking, was able to prevent disturbances in cardiac glycolysis regulation in ovx female and the glycogen synthesis pathway in male rats. In terms of human health, although molecular mechanisms of beneficial effects of exercise on cardiac glucose metabolism vary between genders, low-intensity running may be a useful non-pharmacological approach in the prevention of cardiac metabolic disorders in both men and postmenopausal women.
Keyphrases
  • high intensity
  • physical activity
  • left ventricular
  • resistance training
  • postmenopausal women
  • metabolic syndrome
  • heart failure
  • blood pressure
  • mouse model
  • cell proliferation
  • blood glucose
  • atrial fibrillation