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

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) femal...

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Veröffentlicht in:Journal of food biochemistry 2021-10, Vol.45 (10), p.e13930-n/a
Hauptverfasser: Stanisic, Jelena, Koricanac, Goran, Culafic, Tijana, Romic, Snjezana, Stojiljkovic, Mojca, Kostic, Milan, Ivkovic, Tamara, Tepavcevic, Snezana
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container_issue 10
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container_title Journal of food biochemistry
container_volume 45
creator Stanisic, Jelena
Koricanac, Goran
Culafic, Tijana
Romic, Snjezana
Stojiljkovic, Mojca
Kostic, Milan
Ivkovic, Tamara
Tepavcevic, Snezana
description 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 
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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 &lt; .001 vs. SF). It also prevented a decrease in PFK‐2 phosphorylation in ovx females (p &lt; .001 vs. SF) and increased the expression of PFK‐2 in males (p &lt; .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 &lt; .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. Fructose‐rich diet affected cardiac glucose metabolism in male and ovx female rats differently. In fructose‐fed ovx female rats, low‐intensity exercise, equivalent to brisk walking, was able to prevent disturbances in phosphorylation of PFK‐2, which implicates increased glycolysis. 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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 &lt; .001 vs. SF). It also prevented a decrease in PFK‐2 phosphorylation in ovx females (p &lt; .001 vs. SF) and increased the expression of PFK‐2 in males (p &lt; .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 &lt; .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. Fructose‐rich diet affected cardiac glucose metabolism in male and ovx female rats differently. In fructose‐fed ovx female rats, low‐intensity exercise, equivalent to brisk walking, was able to prevent disturbances in phosphorylation of PFK‐2, which implicates increased glycolysis. 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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 &lt; .001 vs. SF). It also prevented a decrease in PFK‐2 phosphorylation in ovx females (p &lt; .001 vs. SF) and increased the expression of PFK‐2 in males (p &lt; .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 &lt; .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. 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subjects cardiac insulin resistance
glucose transporters
glycogen synthase kinase 3
hexokinase 2,6‐phosphofructo‐2‐kinase
title The effects of low‐intensity exercise on cardiac glycogenesis and glycolysis in male and ovariectomized female rats on a fructose‐rich diet
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