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Abstract: (76 Views)
Abstract
Background: The aim of this study was to determine effect of resistance training on the
expression of PI3K, AKT1 and mTORc1 in the heart tissue of type 2 diabetes rats and their
physiological cardiac hypertrophy.
Methods: 21 male wistar rats (220±20 g) were obese by 6 weeks high fat diet (HFD). After
inducing obesity, T2D induced by intraperitoneal injection of streptozotocin (30 mg/kg) 12
14 rats. Finally, the rat were randomly assigned to 1) non-diabetes, 2) control T2D, 3)
resistance diabetes groups. Rats in the resistance group were completed a resistance
training program, 5 sessions weekly for 6 weeks. PI3K, AKT1 and mTORc1 expression
and the weight ratio of left ventricular to heart, left ventricular to body and heart to body
were compared by ANOVA between groups.
Results: In response to induction of diabetes, the expression of PI3K, AKT1 and mTORc1
in heart tissue decreased significantly compared to the non-diabetic group (p < 0.05).
Resistance training resulted in significant increase in the expression of PI3K, AKT1 and
mTORc1 and the weight ratio of left ventricular to heart, heart to body and left ventricular
to body compared to control diabetes rats (p < 0.05).
Conclusion: Resistance training is associated with physiological cardiac hypertrophy in
diabetic rats, and this improvement can be attributed to the PI3K/AKT1/mTORc1 signaling
pathway.
Background: The aim of this study was to determine effect of resistance training on the
expression of PI3K, AKT1 and mTORc1 in the heart tissue of type 2 diabetes rats and their
physiological cardiac hypertrophy.
Methods: 21 male wistar rats (220±20 g) were obese by 6 weeks high fat diet (HFD). After
inducing obesity, T2D induced by intraperitoneal injection of streptozotocin (30 mg/kg) 12
14 rats. Finally, the rat were randomly assigned to 1) non-diabetes, 2) control T2D, 3)
resistance diabetes groups. Rats in the resistance group were completed a resistance
training program, 5 sessions weekly for 6 weeks. PI3K, AKT1 and mTORc1 expression
and the weight ratio of left ventricular to heart, left ventricular to body and heart to body
were compared by ANOVA between groups.
Results: In response to induction of diabetes, the expression of PI3K, AKT1 and mTORc1
in heart tissue decreased significantly compared to the non-diabetic group (p < 0.05).
Resistance training resulted in significant increase in the expression of PI3K, AKT1 and
mTORc1 and the weight ratio of left ventricular to heart, heart to body and left ventricular
to body compared to control diabetes rats (p < 0.05).
Conclusion: Resistance training is associated with physiological cardiac hypertrophy in
diabetic rats, and this improvement can be attributed to the PI3K/AKT1/mTORc1 signaling
pathway.
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