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High glucose affects the cardiac function of diabetic Akita mice by inhibiting cardiac ATP synthase beta subunit
Yuanfang Ma1, Guang Wang2, Jing Li2
1Department of Endocrinology, Beijing Daxing District People's Hospital, Beijing, China.
Object:
To explore the mechanism of diabetic cardiomyopathy that hyperglycemia may affect the cardiac function by inhibiting the expression of ATPase β subunit.
Method:
Cardiac function, fibrosis levels, and the expression of the ATPase β subunit were observed in Akita mice-a diabetes mice model without lipid metabolism disorders--using morphological, molecular biology, and echocardiographic analyses compared to wild-type mice. The study revealed a connection between the decreased ATPase β subunit and the development of diabetic myocardial injury. Furthermore, study on primary culture of cardiomyocytes hints that the effect of high glucose on myocardium and ATP are related to the decrease of the expression of ATP synthase β subunit.
Result:
With the increase of hyperglycemia time, the heart function of akita mice decreased, AV peak and estimated weight of left ventricle were statistically less than that of wild-type mice, the left ventricular ejection fraction was not statistically different from that of the control group; the E/A ratio of akita mice decreased significantly with age, but did shows significant cardiac dysfunction at the end of the experiment; collagen deposition increased in the heart of akita mice. In the cell level, the protein level of ATPase β subunit in primary cultured cardiomyocytes decreased significantly after high glucose treatment.
Conclusion:
Hyperglycemia may affect the cardiac function by affecting the expression of ATPase β subunit in cardiomyocytes, which may be one of the mechanisms of diabetic cardiomyopathy.
Insights
Hyperglycemia impairs cardiac function in diabetic cardiomyopathy by reducing ATPase β subunit expression in cardiomyocytes. This molecular change is linked to myocardial injury and fibrosis in diabetic mice.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Diabetic cardiomyopathy (DCM) is a cardiac complication of diabetes.
- Hyperglycemia is a key factor in diabetes, but its precise effects on cardiac function are complex.
- The role of specific protein expression, like ATPase β subunit, in DCM pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the mechanism by which hyperglycemia affects cardiac function in diabetic cardiomyopathy.
- To determine if inhibiting ATPase β subunit expression is involved in hyperglycemia-induced cardiac dysfunction.
- To explore the link between hyperglycemia, ATPase β subunit levels, and myocardial injury.
Main Methods:
- Utilized Akita mice, a model for diabetes without lipid metabolism disorders, compared to wild-type mice.
- Employed morphological, molecular biology, and echocardiographic analyses to assess cardiac function, fibrosis, and ATPase β subunit expression.
- Conducted studies on primary cultured cardiomyocytes to examine high glucose effects on myocardial cells and ATP levels.
Main Results:
- Akita mice showed decreased heart function, reduced AV peak, and lower estimated left ventricular weight compared to controls.
- Significant cardiac dysfunction and increased collagen deposition (fibrosis) were observed in Akita mice with prolonged hyperglycemia.
- High glucose treatment in cultured cardiomyocytes led to a significant decrease in ATPase β subunit protein levels.
Conclusions:
- Hyperglycemia may impair cardiac function by downregulating ATPase β subunit expression in cardiomyocytes.
- Reduced ATPase β subunit expression is a potential mechanism contributing to the development of diabetic cardiomyopathy.
- This study highlights a molecular link between hyperglycemia and cardiac dysfunction in diabetes.
