Abstract
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.