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反对非酶糖基化参与糖尿病性心肌病的证据。

Evidence against the involvement of nonenzymatic glycosylation in diabetic cardiomyopathy.

作者信息

Ganguly P K, Thliveris J A, Mehta A

机构信息

Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, Canada.

出版信息

Metabolism. 1990 Jul;39(7):769-73. doi: 10.1016/0026-0495(90)90115-s.

DOI:10.1016/0026-0495(90)90115-s
PMID:2164131
Abstract

There is evidence to suggest that increased nonenzymatic glycosylation (NEG) occurs in hyperglycemic states such as seen in diabetes mellitus. In order to examine the hypothesis that the development of cardiomyopathy in diabetes results from an increased nonenzymatic glycosylation of cardiac sarcolemmal proteins, rats were made diabetic by an intravenous (IV) injection of streptozotocin (65 mg/kg). Twelve weeks after the induction of diabetes, animal showed significantly lower heart rate, left ventricular systolic pressure, rate of contraction (+dp/dt), and rate of relaxation (-dp/dt), whereas left ventricular diastolic pressure was markedly increased. Furthermore, cardiac sarcolemmal Na+, K+ adenosine triphosphatase (ATPase) activity was significantly decreased in diabetic rats. When examined in cardiac crude membranes, as well as in purified sarcolemmal membranes prepared by two different procedures, the levels of NEG did not differ between control and diabetic animals; however, NEG levels were increased in kidney and skeletal muscle. These results indicate that chronic diabetes is associated with functional and biochemical alterations in cardiac muscle and suggest that NEG of cardiac sarcolemma may not play any role in the development of diabetic cardiomyopathy.

摘要

有证据表明,在糖尿病等高血糖状态下,非酶糖基化(NEG)会增加。为了检验糖尿病心肌病的发生是由于心肌肌膜蛋白非酶糖基化增加这一假说,通过静脉注射链脲佐菌素(65mg/kg)使大鼠患糖尿病。糖尿病诱导12周后,动物的心率、左心室收缩压、收缩速率(+dp/dt)和舒张速率(-dp/dt)显著降低,而左心室舒张压明显升高。此外,糖尿病大鼠心肌肌膜钠钾三磷酸腺苷酶(ATP酶)活性显著降低。当在心脏粗膜以及通过两种不同方法制备的纯化肌膜中进行检测时,对照动物和糖尿病动物的NEG水平没有差异;然而,肾脏和骨骼肌中的NEG水平升高。这些结果表明,慢性糖尿病与心肌的功能和生化改变有关,并提示心肌肌膜的NEG可能在糖尿病心肌病的发生中不起任何作用。

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Evidence against the involvement of nonenzymatic glycosylation in diabetic cardiomyopathy.反对非酶糖基化参与糖尿病性心肌病的证据。
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