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高糖通过抑制心脏ATP合酶β亚基影响糖尿病阿基塔小鼠的心脏功能。

High glucose affects the cardiac function of diabetic Akita mice by inhibiting cardiac ATP synthase beta subunit.

作者信息

Ma Yuanfang, Wang Guang, Li Jing

机构信息

Department of Endocrinology, Beijing Daxing District People's Hospital, Beijing, China.

Beijing Chaoyang Hospital, Capital Medical University, Department of Endocrinology, Beijing, China.

出版信息

Int J Cardiol Cardiovasc Risk Prev. 2025 Jan 9;24:200369. doi: 10.1016/j.ijcrp.2025.200369. eCollection 2025 Mar.

DOI:10.1016/j.ijcrp.2025.200369
PMID:39872632
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11770494/
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.

摘要

目的

探讨糖尿病心肌病的发病机制,即高血糖可能通过抑制ATP酶β亚基的表达来影响心脏功能。

方法

利用形态学、分子生物学和超声心动图分析方法,在秋田小鼠(一种无脂质代谢紊乱的糖尿病小鼠模型)中观察心脏功能、纤维化水平以及ATP酶β亚基的表达,并与野生型小鼠进行比较。该研究揭示了ATP酶β亚基减少与糖尿病心肌损伤发展之间的联系。此外,对心肌细胞原代培养的研究表明,高糖对心肌和ATP的影响与ATP合酶β亚基表达的降低有关。

结果

随着高血糖时间的增加,秋田小鼠的心脏功能下降,房室峰和左心室预估重量在统计学上低于野生型小鼠,左心室射血分数与对照组无统计学差异;秋田小鼠的E/A比值随年龄显著下降,但在实验结束时确实出现了明显的心脏功能障碍;秋田小鼠心脏中的胶原沉积增加。在细胞水平上,高糖处理后原代培养心肌细胞中ATP酶β亚基的蛋白水平显著降低。

结论

高血糖可能通过影响心肌细胞中ATP酶β亚基的表达来影响心脏功能,这可能是糖尿病心肌病的发病机制之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ab/11770494/0bea17cde0ea/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ab/11770494/3d6a6f5503f7/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ab/11770494/9a44b62a71aa/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ab/11770494/e9fa72d7fc27/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ab/11770494/87c26ef9c0b2/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ab/11770494/0bea17cde0ea/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ab/11770494/3d6a6f5503f7/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ab/11770494/9a44b62a71aa/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ab/11770494/e9fa72d7fc27/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ab/11770494/87c26ef9c0b2/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ab/11770494/0bea17cde0ea/gr5.jpg

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