心肌收缩功能障碍与2型糖尿病患者的线粒体功能和动态受损有关,但在肥胖患者中并非如此
David Montaigne1, Xavier Marechal2, Augustin Coisne2
1From the Department of Physiology, Faculty of Medicine Lille, Lille, France (D.M., X.M., A.C., N.D., C.P., S.M., S.P., R.N.); Service d'Explorations Fonctionnelles CardioVasculaires (D.M., A.C., S.M.), Department of Cardiovascular Surgery (T.M., G.F., J.-M.E.A., M.K.), and Biochemistry Division, Pathology and Biology Center (F.Z.), University Hospital of Lille, Lille, France; Université Lille 2, Inserm, U1011, and Institut Pasteur de Lille, Lille, France (D.M., X.M., Y.S., H.D., P.L., B.S.); University Hospital of Lille, Lille, France; INSERM U1096, University of Rouen, Institute for Research and Innovation in Biomedicine, Rouen, France (I.R.-J., V.R.); and EA4483-Département de Médecine du Travail, Faculty of Medicine; University Lille 2, Lille, France (J.-L.E.). davidmontaigne@hotmail.com bart.staels@pasteur-lille.fr.
糖尿病严重损害心肌收缩和线粒体功能,甚至在心力衰竭发生之前. 仅仅肥胖对心脏功能和线粒体的影响较小.
科学领域:
- 心血管科学 心血管科学
- 代谢性疾病研究研究
- 线粒体生物学 线粒体生物学
背景情况:
- 肥胖和糖尿病是心力衰竭的独立危险因素.
- 研究了这些条件对人类心肌功能早期的影响.
研究的目的:
- 确定肥胖,胰岛素抵抗和糖尿病对心肌收缩和线粒体功能的明显影响.
- 在心肌病发作之前评估这些影响.
主要方法:
- 来自141名没有心肌病的患者的右心房心肌的分析.
- 在体外评估同位数收缩,线粒体呼吸,保留和氧化应激.
- 测量呼吸链复杂活动和MFN1蛋白表达.
主要成果:
- 糖尿病导致显著的收缩功能障碍,线粒体功能障碍和氧化应激,无论体重如何.
- 仅仅肥胖就导致了较轻的收缩问题,没有主要的线粒体或氧化应激变化.
- 高血红蛋白A1C与线粒体功能受损相关;糖尿病与线粒体碎片化和减少MFN1.1有关.
结论:
- 从肥胖到糖尿病的心肌收缩的恶化与心脏线粒体功能下降有关.
- 缺陷的线粒体功能,动力学和收缩功能障碍在糖尿病患者中很明显,但在新陈代谢健康的肥胖个体中并非如此.
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