Fiordelisi Antonella, Cerasuolo Federica Andrea, Avvisato Roberta, Buonaiuto Antonietta, Maisto Marianna, Bianco Antonio, D'Argenio Valeria, Mone Pasquale, Perrino Cinzia, D'Apice Stefania, Paolillo Roberta, Pezone Antonio, Varzideh Fahimeh, Santulli Gaetano, Sorriento Daniela, Iaccarino Guido, Gambardella Jessica
Department of Molecular Medicine and Medical Biotechnologies, Federico II University, Naples, Italy.
Department of Statistics, Computer Science, Applications (DiSIA), University of Florence, Florence, Italy.
Cardiovasc Diabetol. 2024 Dec 20;23(1):450. doi: 10.1186/s12933-024-02490-x.
In patients with type II diabetes, the development of diabetic cardiomyopathy (DC) is associated with a high risk of mortality. Left ventricular hypertrophy, diastolic dysfunction, and exercise intolerance are the first signs of DC. The underlying mechanisms are not fully elucidated, and there is an urgent need for specific biomarkers and molecular targets for early diagnosis and treatment. Mitochondrial alterations play a key role in the development of DC, and microRNAs regulating mitochondrial function are emerging as potential biomarkers of metabolic stress in DC. L-Arginine (Arg) supplementation has been shown to be an effective strategy for improving mitochondrial function and energetics, with a significant impact on physical performance. The aim of the current study was to evaluate the effects of Arg supplementation on cardiac mitochondrial function, DC development, and relative phenotypes including exercise intolerance. We used db/db mice as a model of type II diabetes, chronically treated with Arg (1 mg/kg/day) for 12 weeks. Arg-treated db/db mice showed preserved diastolic function and left ventricular morphology compared with untreated diabetic mice. Arg supplementation also improved exercise tolerance and the propensity to physical activity. Mitochondrial respiration was significantly increased in cardiomyocytes isolated from treated db/db mice, as well as in diabetic cardiomyocytes treated with Arg in vitro. The improvement of cardiac mitochondrial function in db/db + Arg mice was associated with an increase in PGC-1-alpha levels, mitochondrial biogenesis, recycling, and antioxidant capacity. Arg treatment prevented the accumulation of circulating and cardiac miR-143 in db/db mice, which is an index of metabolic stress and activation of mitochondrial damage mechanisms. In conclusion, Arg supplementation is effective in preventing the development of DC, preserving diastolic function and exercise tolerance by improving mitochondrial fitness and homeostasis. Additionally, miR-143 could potentially be employed to monitor cardiac metabolic stress and the effects of Arg treatment in diabetes.
在2型糖尿病患者中,糖尿病性心肌病(DC)的发展与高死亡率风险相关。左心室肥厚、舒张功能障碍和运动不耐受是DC的最初迹象。其潜在机制尚未完全阐明,迫切需要用于早期诊断和治疗的特异性生物标志物和分子靶点。线粒体改变在DC的发展中起关键作用,调节线粒体功能的微小RNA正成为DC中代谢应激的潜在生物标志物。补充L-精氨酸(Arg)已被证明是改善线粒体功能和能量代谢的有效策略,对身体机能有显著影响。本研究的目的是评估补充Arg对心脏线粒体功能、DC发展以及包括运动不耐受在内的相关表型的影响。我们使用db/db小鼠作为2型糖尿病模型,用Arg(1毫克/千克/天)长期治疗12周。与未治疗的糖尿病小鼠相比,接受Arg治疗的db/db小鼠舒张功能和左心室形态得以保留。补充Arg还改善了运动耐量和体力活动倾向。从接受治疗的db/db小鼠分离的心肌细胞以及体外接受Arg治疗的糖尿病心肌细胞中线粒体呼吸显著增加。db/db + Arg小鼠心脏线粒体功能的改善与PGC-1-α水平升高、线粒体生物发生、循环和抗氧化能力增强有关。Arg治疗可防止db/db小鼠循环和心脏中miR-143的积累,miR-143是代谢应激和线粒体损伤机制激活的指标。总之,补充Arg可有效预防DC的发展,通过改善线粒体健康和内环境稳态来保留舒张功能和运动耐量。此外,miR-143可能潜在地用于监测糖尿病患者的心脏代谢应激和Arg治疗的效果。