Application of leptin as a protective tool for myocardial damage

瘦素的发现是分子生物学对理解经典生理学研究中最初假设的机制所做贡献的一个最好的例子。瘦素在脂肪组织中产生并调节多种神经内分泌。我们假设心肌损伤患者的瘦素浓度降低，瘦素可能是心力衰竭患者发病率的敏感标志物。因此，我们检测了21例急性心肌梗死患者和15名年龄匹配的对照者的瘦素，我们观察到瘦素和白细胞介素-6的峰值浓度之间存在显著的负相关性。瘦素分泌减少的患者在心力衰竭的发展中可能缺乏调节心脏稳态的能力。瘦素可能在心力衰竭患者心脏损害的发展中起调节作用。接下来，为了研究瘦素在病毒性心肌炎和心肌坏死发展中的作用，我们使用了病毒性心肌炎小鼠模型。）我们将脑心肌炎病毒腹腔注射到野生型C57 BL/6小鼠和瘦素基因敲除小鼠。瘦素通过免疫调节作用减轻病毒性心肌炎心肌坏死的严重程度和死亡率，瘦素在心力衰竭中的确切作用有待进一步研究。

The discovery of leptin is a prime example of the contribution molecular biology has made to the understanding of mechanisms initially hypothesized in classic physiologic studies. Leptin is produced in adipose tissue and regulates multiple neuroendocrine secretions. We hypothesized that leptin concentrations are reduced in patients with myocardial damages and that leptin may be a sensitive marker of morbidity in patients with heart failure. So we measured leptin in 21 patients with acute myocardial infarction and 15 age-matched controls.We observed a significant negative correlation between the peak concentrations of leptin and interleukin-6. Patients with reduced leptin secretion may lack the ability to regulate cardiac homeostasis in the development of heart failure. Leptin may play a role in the regulation of the development of cardiac damage in patients with heart failure.In next, to investigate the role of leptin in the development of viral myocarditis and cardiac necrosis, we used a murine model of viral myocarditis.) We injected encephalomyocarditis virus intraperitoneally to wild type C57 BL/6 mice and leptin knockolut mice. leptin reduces the severity of myocardial nerosis and lethality in viral myocarditis by immunomodulation.Future investigation will be needed for the definite role of leptin for heart failure.