Myocardial metabolism and cardiac performance in obesity and insulin resistance

被引:24
作者
Banerjee S. [1 ]
Peterson L.R. [1 ]
机构
[1] Washington University School of Medicine, Department of Medicine, St. Louis, MO 63110
基金
美国国家卫生研究院;
关键词
Insulin Resistance; Left Ventricular Diastolic Dysfunction; Left Ventricular Diastolic Function; Myocardial Metabolism; Myocardial Fatty Acid;
D O I
10.1007/BF02938341
中图分类号
学科分类号
摘要
Obesity, insulin resistance, and their frequent complication of type 2 diabetes are risk factors for left ventricular diastolic dysfunction, systolic dysfunction, and clinical heart failure. Although obesity, insulin resistance, and diabetes are risk factors for coronary artery disease, and hence ischemic cardiomyopathy-related heart failure, there is increasing evidence that these three risk factors are implicated in the development of cardiac dysfunction not related to epicardial coronary disease. There are several mechanisms by which this triad may cause cardiac dysfunction, including alterations in myocardial metabolism, which may initially be adaptations but evolve into maladaptive responses over time. Recent advances in our understanding of these mechanisms will aid in the development of novel therapies, including metabolic manipulations that could prevent and treat cardiac dysfunction in patients with obesity, insulin resistance, and diabetes. Copyright © 2007 by Current Medicine Group LLC.
引用
收藏
页码:143 / 149
页数:6
相关论文
共 50 条
[31]  
Kates A.M., Herrero P., Dence C., Et al., Impact of aging on substrate metabolism by the human heart, J Am Coll Cardiol, 41, pp. 293-299, (2003)
[32]  
Zhou Y.T., Grayburn P., Karim A., Et al., Lipotoxic heart disease in obese rats: Implications for human obesity, Proc Natl Acad Sci U S A, 97, pp. 1784-1789, (2000)
[33]  
Young M.E., Guthrie P.H., Razeghi P., Et al., Impaired long-chain fatty acid oxidation and contractile dysfunction in the obese Zucker rat heart, Diabetes, 51, pp. 2587-2595, (2002)
[34]  
Alavaikko M., Elfving R., Hirvonen J., Jarvi J., Triglycerides, cholesterol, and phospholipids in normal heart papillary muscle and in patients suffering from diabetes, cholelithiasis, hypertension, and coronary atheroma, J Clin Pathol, 26, pp. 285-293, (1973)
[35]  
Szczepaniak L.S., Dobbins R.L., Metzger G.J., Et al., Myocardial triglycerides and systolic function in humans: In vivo evaluation by localized proton spectroscopy and cardiac imaging, Magn Reson Med, 49, pp. 417-423, (2003)
[36]  
Herrero P., Peterson L.R., McGill J.B., Et al., Increased myocardial fatty acid metabolism in patients with type 1 diabetes mellitus, J Am Coll Cardiol, 47, pp. 598-604, (2006)
[37]  
Iozzo P., Chareonthaitawee P., Rimoldi O., Et al., Mismatch between insulin-mediated glucose uptake and blood flow in the heart of patients with Type II diabetes, Diabetologia, 45, pp. 1404-1409, (2002)
[38]  
Scheuermann-Freestone M., Madsen P.L., Manners D., Et al., Abnormal cardiac and skeletal muscle energy metabolism in patients with type 2 diabetes, Circulation, 107, pp. 3040-3046, (2003)
[39]  
Taegtmeyer H., Wilson C.R., Razeghi P., Sharma S., Metabolic energetics and genetics in the heart, Ann N Y Acad Sci, 1047, pp. 208-218, (2005)
[40]  
Sawyer D.B., Colucci W.S., Mitochondrial oxidative stress in heart failure: "oxygen wastage" revisited, Circ Res, 86, pp. 119-120, (2000)