Navab Mohamad, Gharavi Nima, Watson Andrew D
Division of Cardiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095, USA.
Curr Opin Clin Nutr Metab Care. 2008 Jul;11(4):459-64. doi: 10.1097/MCO.0b013e32830460c2.
Poor nutrition, overweight and obesity have increasingly become a public health concern as they affect many metabolic disorders, including heart disease, diabetes, digestive system disorders, and renal failure. Study of the effects of life style including healthy nutrition will help further elucidate the mechanisms involved in the adverse effects of poor nutrition.
Unhealthy life style including poor nutrition can result in imbalance in our oxidation/redox systems. Lipids can undergo oxidative modification by lipoxygenases, cyclooxygenases, myeloperoxidase, and other enzymes. Oxidized phospholipids can induce inflammatory molecules in the liver and other organs. This can contribute to inflammation, leading to coronary heart disease, stroke, renal failure, inflammatory bowl disease, metabolic syndrome, bone and joint disorders, and even certain types of cancer.
Our antioxidant and antiinflammatory defense mechanisms contribute to a balance between the stimulators and the inhibitors of inflammation. Beyond a point, however, these systems might be overwhelmed and eventually fail. High-density lipoprotein is a potent inhibitor of the formation of toxic oxidized lipids. High-density lipoprotein is also an effective system for stimulating the genes whose products are active in the removal, inactivation, and elimination of toxic lipids. Supporting the high-density lipoprotein function should help maintain the balance in these systems. It is hoped that the present report would elucidate some of the ongoing work toward this goal.
营养不良、超重和肥胖日益成为公共卫生问题，因为它们会影响多种代谢紊乱，包括心脏病、糖尿病、消化系统疾病和肾衰竭。对包括健康营养在内的生活方式影响的研究将有助于进一步阐明营养不良不良影响所涉及的机制。
包括营养不良在内的不健康生活方式会导致我们氧化/氧化还原系统失衡。脂质可被脂氧合酶、环氧化酶、髓过氧化物酶和其他酶进行氧化修饰。氧化磷脂可在肝脏和其他器官中诱导炎症分子。这会导致炎症，进而引发冠心病、中风、肾衰竭、炎症性肠病、代谢综合征、骨骼和关节疾病，甚至某些类型的癌症。
我们的抗氧化和抗炎防御机制有助于炎症刺激物和抑制剂之间的平衡。然而，超过一定程度后，这些系统可能会不堪重负并最终失效。高密度脂蛋白是有毒氧化脂质形成的有效抑制剂。高密度脂蛋白也是刺激那些其产物在清除、灭活和消除有毒脂质方面具有活性的基因的有效系统。支持高密度脂蛋白功能应有助于维持这些系统的平衡。希望本报告能阐明朝着这一目标正在进行的一些工作。
