Earticle

초록

영어

Diabetic complications are a leading cause of blindness, renal failure, and nerve damage. Additionally, diabetes-accelerated atherosclerosis leads to increased risk of myocardial infarction, stroke, and limb amputation. At the present time, 4main molecular mechanisms have been implicated in hyperglyceamia-mediated vascular damage. In particular, advancedglycation endproducts (AGE), which are formed by complex, heterogeneous, sugar-derived protein modifications, have beenimplicated as a major pathogenic process for diabetic complications. Recently, AGE inhibitors such as aminoguanidin, ALT-946, and pyridoxamine have been reported. Such an integrating paradigm provides a new conceptual framework for futureresearch on diabetes complications and on discovering drugs to prevent the progression of AGE-induced maladies.

목차

Abstract
 Introduction
 Mechanisms of Diabetic Complications
  A. Polyol pathway
  B. PKC activation
  C. Increased hexosamine pathway
  D. Advanced AGEs
 AGEs and Diabetic Complications
 Formation of Various AGEs in vivo and RelatedToxicity
 AGE Formation During Diabetic Conditions
 ROS and Diabetes
 Pharmacological Inhibition of AGEs
 Conclusion
 Acknowledgments
 References

키워드

저자

• Hyun-Sun Lee [ Institute of Life Science and Natural Resource, Korea University, Seoul 136-701, Korea ]
• Chung-Oui Hong [ Division of Food Bioscience and Technology, College of Life Science and Biotechnology, Korea University, Seoul 136-701, Korea ]
• Kwang-Won Lee [ Division of Food Bioscience and Technology, College of Life Science and Biotechnology, Korea University, Seoul 136-701, Korea ] Corresponding author

참고문헌

발행기관

간행물

표지보기 관심저널 등록

• 간행물명

  Food Science and Biotechnology

• 간기

  격월간

• pISSN

  1226-7708

• 수록기간

  1992~2009

• 십진분류

  KDC 574 DDC 664