Abstract |
Glucose or other reducing sugars in plasma or tissue fluids react with proteins by a nonenzymatic, post-translational process called glycation or Maillard reaction which leads to the formation of advanced glycation end products (AGEs). AGEs are implicated in the multiorgan complications of diabetes because of their multipotent bioactivities through their receptors as well as the functional and structural derangement of the AGE-bearing proteins. AGE inhibitors such as aminoguanidine have been shown to have beneficial effects on the progression of a full range of diabetic complications in animal models. Furthermore, a recent clinical study showed that aminoguanidine therapy resulted in significant improvements in several key measurements; it reduced urinary protein, LDL-cholesterol and triglycerides as well as blood pressure. A novel class of AGE-antagonists, AGE breakers have been also developed and waiting for the clinical evaluation.
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Authors | M Kawakami, M Kuroki |
Journal | Nihon rinsho. Japanese journal of clinical medicine
(Nihon Rinsho)
Vol. 57
Issue 3
Pg. 567-72
(Mar 1999)
ISSN: 0047-1852 [Print] Japan |
PMID | 10199135
(Publication Type: Journal Article, Review)
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Chemical References |
- Glycation End Products, Advanced
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Topics |
- Diabetic Angiopathies
(etiology, prevention & control)
- Glycation End Products, Advanced
(antagonists & inhibitors, physiology)
- Humans
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