Abstract
Advanced glycation end products accumulate as a function of the level of chronic hyperglycemia via generation of reactive dicarbonyl intermediates. Inside cells, advanced glycation end products accumulate rapidly and cause altered function of intracellular proteins. Outside cells, advanced glycation end products accumulate over longer periods of time, interfering with normal extracellular matrix interactions and causing advanced glycation end product receptor-mediated pathologic changes in gene expression. In animal models, pharmacologic inhibition of advanced glycation end product formation prevents diabetic complications in the retina, glomerulus, peripheral nerve, and artery. Efficacy results from a study in type I diabetic patients with overt nephropathy are anticipated in the third quarter of 1998.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 291-297 |
| Number of pages | 7 |
| Journal | Current Opinion in Endocrinology and Diabetes |
| Volume | 3 |
| Issue number | 4 |
| DOIs | |
| State | Published - 1996 |
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism
- Endocrinology
