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- November 19, 2008 |
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"Advanced Glycation in Diabetic Complications"Dr. Stephen Twigg (biography)
English - 2005-03-15 - 47 minutes
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Summary :
Advanced glycation end-products (AGEs) are increased in diabetes and can be formed endogenously or be derived from dietary sources or cigarette tar. The AGE pathway is one of several mechanisms that have been implicated in glucose-mediated vascular damage (1).
AGEs can exert their pathological effects for example through covalent cross-linking with proteins and lipids or by activating cell surface receptors for AGEs. Dr. Twigg reviews studies done in animal models of diabetes showing: the effects of inhibition of advanced glycation with aminoguanidine on the regulation of CTGF (connective tissue growth factor) and fibronectin in diabetic nephropathy (2), the effect of cleavage of pre-formed AGE crosslinks with ALT-711 on diabetes-induced cardiac disease (3) and the apparent association between dietary AGEs and diabetes-accelerated atherosclerosis (4).
Dr. Twigg concludes his presentation with a look at preliminary data in human diabetic subjects from Vlassara and colleagues showing increased inflammatory mediators associated with a diet high in AGEs (5).
Copyright © 2005 E-MedHosting.com Inc.
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- The formation and pathological effects of advanced glycation end-products (AGEs);
- Effects of the inhibition of AGE formation and cleavage of pre-formed AGE crosslinks in animal models of diabetes;
- Preliminary data in human diabetic subjects on the effects of dietary AGEs.
Bibliographic references :
1. MICHAEL BROWNLEE. Biochemistry and molecular cell biology of diabetic complicationsNature. 2001;414:813-820.
2. Stephen M. Twigg, Zemin Cao, Sue V. MCLennan, Wendy C. Burns, Gail Brammar, Josephine M. Forbes and Mark E. Cooper. Renal Connective Tissue Growth Factor Induction in Experimental Diabetes Is Prevented by Aminoguanidine Endocrinology. 2002; 143(12):4907-4915.
3. Riccardo Candido, Josephine M. Forbes, Merlin C. Thomas, Vicki Thallas, Rachael G. Dean, Wendy C. Burns, Christos Tikellis, Rebecca H. Ritchie, Stephen M. Twigg, Mark E. Cooper, Louise M. Burrell
A Breaker of Advanced Glycation End Products Attenuates Diabetes-Induced Myocardial Structural Changes Circulation Research. 2003;92:785.
4. Reigh-Yi Lin, Robin P. Choudhury, Weijing Cai, Min Lu, John T. Fallon, Edward A. Fisher and Helen Vlassara. Dietary glycotoxins promote diabetic atherosclerosis in apolipoprotein E-deficient mice Atherosclerosis. Volume 168, Issue 2 , June 2003, Pages 213-220.
5. Vlassara H, Cai W, Crandall J, Goldberg T, Oberstein R, Dardaine V, Peppa M, Rayfield EJ. Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy.
Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15596-601.
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