PMID- 17378134
OWN - NLM
STAT- MEDLINE
DCOM- 20070613
LR  - 20171116
IS  - 1769-7255 (Print)
IS  - 1769-7255 (Linking)
VI  - 2 Suppl 1
DP  - 2006 Jan
TI  - [Glycation, glycoxidation and diabetes mellitus].
PG  - S8-16
AB  - Advanced glycation end-products (AGEs) result from a reaction between 
      carbohydrates and the free amino groups of proteins, lipids, and DNA. Non 
      enzymatic glycation, glycoxidation with glucose auto-oxidation and the polyol 
      pathway are involved in glycated protein formation. AGEs also named glycotoxins 
      are found in excess in pathological situations such as diabetes mellitus, renal 
      failure, and aging or after absorption of food containing glycated products. 
      Three major pathophysiological mechanisms are described to explain AGE toxicity, 
      first AGEs can accumulate in the vessel wall and in collagen of different 
      tissues; second in situ glycation is possible; third, AGEs bind to cell receptors 
      inducing deleterious consequences. AGE receptor RAGE is a multiligand member of 
      the immunoglobulin superfamily of cell surface molecules. AGE-receptor 
      interaction can alter, macrophage, endothelial cell, mesangial and mesothelial 
      cell functions and can induce inflammation. Oxidant stress, vascular 
      hyperpermeability, vascular cell adhesion molecule-1 (VCAM-1) overexpression and 
      monocytes chemotactic Protein-1 (MCP-1) production have been observed after cell 
      activation by AGEs. AGEs appear to be involved in the genesis of diabetic macro 
      but also microangiopathy such as retinopathy and glomerulosclerosis. New drugs 
      are tested to prevent or break the AGE-protein cross-linkage, or to control the 
      AGE-receptor interaction and their consequences. Dietary treatment, strict 
      glycemic control and preservation of renal function remain the best approach for 
      preventing AGE formation and limiting their deleterious effects.
FAU - Boulanger, Eric
AU  - Boulanger E
AD  - Clinique de nephrologie, hopital Albert-Calmette, CHRU, boulevard Jules-Leclerc, 
      59037 Lille, France. eboulanger@chru-lille.fr
FAU - Wautier, Jean-Luc
AU  - Wautier JL
FAU - Dequiedt, Philippe
AU  - Dequiedt P
FAU - Schmidt, Anne-Marie
AU  - Schmidt AM
LA  - fre
PT  - Journal Article
PT  - Review
TT  - Glycation, glycoxydation et diabete.
PL  - France
TA  - Nephrol Ther
JT  - Nephrologie & therapeutique
JID - 101248950
RN  - 0 (Glycation End Products, Advanced)
RN  - 0 (Receptor for Advanced Glycation End Products)
RN  - 0 (Receptors, Immunologic)
SB  - IM
MH  - Diabetes Mellitus/*metabolism
MH  - Glycation End Products, Advanced/physiology
MH  - Glycosylation
MH  - Humans
MH  - Receptor for Advanced Glycation End Products
MH  - Receptors, Immunologic/physiology
RF  - 64
EDAT- 2007/03/24 09:00
MHDA- 2007/06/15 09:00
CRDT- 2007/03/24 09:00
PHST- 2007/03/24 09:00 [pubmed]
PHST- 2007/06/15 09:00 [medline]
PHST- 2007/03/24 09:00 [entrez]
PST - ppublish
SO  - Nephrol Ther. 2006 Jan;2 Suppl 1:S8-16.