title: Advanced glycation endproducts and its receptor for advanced glycation endproducts in obesity.
abstract: OBJECTIVE
  To highlight the potential importance of advanced glycation endproducts (AGEs) and advanced-lipoxidation endproducts (ALEs) in obesity and obesity-related complications, and the contribution of the receptor for advanced glycation endproducts (RAGE) and the glyoxylase defense system therein.
  
  
  RESULTS
  Formation of AGEs/ALEs and its precursors, including methylglyoxal (MGO), are increased in conditions characterized by hyperglycemia, hyperlipidemia and enhanced oxidative stress. This metabolic profile is generally considered typical for obesity. Increased plasma and/or tissue levels of MGO and of specific AGEs/ALEs, such as N(ε)-(carboxymethyl)lysine (CML), in obesity have recently been described. In addition to increased formation, the suppressed defense system in obesity against AGEs/ALEs formation, that is, the glyoxylase system, will further contribute to AGEs/ALEs formation in obesity. AGEs/ALEs are not inert. In-vitro studies showed that AGEs induced the production of inflammatory mediators in adipocytes and macrophages via RAGE activation, which may subsequently contribute to the development of obesity-related complications.
  
  
  CONCLUSIONS
  The recognition of an enhanced AGEs/ALEs formation in adipose tissue and the biological consequences thereof may lead to a further understanding of underlying mechanisms in dysregulated production of adipokines in obesity.
authors.affiliation: Department of Internal Medicine, Maastricht University Medical Center, Maastricht, the Netherlands.
authors.forename: Katrien H J
authors.initials: KH
authors.lastname: Gaens
authors.forename: Coen D A
authors.initials: CD
authors.lastname: Stehouwer
authors.forename: Casper G
authors.initials: CG
authors.lastname: Schalkwijk
mesh_terms: D017667:Adipocytes / Q000378:metabolism / Q000473:pathology; D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D006801:Humans; D006949:Hyperlipidemias / Q000378:metabolism / Q000473:pathology; D007791:Lactoylglutathione Lyase / Q000378:metabolism; D015227:Lipid Peroxidation; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D009765:Obesity / Q000378:metabolism / Q000473:pathology*; D018384:Oxidative Stress; D011765:Pyruvaldehyde / Q000378:metabolism; D000067759:Receptor for Advanced Glycation End Products / Q000378:metabolism; D011971:Receptors, Immunologic / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D017127:Glycation End Products, Advanced; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D011765:Pyruvaldehyde; D007791:Lactoylglutathione Lyase