N ε -(Carboxymethyl)lysine-Receptor for Advanced Glycation End Product Axis Is a Key Modulator of Obesity-Induced Dysregulation of Adipokine Expression and Insulin Resistance
Author(s) -
Katrien H.J. Gaens,
Gijs H. Goossens,
Petra Niessen,
Marleen M. J. van Greevenbroek,
Carla Kallen,
Hans W.M. Niessen,
Sander S. Rensen,
Wim A. Buurman,
Jan Greve,
Ellen E. Blaak,
Marc A. van Zandvoort,
Angelika Bierhaus,
Coen D.A. Stehouwer,
Casper G. Schalkwijk
Publication year - 2014
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.113.302281
Subject(s) - adipokine , insulin resistance , glycation , advanced glycation end product , lysine , endocrinology , medicine , receptor , chemistry , insulin , obesity , insulin receptor , microbiology and biotechnology , biology , biochemistry , amino acid
Dysregulation of inflammatory adipokines by the adipose tissue plays an important role in obesity-associated insulin resistance. Pathways leading to this dysregulation remain largely unknown. We hypothesized that the receptor for advanced glycation end products (RAGE) and the ligand N(ε)-(carboxymethyl)lysine (CML) are increased in adipose tissue and, moreover, that activation of the CML-RAGE axis plays an important role in obesity-associated inflammation and insulin resistance.
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