PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: 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.
PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: 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: Lucas M M Vianna; Christopher G Stoeger; Joshua D Galloway; Mark Terry; Leslie Cope; Rubens Belfort; Albert S Jun Journal: Am J Ophthalmol Date: 2015-01-30 Impact factor: 5.258
Authors: Jeanette E Eckel-Passow; Daniel J Serie; Brian M Bot; Richard W Joseph; Steven N Hart; John C Cheville; Alexander S Parker Journal: Carcinogenesis Date: 2013-12-28 Impact factor: 4.944
Authors: R Cordova; V Knaze; V Viallon; P Rust; C G Schalkwijk; E Weiderpass; K-H Wagner; A-L Mayen-Chacon; E K Aglago; C C Dahm; K Overvad; A Tjønneland; J Halkjær; F R Mancini; M-C Boutron-Ruault; G Fagherazzi; V Katzke; T Kühn; M B Schulze; H Boeing; A Trichopoulou; A Karakatsani; P Thriskos; G Masala; V Krogh; S Panico; R Tumino; F Ricceri; A Spijkerman; J Boer; G Skeie; C Rylander; K B Borch; J R Quirós; A Agudo; D Redondo-Sánchez; P Amiano; J-H Gómez-Gómez; A Barricarte; S Ramne; E Sonestedt; I Johansson; A Esberg; T Tong; D Aune; K K Tsilidis; M J Gunter; M Jenab; Heinz Freisling Journal: Eur J Nutr Date: 2019-11-07 Impact factor: 5.614