Jean L J M Scheijen1, Nordin M J Hanssen2, Marleen M van Greevenbroek3, Carla J Van der Kallen4, Edith J M Feskens5, Coen D A Stehouwer6, Casper G Schalkwijk7. 1. Department of Internal Medicine, Laboratory for Metabolism and Vascular Medicine, Maastricht University, Maastricht, The Netherlands; Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands. Electronic address: j.scheijen@maastrichtuniversity.nl. 2. Department of Internal Medicine, Laboratory for Metabolism and Vascular Medicine, Maastricht University, Maastricht, The Netherlands; Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands. Electronic address: nmj.hanssen@maastrichtuniversity.nl. 3. Department of Internal Medicine, Laboratory for Metabolism and Vascular Medicine, Maastricht University, Maastricht, The Netherlands; Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands. Electronic address: m.vangreevenbroek@maastrichtuniversity.nl. 4. Department of Internal Medicine, Laboratory for Metabolism and Vascular Medicine, Maastricht University, Maastricht, The Netherlands; Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands. Electronic address: c.vanderkallen@maastrichtuniversity.nl. 5. Division of Human Nutrition, Section Nutrition and Epidemiology, Wageningen University, Wageningen, The Netherlands. Electronic address: edith.feskens@wur.nl. 6. Department of Internal Medicine, Laboratory for Metabolism and Vascular Medicine, Maastricht University, Maastricht, The Netherlands; Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands. Electronic address: cda.stehouwer@mumc.nl. 7. Department of Internal Medicine, Laboratory for Metabolism and Vascular Medicine, Maastricht University, Maastricht, The Netherlands; Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands. Electronic address: c.schalkwijk@maastrichtuniversity.nl.
Abstract
BACKGROUND & AIMS: Advanced glycation endproducts (AGEs) are formed by the reaction between reducing sugars and proteins. AGEs in the body have been associated with several age-related diseases. High-heat treated and most processed foods are rich in AGEs. The aim of our study was to investigate whether dietary AGEs, are associated with plasma and urinary AGE levels. METHODS: In 450 participants of the Cohort on Diabetes and Atherosclerosis Maastricht study (CODAM study) we measured plasma and urine concentrations of the AGEs Nε-(carboxymethyl)lysine (CML), Nε-(1-carboxyethyl)lysine (CEL) and Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1) using UPLC-MS/MS. We also estimated dietary intake of CML, CEL and MG-H1 with the use of a dietary AGE database and a food frequency questionnaire (FFQ). We used linear regression to investigate the association between standardized dietary AGE intake and standardized plasma or urinary AGE levels, after adjustment for age, sex, glucose metabolism status, waist circumference, kidney function, energy- and macro-nutrient intake, smoking status, physical activity, alcohol intake, LDL-cholesterol and markers of oxidative stress. RESULTS: We found that higher intake of dietary CML, CEL and MG-H1 was associated with significantly higher levels of free plasma and urinary CML, CEL and MG-H1 (βCML = 0.253 (95% CI 0.086; 0.415), βCEL = 0.194 (95% CI 0.040; 0.339), βMG-H1 = 0.223 (95% CI 0.069; 0.373) for plasma and βCML = 0.223 (95% CI 0.049; 0.393), βCEL = 0.180 (95% CI 0.019; 0.332), βMG-H1 = 0.196 (95% CI 0.037; 0.349) for urine, respectively). In addition, we observed non-significant associations of dietary AGEs with their corresponding protein bound plasma AGEs. CONCLUSION: We demonstrate that higher intake of dietary AGEs is associated with higher levels of AGEs in plasma and urine. Our findings may have important implications for those who ingest a diet rich in AGEs.
BACKGROUND & AIMS: Advanced glycation endproducts (AGEs) are formed by the reaction between reducing sugars and proteins. AGEs in the body have been associated with several age-related diseases. High-heat treated and most processed foods are rich in AGEs. The aim of our study was to investigate whether dietary AGEs, are associated with plasma and urinary AGE levels. METHODS: In 450 participants of the Cohort on Diabetes and Atherosclerosis Maastricht study (CODAM study) we measured plasma and urine concentrations of the AGEs Nε-(carboxymethyl)lysine (CML), Nε-(1-carboxyethyl)lysine (CEL) and Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1) using UPLC-MS/MS. We also estimated dietary intake of CML, CEL and MG-H1 with the use of a dietary AGE database and a food frequency questionnaire (FFQ). We used linear regression to investigate the association between standardized dietary AGE intake and standardized plasma or urinary AGE levels, after adjustment for age, sex, glucose metabolism status, waist circumference, kidney function, energy- and macro-nutrient intake, smoking status, physical activity, alcohol intake, LDL-cholesterol and markers of oxidative stress. RESULTS: We found that higher intake of dietary CML, CEL and MG-H1 was associated with significantly higher levels of free plasma and urinary CML, CEL and MG-H1 (βCML = 0.253 (95% CI 0.086; 0.415), βCEL = 0.194 (95% CI 0.040; 0.339), βMG-H1 = 0.223 (95% CI 0.069; 0.373) for plasma and βCML = 0.223 (95% CI 0.049; 0.393), βCEL = 0.180 (95% CI 0.019; 0.332), βMG-H1 = 0.196 (95% CI 0.037; 0.349) for urine, respectively). In addition, we observed non-significant associations of dietary AGEs with their corresponding protein bound plasma AGEs. CONCLUSION: We demonstrate that higher intake of dietary AGEs is associated with higher levels of AGEs in plasma and urine. Our findings may have important implications for those who ingest a diet rich in AGEs.
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
Authors: Armand Ma Linkens; Simone Jmp Eussen; Alfons Jhm Houben; Abraham A Kroon; Miranda T Schram; Koen D Reesink; Pieter C Dagnelie; Ronald Ma Henry; Marleen van Greevenbroek; Anke Wesselius; Coen Da Stehouwer; Casper G Schalkwijk Journal: J Nutr Date: 2021-07-01 Impact factor: 4.798