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Academic Journal
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van Dongen KCW; Division of Toxicology, Wageningen University and Research, Stippeneng 4, 6708 WE Wageningen, the Netherlands. Electronic address: katja.vandongen@wur.nl.
Linkens AMA; Department of Internal Medicine, Maastricht University Medical Centre, Universiteitssingel 50, 6200MD Maastricht, the Netherlands; CARIM School for Cardiovascular Diseases, Maastricht University, Universiteitssingel 50, 6229ER Maastricht, the Netherlands. Electronic address: Armand.linkens@maastrichtuniversity.nl.
Wetzels SMW; CARIM School for Cardiovascular Diseases, Maastricht University, Universiteitssingel 50, 6229ER Maastricht, the Netherlands; Department of Pathology, Maastricht University Medical Centre, P. Debyelaan 25, 6229HX, the Netherlands. Electronic address: suzan.wetzels@mumc.nl.
Wouters K; Department of Internal Medicine, Maastricht University Medical Centre, Universiteitssingel 50, 6200MD Maastricht, the Netherlands; CARIM School for Cardiovascular Diseases, Maastricht University, Universiteitssingel 50, 6229ER Maastricht, the Netherlands. Electronic address: kristiaan.wouters@maastrichtuniversity.nl.
Vanmierlo T; Department of Psychiatry & Neuropsychology, School for Mental Health and Neuroscience, Maastricht University, Dr Tanslaan 10, 6229ET Maastricht, the Netherlands; Department of Neuroimmunology, Biomedical Research Institute, Hasselt University, Agoralaan gebouw D, BE3590 Diepenbeek, Belgium. Electronic address: tim.vanmierlo@uhasselt.be.
van de Waarenburg MPH; Department of Internal Medicine, Maastricht University Medical Centre, Universiteitssingel 50, 6200MD Maastricht, the Netherlands; CARIM School for Cardiovascular Diseases, Maastricht University, Universiteitssingel 50, 6229ER Maastricht, the Netherlands. Electronic address: m.vandewaarenburg@maastrichtuniversity.nl.
Scheijen JLJM; Department of Internal Medicine, Maastricht University Medical Centre, Universiteitssingel 50, 6200MD Maastricht, the Netherlands; CARIM School for Cardiovascular Diseases, Maastricht University, Universiteitssingel 50, 6229ER Maastricht, the Netherlands. Electronic address: j.scheijen@maastrichtuniversity.nl.
de Vos WM; Laboratory of Microbiology, Wageningen University and Research, Stippeneng 4, 6708 WE Wageningen, the Netherlands; Human Microbiome Research Program, Faculty of Medicine, University of Helsinki, Haartmaninkatu 3, Finland. Electronic address: willem.devos@wur.nl.
Belzer C; Laboratory of Microbiology, Wageningen University and Research, Stippeneng 4, 6708 WE Wageningen, the Netherlands. Electronic address: clara.belzer@wur.nl.
Schalkwijk CG; Department of Internal Medicine, Maastricht University Medical Centre, Universiteitssingel 50, 6200MD Maastricht, the Netherlands; CARIM School for Cardiovascular Diseases, Maastricht University, Universiteitssingel 50, 6229ER Maastricht, the Netherlands. Electronic address: C.Schalkwijk@maastrichtuniversity.nl. -
Food research international (Ottawa, Ont.) [Food Res Int] 2021 Sep; Vol. 147, pp. 110547. Date of Electronic Publication: 2021 Jun 18.
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English
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Scope: Dietary advanced glycation endproducts (AGEs) are associated with negative biological effects, possibly due to accumulation in plasma and tissues and through modulation of inflammation and gut microbiota. Whether these biological consequences are reversible by limiting dietary AGE intake is unknown.
Methods and Results: Young healthy C57BL/6 mice were fed a standard chow (n = 10) or a baked chow high AGE-diet (n = 10) (~1.8-6.9 fold increased protein-bound Nε-(carboxymethyl)lysine (CML), Nε-(1-carboxyethyl)lysine (CEL), and Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1)) for 10 weeks or a switch diet with baked chow for 5 weeks followed by 5 weeks of standard chow (n = 10). We assessed accumulation of AGEs in plasma, kidney, and liver and measured inflammatory markers and gut microbial composition. After 10 weeks of baked chow, a substantial panel of AGEs were increased in plasma, liver, and kidney. These increases were normalized after the switch diet. The inflammatory z-score increased after the baked chow diet. Gut microbial composition differed significantly between groups, with enriched Dubosiella spp. dominating these alterations.
Conclusion: A high AGE-diet led to an increase of AGEs in plasma, kidney, and liver and to more inflammation and modification of the gut microbiota. These effects were reversed or discontinued by a diet lower in AGEs.
(Copyright © 2021. Published by Elsevier Ltd.)
Additional Information
Publisher: Published on behalf of the Canadian Institute of Food Science and Technology by Elsevier Applied Science Country of Publication: Canada NLM ID: 9210143 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-7145 (Electronic) Linking ISSN: 09639969 NLM ISO Abbreviation: Food Res Int Subsets: MEDLINE
Original Publication: Ottawa, Ontario, Canada : Published on behalf of the Canadian Institute of Food Science and Technology by Elsevier Applied Science, c1992-
Keywords: 16S rRNA sequencing; Dietary advanced glycation endproducts; Gut microbiota; Ultra-performance liquid chromatography tandem mass spectrometry
0 (Glycation End Products, Advanced)
Date Created: 20210817 Date Completed: 20210906 Latest Revision: 20210906
20230925
10.1016/j.foodres.2021.110547
34399524