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The Role of Dietary Advanced Glycation End Products on Chronic Diseases

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Clinical Nutrition".

Deadline for manuscript submissions: 5 July 2024 | Viewed by 2553

Special Issue Editors


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Guest Editor
Advanced Glycoscience Research Cluster, School of Biological and Chemical Sciences, National University of Ireland Galway, University Road, H91 W2TY Galway, Ireland
Interests: glycosciences; diagnostics; biomarkers; therapeutics; molecular biomimics; host-microbe interactions
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Guest Editor
Department of Neuroscience “Rita Levi Montalcini”, University of Turin, 10125 Turin, Italy
Interests: metabolic inflammation; NLRP3 inflammasome; diet-induced metabolic diseases; advanced glycation and products
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are excited to invite you to contribute original research papers and/or review articles on the “Role of Advanced Glycation End Products (AGEs) on Chronic Diseases.”

Non-enzymatic glycation is a set of chemical reactions that occur over a period of time when sugars, typically reducing sugars such as glucose or fructose, react with proteins, lipids, or nucleic acids without the involvement of enzymes.

The non-enzymatic glycation process results in a covalent bond between sugars and target molecules, such as amino acid residues of proteins and the lipid molecules, through a series of reactions, including the formation of Schiff base, Amadori product, and Maillard reaction.  These reactions lead to the formation of more stable and irreversible end products known as advanced glycation end products (AGEs). The formation of AGEs is influenced by various factors, including the concentration of reducing sugars, the length of exposure, temperature, pH, and the presence of catalysts, such as metal ions. AGEs can accumulate in various tissues and organs throughout the body, particularly in long-lived proteins such as collagen, leading to tissue damage and dysfunction.

Non-enzymatic glycation and the subsequent formation of AGEs have been implicated in various pathological conditions and chronic diseases, including diabetes, atherosclerosis, chronic kidney disease, neurodegenerative diseases, and aging. The presence of AGEs can alter the structure and function of proteins and lipids, promote inflammation and oxidative stress, and contribute to cellular dysfunction and tissue damage.

There are several dietary sources of advanced glycation end products (AGEs). AGEs can form during food processing, cooking, and storage, of both animal- and plant-derived products. The exact AGE content of foods can vary depending on factors, such as cooking methods, cooking time, temperature, and ingredient composition. Additionally, the total AGE content of a meal can be influenced by the cooking techniques used and the combination of ingredients.

This Special Issue will focus on dietary sources of AGEs and their impact/role in chronic diseases and how to prevent AGE-led diseases through alternative dietary behaviour.

We, thus, invite investigators to contribute with original research articles, as well as review articles, that seek to offer new advances on dietary AGEs and  to explore the pathological manifestations and molecular insights linked to AGEs accumulation, as well as innovative strategies aimed at the prevention/management of the harmful effects of AGEs on health.

Prof. Dr. Lokesh Joshi
Prof. Dr. Massimo Collino
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • advanced glycation end products (AGEs)
  • diet
  • oxidative stress
  • inflammation
  • insulin resistance
  • hyperglycaemia

Published Papers (2 papers)

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Research

13 pages, 466 KiB  
Article
Dietary Advanced Glycation End Products (AGEs) and Urinary Fluorescent AGEs in Children and Adolescents: Findings from the Italian I.Family Project
by Marika Dello Russo, Ivana Sirangelo, Fabio Lauria, Annarita Formisano, Clara Iannuzzi, Antje Hebestreit, Valeria Pala, Alfonso Siani and Paola Russo
Nutrients 2024, 16(12), 1831; https://doi.org/10.3390/nu16121831 - 11 Jun 2024
Viewed by 330
Abstract
Advanced glycation end products (AGEs) have been implicated in chronic diseases in adults, but their role in paediatric populations remains uncertain. This study, conducted on the Italian sample of the I.Family project, aimed to investigate the relationship between dietary and urinary fluorescent AGEs [...] Read more.
Advanced glycation end products (AGEs) have been implicated in chronic diseases in adults, but their role in paediatric populations remains uncertain. This study, conducted on the Italian sample of the I.Family project, aimed to investigate the relationship between dietary and urinary fluorescent AGEs in children and adolescents. The secondary objective was to investigate the sources of dietary AGEs (dAGEs) and their association with dietary composition and anthropometric parameters. Dietary data were collected from 1048 participants via 24 h dietary recall in 2013/2014 to estimate dAGEs intake, while urinary fluorescent AGE levels were measured in 544 individuals. Participants were stratified based on dAGEs intake and compared with respect to urinary fluorescent AGE levels, anthropometric measurements, and dietary intake. The results showed no significant correlation between dietary and urinary fluorescent AGE levels, nor between dAGEs and anthropometric parameters. Notably, higher dAGEs were associated with a diet richer in protein (especially from meat sources) and fat and lower in carbohydrates. In addition, the consumption of ultra-processed foods was lower in participants with a higher DAGE intake. This study highlights the lack of a clear association between dietary and urinary fluorescent AGEs in children, but suggests a distinctive dietary pattern associated with increased dAGEs intake. Further investigation is warranted to elucidate the potential health implications of dAGEs in paediatric populations. Full article
23 pages, 5705 KiB  
Article
Different Effects of High-Fat/High-Sucrose and High-Fructose Diets on Advanced Glycation End-Product Accumulation and on Mitochondrial Involvement in Heart and Skeletal Muscle in Mice
by Eleonora Aimaretti, Guglielmina Chimienti, Chiara Rubeo, Rosa Di Lorenzo, Lucia Trisolini, Federica Dal Bello, Atefeh Moradi, Massimo Collino, Angela Maria Serena Lezza, Manuela Aragno and Vito Pesce
Nutrients 2023, 15(23), 4874; https://doi.org/10.3390/nu15234874 - 22 Nov 2023
Cited by 2 | Viewed by 1796
Abstract
Diets with an elevated content of fat, sucrose, or fructose are recognized models of diet-induced metabolic alterations, since they induce metabolic derangements, oxidative stress, and chronic low-grade inflammation associated with local and systemic accumulation of advanced glycation end-products (AGEs). This study used four-week-old [...] Read more.
Diets with an elevated content of fat, sucrose, or fructose are recognized models of diet-induced metabolic alterations, since they induce metabolic derangements, oxidative stress, and chronic low-grade inflammation associated with local and systemic accumulation of advanced glycation end-products (AGEs). This study used four-week-old C57BL/6 male mice, randomly assigned to three experimental dietary regimens: standard diet (SD), high-fat high-sucrose diet (HFHS), or high fructose diet (HFr), administered for 12 weeks. Plasma, heart, and tibialis anterior (TA) skeletal muscle were assayed for markers of metabolic conditions, inflammation, presence of AGEs, and mitochondrial involvement. The HFHS diet induced a tissue-specific differential response featuring (1) a remarkable adaptation of the heart to HFHS-induced heavy oxidative stress, demonstrated by an increased presence of AGEs and reduced mitochondrial biogenesis, and efficaciously counteracted by a conspicuous increase in mitochondrial fission and PRXIII expression; (2) the absence of TA adaptation to HFHS, revealed by a heavy reduction in mitochondrial biogenesis, not counteracted by an increase in fission and PRXIII expression. HFr-induced mild oxidative stress elicited tissue-specific responses, featuring (1) a decrease in mitochondrial biogenesis in the heart, likely counteracted by a tendency for increased fission and (2) a mild reduction in mitochondrial biogenesis in TA, likely counteracted by a tendency for increased fusion, showing the adaptability of both tissues to the diet. Full article
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