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Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease
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Abstract
The rapid increase in metabolic diseases, which occurred in the last three decades in both industrialized and developing countries, has been related to the rise in sugar-added foods and sweetened beverages consumption. An emerging topic in the pathogenesis of metabolic diseases related to modern nutrition is the role of Advanced Glycation Endproducts (AGEs). AGEs can be ingested with high temperature processed foods, but also endogenously formed as a consequence of a high dietary sugar intake. Animal models of high sugar consumption, in particular fructose, have reported AGE accumulation in different tissues in association with peripheral insulin resistance and lipid metabolism alterations. The in vitro observation that fructose is one of the most rapid and effective glycating agents when compared to other sugars has prompted the investigation of the in vivo fructose-induced glycation. In particular, the widespread employment of fructose as sweetener has been ascribed by many experimental and observational studies for the enhancement of lipogenesis and intracellular lipid deposition. Indeed, diet-derived AGEs have been demonstrated to interfere with many cell functions such as lipid synthesis, inflammation, antioxidant defences, and mitochondrial metabolism. Moreover, emerging evidence also in humans suggest that this impact of dietary AGEs on different signalling pathways can contribute to the onset of organ damage in liver, skeletal and cardiac muscle, and the brain, affecting not only metabolic control, but global health. Indeed, the most recent reports on the effects of high sugar consumption and diet-derived AGEs on human health reviewed here suggest the need to limit the dietary sources of AGEs, including added sugars, to prevent the development of metabolic diseases and related comorbidities.
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“In addition to nonenzymatic glycation, AGEs can be formed through the polyol pathway and lipid peroxidation in the presence and absence of hyperglycemia, depending on the substrate type, reactant concentration, exposure time, and host cellular context14–17.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [14]
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Metadata
- Authors
- Aragno, M., & Mastrocola, R.
- Affiliations
- University of Turin (IT)
- Corresponding author
- Mastrocola, Raffaella
- Venue
- Nutrients
- Publisher
- MDPI AG
- Published
- 2017-04-14
- Volume
- 9
- Issue
- 4
- Pages
- 385
- ISSN
- 2072-6643 (ISSN-L)
- PMC
- PMC5409724
- OpenAlex
- W2593393776
- Cited by
- 239
- References
- 114
- Citations by year
- 2026: 10 · 2025: 23 · 2024: 27 · 2023: 24 · 2022: 34 · 2021: 36 · 2020: 28 · 2019: 33 · 2018: 14 · 2017: 10
- FWCI
- 3.04
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nutrients (publishedVersion, cc-by)
- Preprints.org (acceptedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion, other-oa)
- Funders
- Università degli Studi di Torino
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Life Sciences › Agricultural and Biological Sciences › Food Science › Potato Plant Research
- Keywords
- advanced glycation end products, dietary sugar, fructose, insulin resistance, lipid metabolism, lipogenesis, inflammation, mitochondrial metabolism, antioxidant defense, metabolic disorders, organ damage, sweetened beverages, added sugars
- MeSH terms
- Animals, Brain, Diet, Feeding Behavior, Fructose, Glycosylation, Heart, Humans, Insulin Resistance, Liver, Metabolic Diseases, Muscles, Sweetening Agents, Glycation End Products, Advanced, Lipid Metabolism
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