CoChat
Sign Up
Cited by 239Advanced Glycation End Products researchDiet, Metabolism, and DiseasePotato Plant Research

The DOI matches its Crossref record; 113 of the 114 references it cites were found in a registry or an index.

Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease

Open access
Aragno, Manuela, Mastrocola, Raffaella·2017·Nutrients
DOI 10.3390/nu9040385PMC PMC5409724

Published version of a preprint

Open this paper in CoChat — free accountOpen PDF

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.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3390/nu9040385

Cites

113 of 113 references verified0 citation errors · 0 not checkable

Statistics

Figures

Scheme 1 Fructose and glucose metabolism and proposed effects for dietary sugar-induced glycation. Fructose bypasses the rate limiting step of glycolysis leading to a faster generation of dicarbonyl precursors than glucose. AGE accumulation in tissues can interfere with many protein functions contributing to the onset of metabolic diseases and related comorbidities.
Scheme 1 Fructose and glucose metabolism and proposed effects for dietary sugar-induced glycation. Fructose bypasses the rate limiting step of glycolysis leading to a faster generation of dicarbonyl precursors than glucose. AGE accumulation in tissues can interfere with many protein functions contributing to the onset of metabolic diseases and related comorbidities.CC BY · PubMed Central
Scheme 2 The polyol pathway. In conditions of excess of glucose, as occurring in diabetes, glucose undertakes the polyol pathway to be converted to fructose through the consecutive action of aldose reductase and sorbitol dehydrogenase. This alternative pathway for the metabolism of glucose leads to the increase in fructose levels in tissues of diabetic patients and of the NADH/NAD+ ratio that contrasts GAP-dehydrogenase activity leading to accumulation of the triose phosphates GAP and DHAP, precursors of the dicarbonyls compounds glyoxal (GO) and methylglyoxal (MGO).
Scheme 2 The polyol pathway. In conditions of excess of glucose, as occurring in diabetes, glucose undertakes the polyol pathway to be converted to fructose through the consecutive action of aldose reductase and sorbitol dehydrogenase. This alternative pathway for the metabolism of glucose leads to the increase in fructose levels in tissues of diabetic patients and of the NADH/NAD+ ratio that contrasts GAP-dehydrogenase activity leading to accumulation of the triose phosphates GAP and DHAP, precursors of the dicarbonyls compounds glyoxal (GO) and methylglyoxal (MGO).CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

1 retracted

Show all 114 references

Cited by

Sorted by citations

Related

See all

Metadata

Authors
Aragno, M., & Mastrocola, R.
Affiliations
University of Turin (IT)
Corresponding author
Mastrocola, Raffaella
ORCID
Venue
Nutrients
Publisher
MDPI AG
Published
2017-04-14
Volume
9
Issue
4
Pages
385
ISSN
2072-6643 (ISSN-L)
DOI
10.3390/nu9040385
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
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review