Cited by 594Advanced Glycation End Products researchPotato Plant ResearchAdipokines, Inflammation, and Metabolic Diseases

Advanced Glycation End Products (AGE) and Diabetes: Cause, Effect, or Both?

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Vlassara, Helen, Uribarri, Jaime·2014·Current Diabetes Reports

Abstract

Despite new and effective drug therapies, insulin resistance (IR), type 2 diabetes mellitus (T2D) and its complications remain major medical challenges. It is accepted that IR, often associated with over-nutrition and obesity, results from chronically elevated oxidant stress (OS) and chronic inflammation. Less acknowledged is that a major cause for this inflammation is excessive consumption of advanced glycation end products (AGEs) with the standard western diet. AGEs, which were largely thought as oxidative derivatives resulting from diabetic hyperglycemia, are increasingly seen as a potential risk for islet β-cell injury, peripheral IR and diabetes. Here we discuss the relationships between exogenous AGEs, chronic inflammation, IR, and T2D. We propose that under chronic exogenous oxidant AGE pressure the depletion of innate defense mechanisms is an important factor, which raises susceptibility to inflammation, IR, T2D and its complications. Finally we review evidence on dietary AGE restriction as a nonpharmacologic intervention, which effectively lowers AGEs, restores innate defenses and improves IR, thus, offering new perspectives on diabetes etiology and therapy.

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  • In both animal models and human studies, exposure to high levels of dietary AGEs during fetal development triggers metabolic reprogramming leading to T2DM independently of genetic predisposition.

    “Additionally, in both animal models and human studies exposure to high levels of dietary AGEs during fetal development has been shown to trigger metabolic reprogramming which leads to the development of T2DM independently of any genetic predisposition.[125,126]”

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Authors
Vlassara, H., & Uribarri, J.
Affiliations
Icahn School of Medicine at Mount Sinai (US)
Corresponding author
Uribarri, Jaime
Venue
Current Diabetes Reports
Published
2013-11-29
Volume
14
Issue
1
Pages
453-453
ISSN
  • 1534-4827 (ISSN-L)
  • 1539-0829
OpenAlex
W2153249592
Cited by
594
References
78
Citations by year
2026: 28 · 2025: 38 · 2024: 53 · 2023: 72 · 2022: 69 · 2021: 62 · 2020: 70 · 2019: 47 · 2018: 59 · 2017: 28 · 2016: 30 · 2015: 26 · 2014: 12
FWCI
2.35
Type
journal article
Language
en
Open access
Locations
  • Current Diabetes Reports (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (AG23188, R37AG023188, AG09453, R01AG009453)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK091231)
  • National Center for Research Resources (M01RR000071, M01-RR-00071)
  • NIH Clinical Center
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Potato Plant Research
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
advanced glycation end products, type 2 diabetes, insulin resistance, chronic inflammation, oxidative stress, innate immunity, beta-cell injury, Western diet, diabetes complications
MeSH terms
Diabetes Mellitus, Type 2, Female, Humans, Pregnancy, Diabetes, Gestational, Glycation End Products, Advanced

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