Glucose, Advanced Glycation End Products, and Diabetes Complications: What Is New and What Works
Abstract
Editor’s note: This is one in a series of articles from the various professional section councils of the American Diabetes Association. This installment is from the Council on Complications. The incidence of diabetes, particularly type 2 diabetes, is increasing at an alarming rate. Worldwide, about 124 million people had diabetes by1997; by 2010, this number is estimated to reach 221 million. Because of the large number of severe pathologies complicating the clinical course of diabetes, one can easily speculate on the huge economic and psychosocial impact of diabetes across age groups and geographical regions. A large number of studies have focused on the factors involved in the pathogenesis of diabetic complications, most seeking effective therapies, but the exact cellular or molecular basis of these complications has not yet been fully elucidated. Hyperglycemia is still considered the principal cause of diabetes complications. Its deleterious effects are attributable, among other things, to the formation of sugar-derived substances called advanced glycation end products (AGEs). AGEs form at a constant but slow rate in the normal body, starting in early embryonic development, and accumulate with time. However, their formation is markedly accelerated in diabetes because of the increased availability of glucose. AGEs are a heterogeneous group of molecules formed from the nonenzymatic reaction of reducing sugars with free amino groups of proteins, lipids, and nucleic acids. The initial product of this reaction is called a Schiff base, which spontaneously rearranges itself into an Amadori product, as is the case of the well-known hemoglobin A1c (A1C). These initial reactions are reversible depending on the concentration of the reactants. A lowered glucose concentration will unhook the sugars from the amino groups to which they are attached; conversely, high glucose …
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Endogenous AGEs are produced and slowly accumulated within the body during normal aging and under oxidative stress, inflammatory, and hyperglycemic conditions often observed in diabetes and other metabolic syndromes.
“Endogenous AGEs represent adducts that are produced and slowly accumulated within the body during the normal aging process and under the oxidative stress, inflammatory, and hyperglycemic (high blood sugar) conditions often observed in diabetes and other metabolic syndromes1,4,12,13.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [13]
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Metabolism and Health Effects of Rare Sugars in a CACO-2/HepG2 Coculture Model
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“Fructose may have impacted metabolic health via the AGE-RAGE pathway in HepG2 cells, as a pathway related with diabetes pathology and vascular complications [78,79].”
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“A large body of evidence suggests that AGEs are important pathogenetic mediators of almost all diabetes complication [36, 43].”
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“They are the protagonists in the pathogenesis of diabetes associated diseases and contribute to the DVLC such as hypertension, dyslipidemia and low-level inflammation [29,30].”
BackgroundProdutos da glicação avançada dietéticos e as complicações crônicas do diabetes
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“In the normal body, advanced glycated end products (AGEs) form at a slow rate, while in diabetes their formation accelerates due to chronically high concentration of blood sugar, which enhances the availability of glucose [14].”
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Elderly Adults and Skin Disorders
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“Although biochemical and immunochemical studies of AGEs can provide direct information about the structure, molecular formation and its binding receptors [8–10], it is AGE autofluorescence that allows noninvasive evaluation and quantification of tissue glycation for monitoring of long-term diabetic complications.”
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- Authors
- Peppa, M., Uribarri, J., & Vlassara, H.
- ORCID
- Uribarri, Jaime
- Venue
- Clinical Diabetes
- Publisher
- American Diabetes Association
- Published
- 2003-10-01
- Volume
- 21
- Issue
- 4
- Pages
- 186-187
- ISSN
- 0891-8929 (ISSN-L)
- 1945-4953
- OpenAlex
- W2141098534
- Cited by
- 234
- References
- 0
- Citations by year
- 2026: 6 · 2025: 8 · 2024: 3 · 2023: 10 · 2022: 11 · 2021: 18 · 2020: 8 · 2019: 6 · 2018: 16 · 2017: 14 · 2016: 11 · 2015: 19 · 2014: 14 · 2013: 15 · 2012: 17
- FWCI
- 1.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Diabetes (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Keywords
- advanced glycation end products, hyperglycemia, diabetes complications, type 2 diabetes, glycation, Schiff base, Amadori products, HbA1c, glucose
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