ArticleDiabetes2011
Advanced glycation end products are direct modulators of β-cell function.
Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 151 citations in OpenAlex.
- Dietary Advanced Glycation End Products and Risk Factors for Chronic Disease: A Systematic Review of Randomised Controlled Trials.Nutrients · 2016Pooled it
- Dietary advanced glycation end-product restriction for the attenuation of insulin resistance, oxidative stress and endothelial dysfunction: a systematic review.European journal of clinical nutrition · 2013Pooled it
- Dietary Advanced Glycation End Products in an Elderly Population with Diabetic Nephropathy: An Exploratory Investigation.Nutrients · 2022Trial
- A 4-week high-AGE diet does not impair glucose metabolism and vascular function in obese individuals.JCI insight · 2022Trial
- Trial
- Dysfunctional protection against advanced glycation due to thiamine metabolism abnormalities in gestational diabetes.Glycoconjugate journal · 2016Trial
- Effect of dietary prebiotic supplementation on advanced glycation, insulin resistance and inflammatory biomarkers in adults with pre-diabetes: a study protocol for a double-blind placebo-controlled randomised crossover clinical trial.BMC endocrine disorders · 2014Trial
- Review
- Red meat intake during pregnancy and childhood and risk of type 1 diabetes: findings from the ABIS birth cohort.Diabetologia · 2026Article
- Environmental Mechanisms Influencing the Pathogenesis and Progression of Type 1 Diabetes.International journal of molecular sciences · 2025Review
- Type 1 diabetes mellitus prevention: present and future.Nature reviews. Endocrinology · 2025Review
- Association between enteral carboxymethyllysine intake and daily glycemic variability in critically ill adults: A retrospective cohort study.JPEN. Journal of parenteral and enteral nutrition · 2025Article
- Maternal AGE Precursors During Lactation Alters Offspring Glycemic Homeostasis Early in Life.Biology · 2025Article
- New Glycotoxin Inhibitor fromMolecules (Basel, Switzerland) · 2024Article
- Protein Advanced Glycation End Products and Their Implications in Pancreatic Cancer.Cancer prevention research (Philadelphia, Pa.) · 2023Review
- Alpha cell receptor for advanced glycation end products associate with glucagon expression in type 1 diabetes.Scientific reports · 2023Article
- Biomarkers of aging.Science China. Life sciences · 2023Review
- Review
- Pyroptosis and Insulin Resistance in Metabolic Organs.International journal of molecular sciences · 2022Review
- Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveExcess accumulation of advanced glycation end products (AGEs) contributes to aging and chronic diseases. We aimed to obtain evidence that exposure to AGEs plays a role in the development of type 1 diabetes (T1D). RESEARCH DESIGN AND
methodsThe effect of AGEs was examined on insulin secretion by MIN6N8 cells and mouse islets and in vivo in three separate rodent models: AGE-injected or high AGE-fed Sprague-Dawley rats and nonobese diabetic (NODLt) mice. Rodents were also treated with the AGE-lowering agent alagebrium.
resultsβ-Cells exposed to AGEs displayed acute glucose-stimulated insulin secretory defects, mitochondrial abnormalities including excess superoxide generation, a decline in ATP content, loss of MnSOD activity, reduced calcium flux, and increased glucose uptake, all of which were improved with alagebrium treatment or with MnSOD adenoviral overexpression. Isolated mouse islets exposed to AGEs had decreased glucose-stimulated insulin secretion, increased mitochondrial superoxide production, and depletion of ATP content, which were improved with alagebrium or with MnTBAP, an SOD mimetic. In rats, transient or chronic exposure to AGEs caused progressive insulin secretory defects, superoxide generation, and β-cell death, ameliorated with alagebrium. NODLt mice had increased circulating AGEs in association with an increase in islet mitochondrial superoxide generation, which was prevented by alagebrium, which also reduced the incidence of autoimmune diabetes. Finally, at-risk children who progressed to T1D had higher AGE concentrations than matched nonprogressors.
conclusionsThese findings demonstrate that AGEs directly cause insulin secretory defects, most likely by impairing mitochondrial function, which may contribute to the development of T1D.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.