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The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction
Open accessAbstract
Advanced glycation end products (AGEs) are a heterogeneous group of molecules produced, non‐enzymatically, from the interaction between reducing sugars and the free amino groups of proteins, nucleic acids, and lipids. AGEs are formed as a normal consequence of metabolism but can also be absorbed from the diet. They have been widely implicated in the complications of diabetes affecting cardiovascular health, the nervous system, eyes, and kidneys. Increased levels of AGEs are also detrimental to metabolic health and may contribute to the metabolic abnormalities induced by the Western diet, which is high in processed foods and represents a significant source of AGEs. While increased AGE levels are a consequence of diabetic hyperglycaemia, AGEs themselves activate signaling pathways, which compromise insulin signaling and pancreatic β‐cell function, thus, contributing to the development of type 2 diabetes mellitus (T2DM). Furthermore, AGEs may also contribute to the obesogenic effects of the Western diet by promoting hypothalamic inflammation and disrupting the central control of energy balance. Here, the role of dietary AGEs in metabolic dysfunction is reviewed with a focus on the mechanisms underpinning their detrimental role in insulin resistance, pancreatic β‐cell dysfunction, hypothalamic control of energy balance, and the pathogenesis of T2DM and obesity.
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TL;DR
This review synthesizes mechanisms by which dietary advanced glycation end products (AGEs) contribute to metabolic dysfunction, including insulin resistance, pancreatic β-cell dysfunction, hypothalamic inflammation, obesity, and type 2 diabetes mellitus. It covers AGE formation, absorption, receptor signaling, detoxification, and evidence from cell, animal, and human studies while noting measurement and dietary AGE controversies.
Key findings
- Dietary AGEs are formed via the Maillard reaction during cooking and processing; around 10–30% are absorbed depending on chemical characteristics, with free low-molecular-weight AGEs absorbed more efficiently than protein-bound AGEs. Foods such as peanuts, biscuits, cereals, toast, and heat-processed meats have the highest measured CML, CEL, and MG-H1 levels (2–5 mg, 2–7 mg, and 15–60 mg per 100 g, respectively), whereas coffee, fruits, vegetables, butter, olive oil, and red wine contain negligible amounts.
- AGEs activate RAGE and downstream pathways including JNK, IKK/NF-κB, and NADPH oxidase/ROS, promoting inflammation and oxidative stress that impair insulin signaling, downregulate GLUT4, and contribute to β-cell cytotoxicity, apoptosis, and impaired glucose-induced insulin secretion.
- In animal models, a high-AGE diet containing synthetic MG-BSA at 1 mg per g of diet decreased insulin receptor and IRS phosphorylation and defective AKT activation in skeletal muscle, adipose tissue, and liver. In humans, an AGE-restricted diet improved insulin sensitivity in T2DM and normalized AGER1 and sirtuin1 while decreasing NF-κB acetylation, circulating TNFα, serum AGEs, and leptin; hyperinsulinemic-euglycemic clamp studies showed a low AGE diet improved insulin sensitivity versus a high AGE diet decreasing it.
- AGEs may promote obesity via hypothalamic inflammation and disrupted central energy balance; a high-fat/high-carbohydrate diet increased CML immunoreactivity in POMC and NPY neurons, and RAGE/ALCAM knockdown improved metabolic phenotype and decreased microglial reactivity. A 5-year follow-up study associated AGEs with increased body weight after adjusting for total energy intake and other confounders.
Methods
- Narrative review; no primary experimental data are reported. The paper synthesizes published literature on AGE formation, dietary sources and absorption, receptors, detoxification, and metabolic effects.
- Evidence discussed includes cell culture studies, animal models, human feeding trials, hyperinsulinemic-euglycemic clamps, and cohort follow-up data.
- Main analysis is a qualitative synthesis of mechanisms and cited findings; no systematic search strategy, meta-analysis, or quantitative pooling is described.
Limitations
- The paper states there is debate about the relative importance of dietary AGEs because of limited digestion and absorption, particularly of high-molecular-weight AGEs, while low-molecular dietary AGEs appear to be efficiently disposed of by the kidneys.
- The paper notes intrinsic problems in comparing AGE concentrations across studies due to different measurement techniques and food matrix effects; immunoassays do not give absolute values, whereas mass spectrometry gives absolute concentrations for AGEs such as CML.
- The paper reports conflicting human feeding studies: some show AGE restriction reduces inflammation and improves vascular function, but two feeding studies showed no effect of dietary AGEs on inflammatory and cardiovascular profiles. Evident from the text: as a narrative review, it lacks systematic search, risk-of-bias assessment, and quantitative synthesis.
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In the paper
“These molecules can also be generated from glucose autoxidation, lipid peroxidation, and the polyol pathway.[18]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 2. AGE Formation
What the sources say
- Not checked yetcites [18] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“Despite its ability to react with free amino groups, glucose is a poor glycating agent compared to dicarbonyls such as methylglyoxal.[16]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 2. AGE Formation
What the sources say
- Not checked yetcites [16] source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Excessive AGE formation is particularly associated with cross-linking of matrix proteins such as collagen, vitronectin, and laminin.[2,10,11]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 1. Introduction
What the sources say
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“Additionally, fructose can increase AGE formation independently of glucose by increasing 𝛼-oxoaldehydes levels.[5]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 1. Introduction
What the sources say
- Not checked yetcites [5] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Furthermore, AGEs may also contribute to the obesogenic effects of the Western diet by promoting hypothalamic inflammation and disrupting the central control of energy balance.”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“AGEs themselves activate signaling pathways, which compromise insulin signaling and pancreatic 𝜷-cell function, thus, contributing to the development of type 2 diabetes mellitus (T2DM).”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“The rate of AGE formation in the body is greatly enhanced in diabetes.[2,3]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 1. Introduction
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Factors affecting the AGE content of food depends on the content of protein, fat, and sugar and the types of processing and cooking methods employed, predominantly on the temperature and duration of preparation.[26,27]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 3. Source and Absorption of Dietary AGEs
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Prolonged high temperatures such as those used in the processing of some dairy products and cooking techniques like roasting and frying increase the production of dietary AGEs.[26,27]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 3. Source and Absorption of Dietary AGEs
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“The Maillard reaction generates these highly reactive dicarbonyls, also referred to as 𝛼-oxoaldehydes, which in addition to methylglyoxal include glyoxal and 3deoxyglucosone. [17]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 2. AGE Formation
What the sources say
- Not checked yetcites [17] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- It may state two separate claims as one. 35
- Probably not a substantial claim. 5
In the paper
“making free-AGEs a good marker for dietary AGE intake while plasma protein-bound AGEs better represent endogenously produced AGEs.[31]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 3. Source and Absorption of Dietary AGEs
What the sources say
- Not checked yetcites [31]
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Thus, the absorption of AGEs as single amino acids or dipeptides occurs more efficiently than protein-bound AGEs, evidenced by higher levels of CML in the faeces when protein-bound CML is ingested.[36]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 3. Source and Absorption of Dietary AGEs
What the sources say
- Not checked yetcites [36]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Dietary AGEs are absorbed by the gastrointestinal tract to exert their effects on health with dietary and circulating free-AGEs concentrations highly correlated, [28][29][30]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 3. Source and Absorption of Dietary AGEs
What the sources say
- Not checked yetcites [28]
- Not checked yetcites [29]
- Not checked yetcites [30]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“AGEs are produced both naturally in the body, as part of normal metabolism, and during the cooking and processing of food with a significant proportion being absorbed in the gastrointestinal tract.”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 1. Introduction
What the sources say
- Not checked yetcites [1] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Free CML is absorbed by simple diffusion, [33] with dipeptides requiring the peptide transporter 1, [34] which also transports pyrraline dipeptides.[35]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 3. Source and Absorption of Dietary AGEs
What the sources say
- Not checked yetcites [33]
- Not checked yetcites [34]
- Not checked yetcites [35]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“AGE modification inhibits proteolytic digestion [32,38] thus, low molecular weight AGEs are absorbed more efficiently than protein-bound AGEs.[39]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 3. Source and Absorption of Dietary AGEs
What the sources say
- Not checked yetcites [32]
- Not checked yetcites [38]
- Not checked yetcites [39] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Also, the increased presence of AGEs in collagen across eight mammalian species has been shown to be associated with reduced lifespan, indicating that AGE levels determine lifespan and rate of ageing.[14]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 1. Introduction
What the sources say
- Not checked yetcites [14]
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Furthermore, the Western diet not only contains large amounts of AGEs, due to high levels of food processing, but is also high in fat and sugar, particularly fructose, which increases AGE production in the body, in part, by increasing circulating glucose levels via enhanced hepatic glucose production and insulin resistance.[4]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 1. Introduction
What the sources say
- Not checked yetcites [4] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Some of the most commonly formed AGEs include the hydroimidazolones, the most prevalent of these in human tissues is formed from the interaction of methylglyoxal with arginine residues.[23]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 2. AGE Formation
What the sources say
- Not checked yetcites [23]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Advanced glycation end products (AGEs) are a complex and heterogeneous group of protein, lipid, and DNA adducts implicated in the development of numerous chronic diseases including diabetes related complications, cardiovascular, renal, and neurodegenerative disease, and have recently also been implicated in hypothalamic inflammation and obesity.[1]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 1. Introduction
What the sources say
- Not checked yetcites [1] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Activity of the glyoxolase is upregulated in diabetes to prevent the build-up of reactive dicarbonyls thereby suppressing AGE formation.[69]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 5.1. Glyoxalases (GLO1 and 2)
What the sources say
- Not checked yetcites [69]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In contrast to CML or CEL, the hydroimidazolone MG-H1 does not require attachment to a peptide carrier to exert its effect [47] and as the MG-H1 content of foods is much higher than either CML or CEL, free MG-H1 absorbed from the diet is likely to be a significant activator of mRAGE. [27,48]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 4.1. RAGE
What the sources say
- Not checked yetcites [47]
- Not checked yetcites [27]
- Not checked yetcites [48]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“AGER1 can counteract AGE-induced oxidative stress [61,62] as well as inhibit the activation of NF-𝜅B by promoting a sirtuin1-dependent deacetylation and suppression of NF-𝜅B.[63,64]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 4.2. Other Receptors
What the sources say
- Not checked yetcites [61]
- Not checked yetcites [62]
- Not checked yetcites [63] source
- Not checked yetcites [64]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“AGER1 is present in almost all cells and tissues, is upregulated by AGEs and increases their uptake and removal.[18]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 4.2. Other Receptors
What the sources say
- Not checked yetcites [18]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“It has been estimated that around 99% of all methylglyoxal is broken down via the glyoxalase pathway [67] detailed below.”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 5. Detoxification of AGEs
What the sources say
- Not checked yetcites [67]
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Nonetheless, this protective mechanism begins to fail as the concentration of AGEs increases, with high levels of AGEs leading to a downregulation of both AGER1 and sirtuin1.[64]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 4.2. Other Receptors
What the sources say
- Not checked yetcites [64]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“However, the mass spectrometry techniques used now give absolute concentrations for AGEs such as CML meaning that values can be compared between studies carried out using this methodology.[27,48,110]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 6. AGEs and the Western Diet
What the sources say
- Not checked yetcites [27]
- Not checked yetcites [48]
- Not checked yetcites [110]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Moreover, ROS potentiate the inflammatory response by activating NF-𝜅B, which, once activated, migrates to the nucleus and induces not only the expression of inflammatory mediators, but also upregulates RAGE, thus establishing a positive feedback loop.[55,56]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 4.1. RAGE
What the sources say
- Not checked yetcites [55]
- Not checked yetcites [56]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Nonetheless the restriction of dietary AGEs has been associated with reductions in inflammation and an increase in vascular function in humans, [96,97]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 6. AGEs and the Western Diet
What the sources say
- Not checked yetcites [96] source
- Not checked yetcites [97]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“mRAGE interacts with AGEs, such as CML, CEL, which bind to the V domain of mRAGE to trigger an immunoinflammatory response.CML and CEL can only bind to mRAGE if they are incorporated into larger peptide structures.[45,46]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 4.1. RAGE
What the sources say
- Not checked yetcites [45]
- Not checked yetcites [46]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Indeed, apart from playing a pivotal role in diabetic complications, including cardiovascular, kidney and neurodegenerative diseases such as Alzheimer's and Parkinson's disease, AGEs have also been implicated in the pathogenesis of insulin resistance and type 2 diabetes mellitus (T2DM) as well as obesity.[1,18,[114][115][116][117][118]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
What the sources say
- Not checked yetcites [1,18,[114]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“while high loads of dietary AGEs have been associated with premature cognitive decline in humans [98] and in animal models fed a high MG diet equivalent to 19 𝜇mol per day.[99]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 6. AGEs and the Western Diet
What the sources say
- Not checked yetcites [98]
- Not checked yetcites [99]
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“The impact of AGEs on insulin resistance in humans has also been confirmed using hyperinsulinemic-euglycemic clamps, the gold standard for the assessment of insulin sensitivity [48] with a low AGE diet inducing an improvement in insulin sensitivity compared to a diet high in AGEs, which decreases insulin sensitivity.[48]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
What the sources say
- Not checked yetcites [48]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“PGC 1𝛼 regulates mitochondrial energy metabolism and biogenesis, thus playing a pivotal role in modulating mitochondria bioenergetics, which has been reported to be impaired in individuals affected by T2DM.[128,129]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“In these studies mice fed a high-AGE diet containing synthetic MG-BSA at 1 mg per g of diet showed a decrease in insulin receptor and IRS phosphorylation, and defective downstream activation of AKT in skeletal muscle, adipose tissue, and liver.[64]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
What the sources say
- Not checked yetcites [64]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“In skeletal muscle, a tissue pivotal for the control of glucose homeostasis, AGEs downregulate GLUT4 and promote the activation of inflammatory pathways as well as endoplasmic reticulum stress as indicated by the upregulation of nuclear factor NF-kappa-B p50 subunit and 78 kDa glucose-regulated protein.[124]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
What the sources say
- Not checked yetcites [124]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Importantly, PGC 1𝛼 appears to be instrumental in this process as genes under its control are downregulated in individuals suffering from T2DM and its upregulation has also been shown to have insulin sensitizing effects in vitro as well as in animal models.[129,132,133,134]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“with an AGE-restricted diet improving insulin sensitivity in T2DM with a normalization of the expression of AGER1 and sir-tuin1 as well as a decrease in NF-𝜅B acetylation circulating TNF𝛼, serum AGEs, and leptin.[63]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
What the sources say
- Not checked yetcites [63] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Importantly, AGEs activate both JNK as well as the IKK/NF-𝜅B signaling pathway supporting the relationship between AGEs and insulin resistance.”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Cell culture studies also showed that the molecular mechanism responsible for AGE-induced oxidative stress relies on increased mitochondrial ROS production as well as the activation of JNK which, in turn, activates NADPH oxidase further fueling oxidative stress.[136]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
What the sources say
- Not checked yetcites [136] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Energy balance is controlled by an intricate, finely-tuned neuroendocrine system.[141,142]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.2. AGEs in the Pathogenesis of Obesity
What the sources say
- Not checked yetcites [141]
- Not checked yetcites [142]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“AGEs exert cytotoxic effect on 𝛽-cells and induce apoptosis, which may be dependent on ROS production.”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
What the sources say
- Not checked yetcites [135] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In addition to inflammation, the AGE-RAGE axis also triggers oxidative stress, which is associated with the development of insulin resistance.[122,123]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“AGEs, by inhibiting mitochondrial cytochrome oxidase, [137] compromise 𝛽-cell ATP synthesis capacity causing an impairment in ATP-induced shutdown of K + channels, 𝛽-cell depolarization and consequently the influx of Ca 2+ thereby preventing the exocytosis of insulin-containing granules.[138]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.1. Insulin Resistance and Type 2 Diabetes Mellitus
What the sources say
- Not checked yetcites [137]
- Not checked yetcites [138]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“AGEs can also activate pro-inflammatory pathways; JNK and IKK/NF-𝜅B both of which have been implicated in mediating high-fat diet induced hypothalamic insulin and leptin resistance leading to hypothalamic dysfunction.[145][146][147][148][149]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.2. AGEs in the Pathogenesis of Obesity
What the sources say
- Not checked yetcites [145]
- Not checked yetcites [146]
- Not checked yetcites [147] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The Western diet contains elevated levels of highly processed foods and as such represents a source of AGEs, which contributes to promoting obesity, insulin resistance, and deterioration in metabolic health.”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 8. Conclusions
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Mechanisms observed in cell culture and animal models of AGE exposure translate to human metabolic dysfunction.
None of the sources cited for this claim have been checked yet.
In the paper
“Insulin and leptin are the main anorexigenic hormones and inform the hypothalamus, particularly the arcuate nucleus of the hypothalamus (ARC), the master regulator of energy balance, about longand short-term energy status.[143,144]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.2. AGEs in the Pathogenesis of Obesity
What the sources say
- Not checked yetcites [143] source
- Not checked yetcites [144]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“The role of AGEs in promoting hypothalamic inflammation was confirmed in animals lacking RAGE and ALCAM which have an improved metabolic phenotype and decreased microglial reactivity on a high-fat diet.[1]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.2. AGEs in the Pathogenesis of Obesity
What the sources say
- Not checked yetcites [1] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“The hypothalamus receives and integrates central and peripheral information related to the nutritional status of the individual and responds to these neural, nutritional, and hormonal cues by triggering orexigenic and anorexigenic responses in order to preserve energy homeostasis and maintain body weight within a tight range.[142]”
§ The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction > 7.2. AGEs in the Pathogenesis of Obesity
What the sources say
- Not checked yetcites [142]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
The association between AGEs and increased body weight after adjusting for total energy intake and other confounders is not due to residual confounding.
“Importantly, the ability of AGEs to increase body weight was retained after adjusting for total energy intake and other cofounders, suggesting AGEs directly affect energy balance.”
The paper relies on this without support.
Mechanisms observed in cell culture and animal models of AGE exposure translate to human metabolic dysfunction.
“Studies using primary 𝛽-cells and cell lines demonstrate that inhibition of RAGE or antioxidant treatment prevents AGE-induced cell toxicity.[135]”
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?
In the citing paper
“AGEs are reported to modify energy balance by disrupting hypothalamic function.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [78]
In the citing paper
“Aggregated AGEs can activate the JNK, Iκ-B kinase (IKK), NF-κB, and TNF-α pathways to trigger hypothalamic insulin and leptin resistance, resulting in hypothalamic dysfunction, imbalanced energy control, and subsequently elevated food consumption and body weight with obesity and metabolic syndromes78.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [78]
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Items 101–193 of 193
Borriello, M., Lauria, F., Sirangelo, I., Aleksandrova, K., Hebestreit, A., Siani, A., & Russo, P. (2022) · Nutrients · doi:10.3390/nu14194135 · Cited by 7
“Furthermore, there is growing evidence of the impact of AGEs on metabolic health and the onset of metabolic syndrome as well as obesity [22].”
BackgroundLodi, G., Sergi, D., Dipinto, A., Bompan, F., Secchiero, P., Voltan, R., & Romani, A. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27062660 · Cited by 10
“This reaction generates unstable Schiff bases, which undergo further rearrangements to produce Amadori products that accumulate on proteins, leading to the formation of AGEs [53,54].”
Self-citationLast Five Years Development In Food Safety Perception of n-Carboxymethyl Lysine
Golchinfar, Z., Farshi, P., Mahmoudzadeh, M., Mohammadi, M., Tabibiazar, M., & Smith, J. S. (2021) · Food Reviews International · doi:10.1080/87559129.2021.2011909 · Cited by 6
Akoonjee, A., Lukman, H. Y., Ajao, A. A., Uthman, T. O., & Sabiu, S. (2024) · Journal of Biomolecular Structure and Dynamics · doi:10.1080/07391102.2024.2446672 · Cited by 6
“…et al., 2022; Taguchi & Fukami, 2023) by triggering biochemical processes such as release pro-inflammatory molecules, impair mitochondrial oxidative stress, and epigenetic changes implicated in the pathogenesis of T2DM and its complications (Cervantes Gracia et al., 2017; Sergi et al., 2021).”
Possible effects of dietary advanced glycation end products on maternal and fetal health: a review
Demirer, B., & Samur, G. (2022) · Nutrition Reviews · doi:10.1093/nutrit/nuac090 · Cited by 7
Hosseini, E., Mokhtari, Z., Poustchi, H., Khoshnia, M., Dawsey, S. M., Boffetta, P., Abnet, C. C., Kamangar, F., Etemadi, A., Pourshams, A., et al. (2023) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph20053788 · Cited by 6
Topical Application of Deglycating Enzymes as an Alternative Non-Invasive Treatment for Presbyopia
Delanghe, J., Beeckman, J., Beerens, K., Himpe, J., Bostan, N., Speeckaert, M. M., Notebaert, M., Huizing, M. T., & Aken, E. V. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24087343 · Cited by 6
“The formation of advanced glycation end products (AGEs) is generally described as the Maillard reaction, a very complex nonenzymatic series of chemical reactions [5].”
BackgroundEvaluation of the effects of dietary advanced glycation end products on inflammation
Demirer, B., & Fisunoğlu, M. (2023) · Nutrition Bulletin · doi:10.1111/nbu.12653 · Cited by 6
Chen, S.-Y., Huang, Y.-N., Lin, J., & Yen, G. (2024) · Journal of Food and Drug Analysis · doi:10.38212/2224-6614.3494 · Cited by 6
“Both advanced glycation end products (AGEs) and their precursor methylglyoxal (MG) are involved in lipid and carbohydrate metabolism disorders [5].”
Advanced Glycation End Products and Diabetes
Hadzi‐Petrushev, N., Angelovski, M., & Mladenov, M. I. (2023) · Contemporary Endocrinology · doi:10.1007/978-3-031-39721-9_5 · Cited by 7
Fu, M., Zhengran, L., Li, Y., Tong, W., Liyang, C., Xi, G., Yang, X., Cao, M., & Yi, G. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e36111 · Cited by 5
“This mechanism involves both receptor for RAGE-dependent and -independent pathways [56].”
BackgroundJi, K., Han, M., Yang, M., Xu, Q., & Zhang, Y. (2025) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2025.1454647 · Cited by 5
You, S., Jang, M., & Kim, G. (2022) · Journal of Functional Foods · doi:10.1016/j.jff.2022.104996 · Cited by 5
Choi, J.-H., Park, C. H., Song, I.-B., Lee, S., Choi, H., Youn, D. H., Han, S.-W., Jeon, J. P., & Kwon, J. (2024) · Applied Sciences · doi:10.3390/app14062266 · Cited by 5
Mangiferin modulates lipid metabolism via AKR1B1 in response to advanced glycation end products
Sharda, S., Aher, A., Ghosh, D. K., et al. (2025) · British Journal of Pharmacology · doi:10.1111/bph.70084 · Cited by 5
(2021) · Biointerface Research in Applied Chemistry · doi:10.33263/briac122.22422250 · Cited by 5
Preparation and Characterization of Crosslinked Electrospun Gelatin Fabrics via Maillard Reactions
Dechojarassri, D., Kaneshige, R., Tamura, H., & Furuike, T. (2023) · Materials · doi:10.3390/ma16114078 · Cited by 5
“Meanwhile, intermediate glycation products can be generated via another pathway involving glucose autoxidation, lipid peroxidation, the polyol pathway, and glycolysis [25,26].”
BackgroundUllah, A., Aleem, U., Siddiqui, B. S., et al. (2023) · ChemistrySelect · doi:10.1002/slct.202301884 · Cited by 5
Ferreyro‐Bravo, F., Ceballos-Cruz, Á., Urruchúa-Rodríguez, M. J., et al. (2023) · Medicina · doi:10.3390/medicina59081451 · Cited by 4
“According to the existing literature, it has been suggested that hyperglycemia, oxidative stress, and other pathological metabolic processes may be among the factors that contribute to glycation mechanisms [3].”
BackgroundRutkowska, J., & Baranowski, D. (2024) · NFS Journal · doi:10.1016/j.nfs.2024.100202 · Cited by 6
Tufail, P., Anjum, S., Siddiqui, B. S., Pizzi, M., Jahan, H., & Choudhary, M. I. (2025) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2025.167784 · Cited by 6
Li, X., Wesseling, S., Sang, Y., et al. (2025) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.5c08345 · Cited by 4
Russo, M. D., Sirangelo, I., Lauria, F., Formisano, A., Iannuzzi, C., Hebestreit, A., Pala, V. M., Siani, A., & Russo, P. (2024) · Nutrients · doi:10.3390/nu16121831 · Cited by 4
“Chronic exposure to high levels of dAGEs has been demonstrated to promote chronic inflammation and insulin resistance, both of which are underlying mechanisms of obesity and metabolic syndrome [23], although conclusive evidence of causality or consequentiality remains elusive.”
BackgroundBesinlerde Oluşan İleri Glikasyon Son Ürünlerine Polifenollerin Etkisi
YALÇIN, E., & Rakıcıoğlu, N. (2022) · Journal of Nutrition and Dietetics · doi:10.33076/2022.bdd.1554 · Cited by 4
“Biriken metabolitler, hücre içi ve hücre dışı proteinlerle etkileşime girerek fruktoz-3-fosfat ve dikarbonil türevlerini oluşturur (9).”
BackgroundType 2 Diabetes Mellitus in Tanzania. A Narrative Review of Epidemiology and Disease Trend
Chillo, O., Mzokolo, I. C., Peter, E. G., MALINDISA, E. K., Haji, H. T., Tungu, A. M., Njelekela, M. A., & Balandya, E. (2024) · Current Diabetes Reviews · doi:10.2174/0115733998267513231208100124 · Cited by 4
Tabar, M. S., Nilghaz, M., Hekmatdoost, A., Pashayee-Khamene, F., Mokhtari, Z., Karimi, S., Ahmadzadeh, S., Saberifiroozi, M., Hatami, B., & Yari, Z. (2025) · Scientific Reports · doi:10.1038/s41598-025-89433-y · Cited by 4
Russo, P., Sirangelo, I., & Siani, A. (2025) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2025.104538 · Cited by 4
Lu, Y., Chang, L., Liu, S., et al. (2026) · Food & Function · doi:10.1039/d5fo04604a · Cited by 3
Wang, Y., Hu, C., Cao, L., Liu, Q., Li, Y., Zhu, T., & Zhang, D. (2024) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-024-03217-1 · Cited by 3
“The downstream consequences of the AGE/RAGE axis include impaired insulin signalling, disruption of metabolic homeostasis, RAGE-induced pancreatic β-cell toxicity, and epigenetic modification (Yan et al. 2003; Gąsiorowski et al. 2018; Muthyalaiah et al. 2021; Sergi et al. 2021).”
Mostafa, H. K. K. (2025) · Journal of Microscopy and Ultrastructure · doi:10.4103/jmau.jmau_101_24 · Cited by 3
Sex-specific differences of advanced glycation end products in diabetes
Hellwig, M., Decker, J., Roma, L. P., Schunk, S. J., Ampofo, E., & Rother, S. (2025) · Nutrition and Diabetes · doi:10.1038/s41387-025-00379-6 · Cited by 4
“Adipose tissue-derived cytokines such as tumor necrosis factor-α (TNF-α ) and adipokines play a role in AGE metabolism and clearance, and their dysregulation in obesity can contribute to elevated AGE levels [11, 24, 25].”
An industrially applicable processing method for reducing AGEs in bread based on RSM design
Jiang, G., Yu, H., Chen, L., Zhang, Y., & Liu, L. (2025) · Future Foods · doi:10.1016/j.fufo.2025.100687 · Cited by 3
Nikray, N., Abharian, N., Ashtiani, S. J., Kobarfard, F., & Faizi, M. (2024) · Iranian journal of pharmaceutical research · doi:10.5812/ijpr-153322 · Cited by 3
“One of the primary sources of MG and AGEs is food, particularly Western diets, and alcoholic beverages; however, they can also be produced endogenously as a by-product of the glycolysis pathway (46).”
BackgroundRevisiting the protective effects of ginger phenolic compounds on the kidneys: A narrative review
Moghaddam, S. H., Vatankhah, A., Armide, N., & Keshavarzi, Z. (2024) · Food and Humanity · doi:10.1016/j.foohum.2024.100442 · Cited by 3
The Maillard reaction and food allergy: Impacts on sensitisation and on elicitation
Teodorowicz, G., Bastiaan‐Net, S., Hoppenbrouwers, T., & Wichers, H. J. (2024) · Elsevier eBooks · doi:10.1016/b978-0-323-96018-2.00142-5 · Cited by 3
Epigenetic contributions to cancer: Exploring the role of glycation reactions
Khan, H., Rafi, Z., Khan, M. Y., Maarfi, F., Rehman, S., Kaur, K., Ahmad, M. K., Shahab, U., Ahmad, S., & Ahmad, S. (2024) · International review of cytology · doi:10.1016/bs.ircmb.2024.04.001 · Cited by 2
Mustafa, I., Irfan, S., Hussain, G., et al. (2024) · Bioinformatics and Biology Insights · doi:10.1177/11779322241292239 · Cited by 2
Paiella, M., Raiteri, T., Reano, S., Manfredelli, D., Manenti, T., Gentili, G., Meskine, H., Chiappalupi, S., Bellomo, G., Prodam, F., et al. (2025) · Antioxidants · doi:10.3390/antiox14080900 · Cited by 2
“…consumption of cranberry or cranberry-derived products might be useful in counteracting the metabolic syndrome, a complex condition characterized by multiple cardiovascular risk factors, including obesity, hypertension, and hyperglycemia [47], in which AGEs have been extensively implicated [9,39].”
Ge, Y., Kou, B., Zhang, C., Gu, C., Cheng, L. Z., Shi, Y., Le, G., & Xu, W. (2025) · Foods · doi:10.3390/foods14183220 · Cited by 4
“For instance, AGEs—which were also significantly elevated in the HOP group in our study (Table 1)—are known to impair β -cell function through receptor (RAGE)-mediated activation of oxidative stress and inflammatory pathways, mechanisms that parallel our observations with Dityr [45].”
Li, G., Badar, I. H., Zheng, X., Wang, M., Hu, Y., & Zhang, L. (2026) · Journal of Food Composition and Analysis · doi:10.1016/j.jfca.2026.108865 · Cited by 3
Chen, X., Wang, D., Tao, J., & Zhang, A. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103067 · Cited by 3
Formation of N-carboxymethyllysine in raw and heat-treated hen eggs: Effects of egg freshness
Wu, S., Lai, K., Chen, M., Fan, Y., Li, X., Tan, L., Xiang, X., & Huang, Y. (2023) · Journal of Food Composition and Analysis · doi:10.1016/j.jfca.2023.105177 · Cited by 2
Honarkar-Shafie, E., Hosseinzadeh‐Attar, M. J., Taheri, F., Moosavi, N., Yaseri, M., Alidoosti, M., & Vasheghani‐Farahani, A. (2023) · The Journal of Tehran University Heart Center · doi:10.18502/jthc.v18i1.12574 · Cited by 2
Mitochondrial dysfunction and diabetes in South Africa: A review
Pearce, B., & Pearce, K. M. (2024) · Endocrine and Metabolic Science · doi:10.1016/j.endmts.2024.100157 · Cited by 2
Advances in the study of microparticles in diabetic retinopathy
Hou, Y., Tang, Y., & Cai, S. (2024) · Postgraduate Medical Journal · doi:10.1093/postmj/qgae046 · Cited by 2
Singh, S., & Singh, T. G. (2024) · Journal of Traditional and Complementary Medicine · doi:10.1016/j.jtcme.2024.04.009 · Cited by 3
Toxic AGEs (TAGE) Cause Lifestyle-Related Diseases
Takeuchi, M. (2024) · Antioxidants · doi:10.3390/antiox13111372 · Cited by 2
Klimontov, V. V., Yushin, A. Y., Semenova, J. F., et al. (2025) · Diabetes Mellitus · doi:10.14341/dm13209 · Cited by 2
Antelmann, H. (2024) · Elsevier eBooks · doi:10.1016/b978-0-12-818619-0.00051-4 · Cited by 4
Fructosyl Amino Oxidase as a Therapeutic Enzyme in Age-Related Macular Degeneration
Delanghe, J., Mavungu, J. D. D., Beerens, K., Himpe, J., Bostan, N., Speeckaert, M. M., Vrielinck, H., Vral, A., Broeke, C. V. D., Huizing, M. T., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25094779 · Cited by 1
Salivary metabolites profiling for diagnosis of COPD: an exploratory study
Zherong, Z., Lv, Y., Gong, M., et al. (2025) · Journal of Breath Research · doi:10.1088/1752-7163/adba07 · Cited by 1
“Pyrraline, recognized as a significant advanced glycation end product (AGE), is often associated with adverse health effects and contributes to the progression of various chronic diseases, including diabetes and atherosclerosis [32–34].”
Urinary biomarkers in metabolic syndromes
Saini, A., Dagar, W., Kapoor, K., et al. (2025) · Elsevier eBooks · doi:10.1016/b978-0-443-33574-7.00009-2 · Cited by 1
Targeting reactive carbonyls in metabolic disorders
Amaro, A., Freitas, M., & Matafome, P. N. (2025) · Elsevier eBooks · doi:10.1016/b978-0-443-27370-4.00022-6 · Cited by 1
Başdoğan, H., Pehlivanoğlu, H., Palabıyık, İ., et al. (2025) · Food and Humanity · doi:10.1016/j.foohum.2025.100798 · Cited by 1
Sahoo, S., Howsam, M., Tessier, F. J., & Tupe, R. S. (2025) · Biochimie · doi:10.1016/j.biochi.2025.12.004 · Cited by 3
Tate, D. E., Tanprasertsuk, J., Tarr, D. S., Shmalberg, J. W., & Honaker, R. W. (2026) · Journal of Animal Science · doi:10.1093/jas/skag206 · Cited by 4
“Accordingly, numerous studies have investigated the absorption, metabolism, and biological mechanisms underlying AGE-associated effects (Rowan et al. 2018; Snelson and Coughlan 2019; Chen and Guo 2021; Sergi et al. 2021).”
Liang, Z., Chen, X., Yang, Z., Lu, J., Huang, J., Liu, Y., Chen, L., Xian, H., Mo, J., Huang, X., et al. (2021) · International Journal of Food Science & Technology · doi:10.1111/ijfs.15109 · Cited by 1
Taheri, F., Vasheghani‐Farahani, A., Honarkar-Shafie, E., Poorhosseini, H., Yaseri, M., & Hosseinzadeh‐Attar, M. J. (2023) · Journal of Research in Medical Sciences · doi:10.4103/jrms.jrms_293_23 · Cited by 1
“[27] Several studies have indicated the effect of dietary AGEs limitation on improving insulin resistance and reducing inflammatory markers.”
Background(2023) · Turkish Journal of Biochemistry · doi:10.1515/tjb-2023-48s107 · Cited by 1
Nov, P., Zheng, C., Wang, D., Sou, S., Touch, S., Kouy, S., Ni, P., Kou, Q., Li, Y., Prasai, A., et al. (2024) · Molecular Medicine Reports · doi:10.3892/mmr.2024.13336 · Cited by 1
“AGEs are produced through non‑enzymatic glycation reactions between amino acids and reducing sugars, a process commonly known as the Maillard reaction (38).”
BackgroundAdvanced glycation end-product intake predicts insulin resistance in a sex-dependent fashion
Sergi, D., Angelini, S., Spaggiari, R., Castaldo, F., Zuliani, G., Sanz, J. M., Passaro, A., the PANGEA study group, Nora, E. D., Brombo, G., et al. (2025) · European Journal of Nutrition · doi:10.1007/s00394-025-03672-3 · Cited by 1
“Considering their heterogeneity, AGEs include molecules like carboxyethyl lysine, carboxymethyl lysine, glyoxal lysine dimer, 3-deoxyglucosone lysine dimer and pyrroline [12].”
Self-citationWu, L., Tan, J., Sun, W., Dong, X., He, J., Ali, A. M. M., Chen, M., Zhang, L., & Wang, P. (2025) · Journal of Diabetes Research · doi:10.1155/jdr/3955893 · Cited by 1
“…sugar, the rate of glycation reactions signi fi cantly accelerates, leading to a marked increase in the production of AGEs and their accumulation in the body, triggering various complications of diabetes, including diabetic vascular complications, neurodegenerative diseases, and cancer [15, 16].”
Hayes, A., Klug, M. E., Sharma, M., Kao, A. E., Sun, S., Gonzalez, E. D. J. L., Zhu, H., Dent, J. C., Clark, R. J., Sell, D. R., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.01.07.698065 · Cited by 1
Polycystic Ovary Syndrome and Environmental Toxins
Kandaraki, E., & Papalou, O. (2022) · Cambridge University Press eBooks · doi:10.1017/9781108989831.009
Chen, S., Huang, Y.-N., Lin, J., Chen, Y., & Yen, G. (2023) · SSRN Electronic Journal · doi:10.2139/ssrn.4522856
The RAGE gene crucial function in the etiology and consequences of Type I diabetes
Mohamed, A. A., Mahmoud, M. O., Abd‐Allah, G. M., et al. (2024) · Journal of Medicine in Scientific Research · doi:10.59299/2537-0928.1069
Impact of dietary advanced glycation end products (dAGEs) in processed foods on health
Kunnel, S., Chakraborty, I., Govindaraju, I., Mal, S. S., & Mazumder, N. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-14042-6.00013-0
Lestari, N. D., Agustini, S. M., Dliyauddin, M., Adharini, W. I., Nilamsari, R. V., Widodo, N., Rahayu, S., & Rifa’i, M. (2024) · Medicinski Glasnik · doi:10.17392/1685-21-02
Advanced glycation end products and human diseases
Zahra, H. A. (2025) · Journal of Biological Research - Bollettino della Società Italiana di Biologia Sperimentale · doi:10.4081/jbr.2025.12656
Tian, Y.-Y., Xu, L., Fu, Y., Zhou, S., Yue, C., Hu, L., Yang, Y., Lu, Y.-Q., Sheng, Z., & Liu, L. (2025) · Calcified Tissue International · doi:10.1007/s00223-025-01384-8
“Consistent with previous studies, it was observed that OP correlated with older age, female gender, and lower BMI [26].”
Großkopf, A., Kuru-Schors, M., Schmidt, S., Dienel, J., Höhn, A., Raupbach, J., Wächter, K., Köhler, C., Grune, T., Szabo, G. B., et al. (2025) · Current Research in Food Science · doi:10.1016/j.crfs.2025.101144
Bayram, H. M., & Öztürkcan, A. (2025) · Journal of Hunger & Environmental Nutrition · doi:10.1080/19320248.2025.2545539
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Influential
Metadata
- Authors
- Sergi, D., Boulestin, H., Campbell, F. M., & Williams, L. M.
- Affiliations
- Commonwealth Scientific and Industrial Research Organisation (AU)
- University of Aberdeen (GB)
- Corresponding author
- Williams, Lynda M.
- Venue
- Molecular Nutrition & Food Research
- Publisher
- Wiley
- Published
- 2020-04-20
- Volume
- 65
- Issue
- 1
- Pages
- e1900934-e1900934
- ISSN
- 1613-4125 (ISSN-L)
- 1613-4133
- OpenAlex
- W3014454708
- Semantic Scholar
- 97ca7e276f92fd6912c3817577b53faabeec219d
- Cited by
- 194
- References
- 147
- Citations by year
- 2026: 20 · 2025: 40 · 2024: 42 · 2023: 30 · 2022: 34 · 2021: 24 · 2020: 4
- FWCI
- 2.89
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Molecular Nutrition & Food Research (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Aberdeen University Research Archive (Aberdeen University) (submittedVersion)
- Institutional Research Information System University of Ferrara (University of Ferrara) (submittedVersion, cc-by)
- Funders
- Rural and Environment Science and Analytical Services Division
- Commonwealth Scientific and Industrial Research Organisation
- 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 › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- advanced glycation end products, dietary AGEs, metabolic dysfunction, type 2 diabetes, insulin resistance, beta-cell dysfunction, hypothalamic inflammation, energy balance, Western diet, obesity, hyperglycemia, diabetes complications, signaling pathways
- MeSH terms
- Antigens, Neoplasm, Cooking, Diabetes Mellitus, Type 2, Diet, Enzymes, Humans, Inflammation, Obesity, Glycation End Products, Advanced, Mitogen-Activated Protein Kinases, Insulin-Secreting Cells, Diet, Western
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