The DOI matches its Crossref record; 143 of the 147 references it cites were found in a registry or an index; none of the 123 sources its claims cite is checked for support yet.
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.
Overview
AI snapshot
Written from the paper’s full text.
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.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
74 Not checked yet · 11 Own interpretation
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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In 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
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
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
“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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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]
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It 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]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably 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]
Citations
Cites
López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013) · Cell · doi:10.1016/j.cell.2013.05.039 · Cited by 14,982
Mootha, V. K., Lindgren, C. M., Eriksson, K.-F., Subramanian, A., Sihag, S., Lehar, J., Puigserver, P., Carlsson, E., Ridderstråle, M., Laurila, E., et al. (2003) · Nature Genetics · doi:10.1038/ng1180 · Cited by 10,197
Increased oxidative stress in obesity and its impact on metabolic syndrome
Furukawa, S., Fujita, T., Shimabukuro, M., Iwaki, M., Yamada, Y., Nakajima, Y., Nakayama, O., Makishima, M., Matsuda, M., & Shimomura, I. (2004) · Journal of Clinical Investigation · doi:10.1172/jci21625 · Cited by 5,508
The Pathobiology of Diabetic Complications
Brownlee, M. (2005) · Diabetes · doi:10.2337/diabetes.54.6.1615 · Cited by 5,339
Advanced glycation end-products: A review
Singh, R., Barden, A., Mori, T., & Beilin, L. (2001) · Diabetologia · doi:10.1007/s001250051591 · Cited by 2,597
Inflammation, metaflammation and immunometabolic disorders
Hotamisligil, G. S. (2017) · Nature · doi:10.1038/nature21363 · Cited by 2,570
Reactive oxygen species have a causal role in multiple forms of insulin resistance
Houstis, N., Rosen, E. D., & Lander, E. S. (2006) · Nature · doi:10.1038/nature04634 · Cited by 2,525
Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity
Bray, G. A., Nielsen, S. J., & Popkin, B. M. (2004) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/79.4.537 · Cited by 1,990
Hall, K. D., Ayuketah, A., Brychta, R., Cai, H., Cassimatis, T., Chen, K. Y., Chung, S. T., Costa, E., Courville, A., Darcey, V., et al. (2019) · Cell Metabolism · doi:10.1016/j.cmet.2019.05.008 · Cited by 1,971
Patti, M. E., Butte, A. J., Crunkhorn, S., Cusi, K., Berria, R., Kashyap, S., Miyazaki, Y., Kohane, I., Costello, M., Saccone, R., et al. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1032913100 · Cited by 1,952
Research works printed but not linked: 10
- Maillard L., 1912, C. R. Seances Acad. Sci., 154, 66
- Hammes H. P., 1996, Lab. Invest., 75, 325
- Monnier V. M., 1989, Prog. Clin. Biol. Res., 304, 1
- Liang Z., 2019, Crit. Rev. Food Sci. Nutr., 1
- Lue L., 2009, Funct. Neurol., 4, 167
- Shewfelt R. L., 2016, Defense of Processed Food: It's Not Nearly as Bad as You Think
- Cordova R., 2019, Eur. J. Nutr., 1
- Zick Y., 2005, Sci. Signaling, 268, pe4
- Brobeck J. R., 1943, Yale J. Biol. Med., 15, 831
- Sergi D., 2019, Nutr. Rev.
Cited by
Sorted by citations
Advanced Glycation End Products and Diabetes Mellitus: Mechanisms and Perspectives
Khalid, M., Petroianu, G. A., & Adem, A. (2022) · Biomolecules · doi:10.3390/biom12040542 · Cited by 972
“AGEs can signal through several receptors, however AGEs interactions with AGEs receptors and their role in mediating cellular responses are yet to be fully elucidated [12,25].”
BackgroundInfluentialMetabolic syndrome and cardiovascular diseases: Going beyond traditional risk factors
Rossi, J. L. S., Barbalho, S. M., de Araújo, R. R., Bechara, M. D., Sloan, K. P., & Sloan, L. A. (2021) · Diabetes/Metabolism Research and Reviews · doi:10.1002/dmrr.3502 · Cited by 606
“interact with circulating proteins, amplifying the synthesis of these substances.(82) This class of compounds prominent representatives is glyoxal, methylglyoxal, 3‐deoxyglucosone, glycolaldehyde, and glyceraldehyde.”
BackgroundCOVID-19: The Inflammation Link and the Role of Nutrition in Potential Mitigation
Zabetakis, I., Lordan, R., Norton, C., & Τσούπρας, Α. (2020) · Nutrients · doi:10.3390/nu12051466 · Cited by 553
“The Western diet is highly associated with hyperglycemia and advanced glycation end products (AGEs) that are linked with inflammation, metabolic complications, and chronic disease [134].”
BackgroundRungratanawanich, W., Qu, Y., Wang, X., Essa, M. M., & Song, B.-J. (2021) · Experimental & Molecular Medicine · doi:10.1038/s12276-021-00561-7 · Cited by 411
Lifestyle interventions for the prevention and treatment of hypertension
Valenzuela, P. L., Carrera‐Bastos, P., Gálvez, B. G., Ruiz‐Hurtado, G., Ordovás, J. M., Ruilope, L. M., & Lucía, A. (2020) · Nature Reviews Cardiology · doi:10.1038/s41569-020-00437-9 · Cited by 400
Zhou, M., Zhang, Y., Shi, L., Li, L., Zhang, D., Gong, Z., & Wu, Q. (2024) · Pharmacological Research · doi:10.1016/j.phrs.2024.107282 · Cited by 286
Lima, J. E. B. F., Moreira, N. C. S., & Sakamoto-Hojo, E. T. (2022) · Mutation Research/Genetic Toxicology and Environmental Mutagenesis · doi:10.1016/j.mrgentox.2021.503437 · Cited by 203
Antioxidants in Alzheimer’s Disease: Current Therapeutic Significance and Future Prospects
Pritam, P., Deka, R., Bhardwaj, A., Srivastava, R., Kumar, D., Jha, A. K., Jha, N. K., Villa, C., & Jha, S. K. (2022) · Biology · doi:10.3390/biology11020212 · Cited by 188
“The increase in the level of non-enzymatic glycation of cellular proteins, lipoproteins, and nucleic acids results from increased glucose levels [15].”
BackgroundMuriel, P., López‐Sánchez, P., & Ramos‐Tovar, E. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22136969 · Cited by 171
Toxicity of advanced glycation end products (Review)
Kuzan, A. (2021) · Biomedical Reports · doi:10.3892/br.2021.1422 · Cited by 151
Diet-Derived Antioxidants and Their Role in Inflammation, Obesity and Gut Microbiota Modulation
Deledda, A., Annunziata, G., Tenore, G. C., Palmas, V., Manzin, A., & Velluzzi, F. (2021) · Antioxidants · doi:10.3390/antiox10050708 · Cited by 163
“Their reduction by lowering cooking temperature, the use of some spices and abundance of vegetables should be a part of a dietary treatment [184].”
BackgroundChen, C., Zhang, J., Li, L., Guo, M., He, Y., Dong, Y., Meng, H., & Yi, F. (2022) · Frontiers in Medicine · doi:10.3389/fmed.2022.837222 · Cited by 175
“of dAGEs, which are closely related to the colour, flavour, and taste of food (51).”
BackgroundLee, J., Yun, J., & Ko, S. (2022) · Nutrients · doi:10.3390/nu14153086 · Cited by 161
“Unabsorbed AGEs in the colon are crucial factors for compromised glycemic control [28].”
BackgroundAdvanced glycation end products and their receptors in serum of patients with type 2 diabetes
Indyk, D., Bronowicka-Szydełko, A., Gamian, A., & Kuzan, A. (2021) · Scientific Reports · doi:10.1038/s41598-021-92630-0 · Cited by 120
Krawczyk, M., Burzyńska-Pędziwiatr, I., Woźniak, L. A., & Bukowiecka‐Matusiak, M. (2023) · Biomolecules · doi:10.3390/biom13091402 · Cited by 120
“Their potential detrimental effects on health can be attributed to their capacity to activate transcription factors, such as NF-B, activating protein-1 (AP-1), tumour protein (p53), and Nrf2, as well as cause cell damage through the collapse of the mitochondrial membrane potential, favouring the propagation of reactiv…”
BackgroundInfluentialOxidative Stress in Diabetic Peripheral Neuropathy: Pathway and Mechanism-Based Treatment
Lin, Q., Li, K., Chen, Y., Xie, J., Wu, C., Cui, C., & Deng, B. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03342-7 · Cited by 105
“The binding of AGE and RAGE can trigger a cascade of downstream signaling pathways involving NF-κB, MAPK/ERK, p21Ras, JNK, and others, leading to enhanced cellular oxidative stress and inflammation [33-35].”
BackgroundCannabis: a multifaceted plant with endless potentials
Fordjour, E., Manful, C. F., Sey, A. A., Javed, R., Pham, T. H., Thomas, R., & Cheema, M. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1200269 · Cited by 109
“Cannabis can potentially impact these processes by activating the receptors in the ECS, leading to an increase in food intake and metabolic processes like lipolysis and glucose metabolism (Sergi et al., 2021).”
BackgroundAdvanced Glycation End-Products and Diabetic Neuropathy of the Retina
Oshitari, T. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24032927 · Cited by 101
“Although not all cellular mechanisms are activated under the AGE-RAGE axis [36], the AGE/RAGE interaction is t ought to activate several cellular pathways and to be associated with the pathophysiology of diabetic retinopathy [9].”
BackgroundPathomechanisms of Diabetic Kidney Disease
Sinha, S. K., & Nicholas, S. B. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12237349 · Cited by 98
“Although AGEs can interact with various receptors, the precise interactions and their roles in cellular responses are not fully understood [61,62].”
BackgroundPal, R., & Bhadada, S. K. (2023) · Bone · doi:10.1016/j.bone.2023.116884 · Cited by 96
The Effects of Dietary Advanced Glycation End-Products on Neurocognitive and Mental Disorders
D'Cunha, N. M., Sergi, D., Lane, M. M., Naumovski, N., Gamage, E., Rajendran, A., Kouvari, M., Gauci, S., Dissanayaka, T. D., Marx, W., et al. (2022) · Nutrients · doi:10.3390/nu14122421 · Cited by 84
“The body aims to remove the toxicity of the AGEs dicarbonyl precursors via the glyoxalase detoxifying system that prevents the formation of AGEs, and via proteasomal degradation of formed AGEs [26].”
BackgroundInfluentialSelf-citationDiet’s Role in Modifying Risk of Alzheimer’s Disease: History and Present Understanding
Grant, W. B., & Blake, S. M. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230418 · Cited by 82
“Good evidence indicates that exogenous sources of AGEs have important health effects [158–160].”
Negrini, T. D. C., Carlos, I. Z., Duque, C., Caiaffa, K. S., & Arthur, R. A. (2021) · Frontiers in Oral Health · doi:10.3389/froh.2021.697428 · Cited by 82
Xiong, K., Li, M., Chen, Y., Hu, Y., & Wen, J. (2024) · Journal of Food Protection · doi:10.1016/j.jfp.2024.100338 · Cited by 74
Wei, Y., Xu, S., Wu, Z., Zhang, M., Bao, M., & He, B. (2024) · Medicine · doi:10.1097/md.0000000000040412 · Cited by 68
Dey, S., Murmu, N., Mondal, T., Saha, I., Chatterjee, S., Manna, R., Haldar, S., Dash, S. K., Sarkar, T. R., & Giri, B. (2022) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.113801 · Cited by 58
van Dongen, K. C. W., Kappetein, L., Estruch, I. M., Belzer, C., Beekmann, K., & Rietjens, I. M. C. M. (2022) · Food and Chemical Toxicology · doi:10.1016/j.fct.2022.112987 · Cited by 63
Nomogram-Based Prediction of the Risk of Diabetic Retinopathy: A Retrospective Study
Mo, R., Shi, R., Yuhong, H., & Hu, F. (2020) · Journal of Diabetes Research · doi:10.1155/2020/7261047 · Cited by 53
Cai, Z., Li, Y., Bai, L., Xu, J., Liu, Z., Zhang, T., Gao, S., & Lin, Y. (2023) · ACS Nano · doi:10.1021/acsnano.3c06999 · Cited by 56
Pincemail, J., & Meziane, S. (2022) · Antioxidants · doi:10.3390/antiox11112270 · Cited by 61
Luo, Y., Zhang, J., Ho, C., & Li, S. (2022) · Food Science and Human Wellness · doi:10.1016/j.fshw.2021.12.012 · Cited by 50
Public Health Risks Associated with Food Process Contaminants – A Review
Zahir, A., Ge, Z., & Khan, I. A. (2024) · Journal of Food Protection · doi:10.1016/j.jfp.2024.100426 · Cited by 44
Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development
Du, C., Whiddett, R. O., Buckle, I., Chen, C., Forbes, J. M., & Fotheringham, A. K. (2022) · Cells · doi:10.3390/cells11213503 · Cited by 49
“Exogenous AGEs in foods can be absorbed across the gastrointestinal tract, contributing to the body’s AGE pool [87].”
BackgroundPucci, M., Aria, F., Premoli, M., Maccarinelli, G., Mastinu, A., Bonini, S. A., Memo, M., Uberti, D. L., & Abate, G. (2021) · Food and Chemical Toxicology · doi:10.1016/j.fct.2021.112608 · Cited by 41
Deledda, A., Palmas, V., Heidrich, V., Fosci, M., Lombardo, M., Cambarau, G., Lai, A., Melis, M., Loi, E., Loviselli, A., et al. (2022) · Metabolites · doi:10.3390/metabo12111092 · Cited by 46
“Among the causes of the altered metabolic control typical of T2DM, the most known is the release of proinflammatory cytokines and free fatty acids (FFA) by adipose tissue infiltrated by macrophages [17] and a proinflammatory diet rich in packaged foods [18], industrial fructose [19], low-quality fats [20], and Advance…”
BackgroundBeaulieu, J., Costa, G., Renaud, J., Moitié, A., Glémet, H., Sergi, D., & Martinoli, M. (2021) · Molecular Neurobiology · doi:10.1007/s12035-021-02328-7 · Cited by 37
Self-citationKoerich, S., Parreira, G. M., de Almeida, D. L., Vieira, R. P., & de Oliveira, A. C. P. (2022) · Current Neuropharmacology · doi:10.2174/1570159x20666220922153903 · Cited by 40
“…represented by side chains of lysine and arginine-containing proteins, with carbonyl compounds, including aldohexoses and ketohexoses, such as glucose and fructose, respectively, as well as α -dicarbonyl moieties derived from autoxidation processes, lipid peroxidation and glycolysis [5, 8, 9].”
Li, L., Kong, S., Liu, Y., Huang, Y., Li, Y., & Lai, K. (2021) · Journal of Food Measurement & Characterization · doi:10.1007/s11694-021-01102-6 · Cited by 36
Demirer, B., Yardımcı, H., & Basmaz, S. E. (2022) · Journal of Diabetes and its Complications · doi:10.1016/j.jdiacomp.2022.108354 · Cited by 36
The Protective Effect of Theaflavins on the Kidney of Mice with Type II Diabetes Mellitus
Wang, J., Jiang, J., Zhao, C., et al. (2022) · Nutrients · doi:10.3390/nu15010201 · Cited by 33
“Endogenous AGEs are usually formed from glycolysis in vivo and can accumulate in tissues [12].”
BackgroundSergi, D., Spaggiari, R., Nora, E. D., Angelini, S., Castaldo, F., Omenetto, A., Stifani, G., Sanz, J. M., & Passaro, A. (2025) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2025.112103 · Cited by 35
Self-citationOliveira, T. L. P. S. D. A., Ribeiro, I. D. C., Jurema-Santos, G., Nobre, I. G., dos Santos, R. M., Rodrigues, C. P. S., OLIVEIRA, K. C. N. D., Henrique, R. D. S., Silva, W. T. F. E., & Araújo, A. V. (2020) · Foods · doi:10.3390/foods9111567 · Cited by 34
Metabolic and Mitochondrial Dysregulations in Diabetic Cardiac Complications
Tashkandi, A. J. A., Gorman, A., Mathers, E. M., Carney, G., Yacoub, A., Setyaningsih, W. A. W., Kuburas, R., & Margariti, A. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26073016 · Cited by 35
“The sustained activation of AGE/RAGE-ROS triggers multiple cellular stress-sensitive pathways, such as PKC, NF κ B, mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription 3 (STAT3), amplifying inflammatory and fibrotic responses in diabetic cardiomyopathy [75].”
Nε-carboxymethyl-lysine and Nε-carboxyethyl-lysine contents in commercial meat products
Yu, L., Li, Y., Gao, C., Yang, Y., Zeng, M., & Chen, J. (2022) · Food Research International · doi:10.1016/j.foodres.2022.111048 · Cited by 32
AGEs-related dysfunctions in PCOS: evidence from animal and clinical research
Tatone, C., Emidio, G. D., Placidi, M., Rossi, G., Ruggieri, S., Taccaliti, C., D’Alfonso, A., Amicarelli, F., & Guido, M. (2021) · Journal of Endocrinology · doi:10.1530/joe-21-0143 · Cited by 34
Rezaei, M., Rabizadeh, S., Mirahmad, M., Hajmiri, M. S., Nakhjavani, M., Hemmatabadi, M., & Shirzad, N. (2022) · Diabetology & Metabolic Syndrome · doi:10.1186/s13098-022-00895-w · Cited by 29
“These findings imply that both AGEs and RAGEs are potential therapeutic targets to avoid diabetes-related vascular complications [17, 29, 30].”
BackgroundZahir, A., Khan, I. A., Nasim, M., Azizi, M. N., & Azi, F. (2024) · Food Additives & Contaminants Part A · doi:10.1080/19440049.2024.2381210 · Cited by 29
“Endogenous AGEs (also called biological AGEs) are produced in the body as part of normal metabolism (Sergi et al. 2021).”
Lee, H., Gu, M. J., Lee, J., Lee, S., Kim, Y., & Ha, S. K. (2021) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.202000799 · Cited by 29
Chumroenvidhayakul, S., Thilavech, T., Abeywardena, M. Y., & Adisakwattana, S. (2023) · Antioxidants · doi:10.3390/antiox12051002 · Cited by 35
Gu, M. J., Lee, Y. R., Kim, D., Kim, Y., & Ha, S. K. (2024) · Comprehensive Reviews in Food Science and Food Safety · doi:10.1111/1541-4337.13412 · Cited by 34
Dietary N‐epsilon‐carboxymethyllysine as for a major glycotoxin in foods: A review
Chen, G. (2021) · Comprehensive Reviews in Food Science and Food Safety · doi:10.1111/1541-4337.12817 · Cited by 27
Lim, J.-M., Yoo, H. J., & Lee, K. (2022) · Marine Drugs · doi:10.3390/md20090580 · Cited by 26
“Intestinal barrier dysfunction, often called “leaky gut”, makes individuals vulnerable to various chronic inflammatory intestinal disorders, including diabetes and inflammatory bowel disease (IBD) [1].”
BackgroundInfluentialDietary Advanced Glycation End Products: An Emerging Concern for Processed Foods
Geng, Y., Mou, Y., Xie, Y., Ji, J., Chen, F., Liao, X., Hu, X., & Ma, L. (2023) · Food Reviews International · doi:10.1080/87559129.2023.2169867 · Cited by 26
“[37] AGEs activate both c-Jun N-terminal kinase (JNK) and the IκB kinase (IKK)/transcription factor nuclear-factor-kappa B (NF-κB) signaling pathway, which have been demonstrated to restrain insulin signaling.”
BackgroundWu, Y., Zong, M., Wu, H., He, D., Li, L., Zhang, X., Zhao, D., & Li, B. (2022) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.202200046 · Cited by 26
Exploring Formation and Control of Hazards in Thermal Processing for Food Safety
Liu, Z., Gao, S., Yuan, Z., Yang, R., Zhang, X., El‐Mesery, H. S., Dai, X., Lu, W., & Xu, R. (2025) · Foods · doi:10.3390/foods14132168 · Cited by 28
“These processes contribute to aging and various chronic diseases such as diabetes [192], Alzheimer’s disease [193], atherosclerosis, and uremia [194].”
A Potential Role for Fructosamine-3-Kinase in Cataract Treatment
Bruyne, S. D., van Schie, L., Himpe, J., Somer, F. M. J. J. D., Everaert, I., Derave, W., den Broecke, C. V., Huizing, M. T., Bostan, N., Speeckaert, M. M., et al. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22083841 · Cited by 23
“Advanced glycation end products (AGEs) are synthesized endogenously via the Maillard reaction and several alternative pathways [6].”
BackgroundThe Exposome and Immune Health in Times of the COVID-19 Pandemic
Morales, J. S., Valenzuela, P. L., Castillo‐García, A., Butragueño, J., Jiménez‐Pavón, D., Carrera‐Bastos, P., & Lucía, A. (2021) · Nutrients · doi:10.3390/nu14010024 · Cited by 24
“There is a growing body of evidence that closely links AGEs with chronic diseases [89,91,92].”
BackgroundGeneral Installation of (4 H )-Imidazolone cis -Amide Bioisosteres Along the Peptide Backbone
Wall, B. J., Sharma, K. K., O’Brien, E. A., et al. (2024) · Journal of the American Chemical Society · doi:10.1021/jacs.3c13825 · Cited by 22
Pathogenesis and Therapeutic Perspectives of Tubular Injury in Diabetic Kidney Disease: An Update
Geng, J., Ma, S., Tang, H. R., & Zhang, C. (2025) · Biomedicines · doi:10.3390/biomedicines13061424 · Cited by 26
“This ligand–receptor axis activates three-tiered signaling cascades, including MAP kinase pathways, Ras-mediated ERK phosphorylation, and JAK/STAT transduction systems [31–33].”
Duisenbek, A., López-Armas, G. D. C., Pérez, M., Perez, M. D., Benítez, J. M. A., Pérez, V. R. P., Ortega, J. G., Yessenbekova, A., Аблайханова, Н. Т., Escames, G., et al. (2023) · Antioxidants · doi:10.3390/antiox12061290 · Cited by 24
“The thermal processing of food and conservation and safety processes of food lead to the generation of diverse food-derived AGEs known as glycotoxins [3,4].”
BackgroundSantos, L. D. O., Ribeiro, A. L. S., Lima, K. M. D. O., dos Santos, I. R. P., de Almeida, B. S., de Matos, M. F. R., Krumreich, F. D., Andrade, L. L., Ruggiero, W. F., & Pinto, L. C. (2024) · Food Control · doi:10.1016/j.foodcont.2024.110960 · Cited by 20
Dean, E., Jia, X., JONES, A. Y. M., Vongsirinavarat, M., Lomi, C., Kumar, P. L., Ngeh, E. N., & Storz, M. A. (2024) · Nutrition Journal · doi:10.1186/s12937-024-01018-z · Cited by 23
Effect of Advanced Glycation end Products (AGEs) on Sperm Parameters and Function in C57Bl/6 Mice
Darmishonnejad, Z., Hassan‐Zadeh, V., Tavalaee, M., Kobarfard, F., Hassani, M., Gharagozloo, P., Drevet, J. R., & Nasr‐Esfahani, M. H. (2024) · Reproductive Sciences · doi:10.1007/s43032-024-01507-w · Cited by 18
van Dongen, K. C. W., van der Zande, M., Bruyneel, B., Vervoort, J. J. M., Rietjens, I. M. C. M., Belzer, C., & Beekmann, K. (2021) · Toxicology in Vitro · doi:10.1016/j.tiv.2021.105078 · Cited by 19
Dicks, L. M. T. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26146744 · Cited by 22
“AGEs are also associated with chronic inflammation, diabetes, Crohn’s disease [99,100], and oxidative stress (listed in the light-yellow area) [101].”
Acrylamide and Advanced Glycation End Products in Frying Food: Formation, Effects, and Harmfulness
Rasool, A., Luo, X., Zhang, Q., Jia, C., Zhao, S., Liu, R., Rong, J., Zhou, G., Wang, B., Kuai, J., et al. (2025) · Foods · doi:10.3390/foods14193313 · Cited by 17
“…active dicarbonyl compounds can also be formed through lipid peroxidation via the acetol pathway [22], Schiff base oxidative cracking (Namiki pathway), the polyol pathway, amino acid-derived ketone metabolism [39], and glucose autoxidation [40], in addition to Amadori product rearrangement.”
Wu, Y., Zong, M., Zhang, Z., Wu, Y., Li, L., Zhang, X., Wu, H., & Li, B. (2022) · Food Chemistry · doi:10.1016/j.foodchem.2022.133284 · Cited by 16
Yang, J., & Jiang, S. (2022) · Acta Diabetologica · doi:10.1007/s00592-022-01973-1 · Cited by 15
Mahmoudinezhad, M., Farhangi, M. A., Kahroba, H., & Dehghan, P. (2021) · Scientific Reports · doi:10.1038/s41598-021-99077-3 · Cited by 17
Modulation of Aging Diseases via RAGE Targets: A Dietary Intervention Review
Wu, Q., Yan, J., Zhang, Y., Ming, X., Chen, S., Zou, Z., Feng, N., & Xiao, J. (2025) · Advanced Science · doi:10.1002/advs.202510242 · Cited by 16
Structures of Toxic Advanced Glycation End-Products Derived from Glyceraldehyde, A Sugar Metabolite
Sakai, A., Takeda, K., Suzuki, H., & Takeuchi, M. (2024) · Biomolecules · doi:10.3390/biom14020202 · Cited by 13
“…TAGE levels under oxidative stress and inflammatory/hyperglycemic conditions and showed that they were associated with insulin resistance, endothelial dysfunction, vascular inflammation, and a decreased number and reduced migratory activity of endothelial progenitor cells (EPCs) in humans [23].”
BackgroundYao, M., Xu, F., Yao, Y., Wang, H., Ju, X., & Wang, L. (2022) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.2c03718 · Cited by 15
Ávila, F., Cruz, N., González, M. A., Eduardo Fuentes, Q., Wehinger, S., & Mariane Lutz, R. (2025) · Biochimie · doi:10.1016/j.biochi.2025.06.001 · Cited by 15
Advanced glycation end products are associated with cardiovascular risk in the Mexican population
Robles-Rivera, K., Rivera‐Paredez, B., Quezada-Sanchez, A. D., Velázquez‐Cruz, R., & Salmerón, J. (2023) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2022.12.028 · Cited by 13
Ameera, K., Mukunda, D. C., Basha, S., Rodrigues, J., Biswas, S., Mazumder, N., Prabhu, V. K., Prabhu, M. M., & Mahato, K. K. (2025) · Applied Spectroscopy Reviews · doi:10.1080/05704928.2025.2477237 · Cited by 13
Glycation-induced age-related illnesses, antiglycation and drug delivery strategies
Abdelkader, H., Mustafa, W. W., Alqahtani, A., Alsharani, S., Fatease, A. M. A., & Alany, R. G. (2022) · Journal of Pharmacy and Pharmacology · doi:10.1093/jpp/rgac051 · Cited by 12
Melloni, M., Sergi, D., Simioni, C., Passaro, A., & Neri, L. M. (2023) · Biology · doi:10.3390/biology12030449 · Cited by 12
“Insulin resistance is referred to as a blunted response of insulin tissue targets to this hormone leading to impaired glycaemic control, dyslipidemia along with an increased risk of developing cardiovascular disease and certain types of cancer [4,5].”
BackgroundSelf-citationVitamin B6 and diabetes and its role in counteracting advanced glycation end products
Vernı̀, F. (2024) · Vitamins and hormones · doi:10.1016/bs.vh.2024.02.005 · Cited by 12
The relationship of redox signaling with the risk for atherosclerosis
Lei, S., Liu, C., Zheng, T., Fu, W., & Huang, M.-Z. (2024) · Frontiers in Pharmacology · doi:10.3389/fphar.2024.1430293 · Cited by 14
Xu, F., Zhang, M., Wu, H., et al. (2022) · Pharmaceutical Biology · doi:10.1080/13880209.2022.2067568 · Cited by 12
“AGEs play a significant role in the pathogenesis of multiple diabetic complications (Sergi et al. 2021).”
BackgroundLiu, R., Zhang, M., Xu, L. Z., Liu, J., Yang, P., Li, M., & Qin, J. (2022) · Frontiers in Nutrition · doi:10.3389/fnut.2022.1083872 · Cited by 12
“Advanced glycation end products (AGEs) are generated through the Maillard reaction between reducing sugars (such as glucose and fructose) and amino compounds (1, 2).”
BackgroundInfluentialAydemi̇r, M. E., Arslan, A., Takım, K., Altun, S. K., Yılmaz, M. A., & Çakır, O. (2023) · Meat Science · doi:10.1016/j.meatsci.2023.109362 · Cited by 11
Wu, Y., Yang, Y., Zhong, Y., Wu, Y., Zhang, Z., Yan, Z., Liu, B.-X., & Wang, W. (2024) · Food & Function · doi:10.1039/d4fo01545b · Cited by 13
Zarei, M., Rahimi, K., Hassanzadeh, K., Abdi, M., Hosseini, V., Fathi, A., & Kakaei, K. (2021) · Environmental Research · doi:10.1016/j.envres.2021.111555 · Cited by 11
Ashraf, G. M., Ebada, M. A., Suhail, M., Ali, A., Uddin, M. S., Bilgrami, A. L., Perveen, A., Husain, A., Tarique, M., Hafeez, A., et al. (2021) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2021/4572471 · Cited by 11
Liang, Z., Chen, X., Yang, Z., et al. (2022) · Frontiers in Nutrition · doi:10.3389/fnut.2022.874650 · Cited by 11
“Dietary AGEs can accumulate in the body and have a harmful effect on human health (2).”
BackgroundCalorie restriction mimetics against aging and inflammation
Chaudhary, S., Chaudhary, M. R., Jena, M. K., Rath, P. K., Mishra, B. P., Paital, B., Vyas, A., Sahoo, D. K., Singh, P., & Mehdi, M. M. (2025) · Biogerontology · doi:10.1007/s10522-025-10269-0 · Cited by 13
Blidi, S., Troise, A. D., Ledbetter, M., Cottin, S., Sturrock, K. R., Pascale, S. D., Scaloni, A., & Fiore, A. (2023) · LWT · doi:10.1016/j.lwt.2023.114679 · Cited by 10
Lu, X., Ma, R., Zhan, J., Pan, X., Liu, C., Zhang, S., & Tian, Y. (2024) · Critical Reviews in Food Science and Nutrition · doi:10.1080/10408398.2024.2407894 · Cited by 11
“Several animal and clinical studies ( Khalid , Petroianu, and Adem 2022; Sergi et al. 2021) suggested that they might disrupt glucose homeostasis by interfering with glucose metabolism, pancreatic β-cell function, or insulin signaling pathways.”
Patil, N. A., Kelkar, A., & Sivaram, A. (2022) · BioNanoScience · doi:10.1007/s12668-022-00954-6 · Cited by 8
“Over a period of time, AGE accumulates in the body, damaging the proteins, thereby contributing to the diseases [3].”
BackgroundLitwinowicz, K., Waszczuk, E., Kuzan, A., Bronowicka-Szydełko, A., Gostomska‐Pampuch, K., Naporowski, P., & Gamian, A. (2022) · Nutrients · doi:10.3390/nu14245266 · Cited by 9
Tian, A., Yan, Z., Li, H., Zhang, Z., Du, L., Huang, X., Sun, L., & Wu, H. (2024) · Food & Function · doi:10.1039/d4fo00774c · Cited by 8
RAGE as a Novel Biomarker for Prostate Cancer: A Systematic Review and Meta-Analysis
Applegate, C. C., Nelappana, M. B., Nielsen, E. A., Kalinowski, L., Dobrucki, I. T., & Dobrucki, L. W. (2023) · Cancers · doi:10.3390/cancers15194889 · Cited by 8
“High levels of dietary AGEs are associated with the development of inflammation-related chronic pathologies, including cancer [14,15].”
The dynamic roles of advanced glycation end products
Khalid, M., & Adem, A. (2024) · Vitamins and hormones · doi:10.1016/bs.vh.2024.02.008 · Cited by 11
Antiglycating effects of citrus flavonoids and associated mechanisms
Xiao, Y., Shen, J., Zhan, J., Guo, L., Ho, C., & Li, S. (2024) · Food Science and Human Wellness · doi:10.26599/fshw.2022.9250247 · Cited by 9
Erim, B., & Binici, H. İ. (2024) · Nutrire · doi:10.1186/s41110-024-00298-z · Cited by 8
“These AGEs bind to the RAGE, initiating a cascade of signaling pathways [16]. c-Jun N-terminal kinase (JNK), a key protein within the MAPK family, plays a crucial role in generating stress-induced responses [17].”
Emami, N., Masouleh, A. A. M., Maleki‐Hajiagha, A., Dizavi, A., Vesali, S., & Moini, A. (2023) · Journal of Ovarian Research · doi:10.1186/s13048-023-01224-z · Cited by 8
“Other than being endogenously formed, AGEs are found abundantly in fast-food meals and products [5].”
BackgroundWhat Every Diabetologist Should Know about SARS-CoV-2: State of Knowledge at the Beginning of 2021
Abramczyk, U., & Kuzan, A. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10051022 · Cited by 8
“The consequences of these changes are angiopathies, nephropathies, neuropathies, and other diseases accompanying diabetes [60].”
BackgroundLima, M. T. N. S., Boulanger, É., Tessier, F. J., & Takahashi, J. A. (2022) · Foods · doi:10.3390/foods11121676 · Cited by 8
Diabetes and brain: omics approaches to study diabetic encephalopathy
Lionetti, N., Lago, M. L. F., Brescia, T., Bevilacqua, F., & Gnoni, A. (2025) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1570585 · Cited by 9
“AGEs can increase cellular oxidative stress by binding to their cellular receptors (RAGE), by stimulating the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and JNK (c-Jun N-terminal Kinase), which promote the production of reactive oxygen species (ROS) (62).”
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
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.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
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
