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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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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
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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
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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
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plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
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- Not checked yetcites [5] source
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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.
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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
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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.
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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
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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.
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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
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- Not checked yetcites [17] source
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- 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]
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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
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- Not checked yetcites [36]
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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
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- Not checked yetcites [28]
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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.
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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
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- Not checked yetcites [33]
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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]
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plaindirect- Asserted: passes — The authors put it forward as true.
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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.
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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
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- Not checked yetcites [4] source
plaindirect- Asserted: passes — The authors put it forward as true.
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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
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- Not checked yetcites [23]
plaindirect- Asserted: passes — The authors put it forward as true.
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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.
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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.
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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
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- Not checked yetcites [47]
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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
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- Not checked yetcites [61]
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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]
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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
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- Not checked yetcites [67]
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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]
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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
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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
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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
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- Not checked yetcites [96] source
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plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
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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
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plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
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- Not checked yetcites [98]
- Not checked yetcites [99]
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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.
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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.
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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.
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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.
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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.
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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]
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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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