Higher dietary advanced glycation products intake is associated with increased risk of dementia, independent from genetic predisposition

Zhang, Yebing; Jiang, Fangyuan; Liu, Di; Xue, Liyan; Ma, Zhiyong; Yao, Zhen; Ma, Aiguo; Qin, Liqiang; Chen, Guo-Chong; Wan, Zhongxiao

doi:10.1016/j.clnu.2023.08.006

Cited by 4 publications

(2 citation statements)

References 48 publications

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“…AGEs are also formed during the high-temperature processing of foods. These dietary AGEs, when ingested, may also contribute to disease onset and the progression of non-alcoholic fatty liver disease (NAFLD) [81], pediatric obesity [82], cancer [83], dementia [84], and diabetes [85]. AGEs accelerate diabetes-related atherosclerosis by activating RAGE-NF-kB signaling, thereby promoting low-density lipoprotein (LDL) transcytosis in endothelial cells [78].…”

Section: Oxidative Stress and Advanced Glycation End Products (Ages)mentioning

confidence: 99%

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Oxidative Stress in Health and Disease

Reddy

2023

Biomedicines

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Oxidative stress, resulting from the excessive intracellular accumulation of reactive oxygen species (ROS), reactive nitrogen species (RNS), and other free radical species, contributes to the onset and progression of various diseases, including diabetes, obesity, diabetic nephropathy, diabetic neuropathy, and neurological diseases, such as Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and Parkinson’s disease (PD). Oxidative stress is also implicated in cardiovascular disease and cancer. Exacerbated oxidative stress leads to the accelerated formation of advanced glycation end products (AGEs), a complex mixture of crosslinked proteins and protein modifications. Relatively high levels of AGEs are generated in diabetes, obesity, AD, and other I neurological diseases. AGEs such as Ne-carboxymethyllysine (CML) serve as markers for disease progression. AGEs, through interaction with receptors for advanced glycation end products (RAGE), initiate a cascade of deleterious signaling events to form inflammatory cytokines, and thereby further exacerbate oxidative stress in a vicious cycle. AGE inhibitors, AGE breakers, and RAGE inhibitors are therefore potential therapeutic agents for multiple diseases, including diabetes and AD. The complexity of the AGEs and the lack of well-established mechanisms for AGE formation are largely responsible for the lack of effective therapeutics targeting oxidative stress and AGE-related diseases. This review addresses the role of oxidative stress in the pathogenesis of AGE-related chronic diseases, including diabetes and neurological disorders, and recent progress in the development of therapeutics based on antioxidants, AGE breakers and RAGE inhibitors. Furthermore, this review outlines therapeutic strategies based on single-atom nanozymes that attenuate oxidative stress through the sequestering of reactive oxygen species (ROS) and reactive nitrogen species (RNS).

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Section: Oxidative Stress and Advanced Glycation End Products (Ages)mentioning

confidence: 99%

Section: Oxidative Stress and Advanced Glycation End Products (Ages)mentioning

confidence: 99%

Oxidative Stress in Health and Disease

Reddy

2023

Biomedicines

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Polyphenols as Reactive carbonyl substances Regulators: A comprehensive review of thermal processing hazards mitigation

Chen,

Xu,

Yang

et al. 2024

Food Research International

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The contribution of dietary advanced glycation end‐products and genetic risk in the development of inflammatory bowel disease: a prospective cohort study

Jiang,

Yang,

Cao

et al. 2024

Aliment Pharmacol Ther

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SummaryBackgroundDietary advanced glycation end products (AGEs) may promote oxidative stress and inflammation in the gastrointestinal tract.AimsThe aim of this study is to investigate the association between dietary AGE intake and the risk of inflammatory bowel disease (IBD).MethodsWe included 121,978 participants without IBD at baseline from the UK Biobank. We estimated consumption of three common AGEs (Nε‐(carboxymethyl)‐lysine (CML), Nε‐(1‐carboxyethyl)‐lysine (CEL), and Nδ‐(5‐hydro‐5‐methyl‐4‐imidazolon‐2‐yl)‐ornithine (MG‐H1)) by matching 24‐h dietary questionnaires to a validated dietary AGE database. We used Cox proportional hazards regression models to calculate the hazard ratio (HR) and 95% CI of the association between dietary AGEs and IBD risk.ResultsDuring a median follow‐up of 13.72 years, 671 participants developed IBD (192 with Crohn's disease (CD) and 478 with ulcerative colitis (UC)). Among the assessed dietary AGEs, only CEL was associated with an increased risk of IBD (HR = 1.09, 95% CI: 1.01–1.18, p = 0.020) and CD (HR = 1.18, 95% CI: 1.03–1.36, p = 0.014), particularly for participants who were overweight, physically inactive, and non‐smokers. Among participants at a high genetic risk of CD, HRs (95% CI) of CD were 1.26 (1.00–1.57) for CML, 1.41 (1.12–1.77) for CEL, and 1.28 (1.01–1.62) for MG‐H1 (p < 0.05 for each). However, none of the dietary AGEs was significantly associated with UC risk, irrespective of genetic predisposition.ConclusionsDietary CEL was associated with an increased risk of IBD and CD, but not UC. Further interventional studies are required to support the potential benefit of AGE restriction, especially for individuals at a high genetic risk of CD.

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Higher dietary advanced glycation products intake is associated with increased risk of dementia, independent from genetic predisposition

Cited by 4 publications

References 48 publications

Oxidative Stress in Health and Disease

Oxidative Stress in Health and Disease

Polyphenols as Reactive carbonyl substances Regulators: A comprehensive review of thermal processing hazards mitigation

The contribution of dietary advanced glycation end‐products and genetic risk in the development of inflammatory bowel disease: a prospective cohort study

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