Differential Effects of Dietary Patterns on Advanced Glycation end Products: A Randomized Crossover Study

Kim, Yoona; Keogh, Jennifer B.; Deo, Permal; Clifton, Peter M.

doi:10.3390/nu12061767

Cited by 26 publications

(16 citation statements)

References 40 publications

(65 reference statements)

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“…The discrepancy in findings between our study and previous studies may also be explained by different measures and methods used to determine AGEs intake or different methods for assessment of allergy outcomes. Previous studies investigating the association between AGEs and disease outcomes used serum levels of AGEs, 31,46 or activity of the age receptor (RAGE) 37,42,43 rather than dietary intake of AGEs as in our study. Some studies measured reported highfructose corn syrup-sweetened soft drinks, fruit drinks, 38 apple juice, and soda intake.…”

Section: Discussionmentioning

confidence: 99%

Advanced glycation end product intake during pregnancy and offspring allergy outcomes: A Prospective cohort study

Venter

Pickett

Starling

et al. 2021

Clin Experimental Allergy

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Background:Associations have been shown between concurrent assessment of dietary intake of advanced glycation end products (AGEs) and childhood allergic outcomes. We examined the association between maternal AGEs intake and development of offspring asthma, wheeze, atopic dermatitis, allergic rhinitis and food allergies, and sought to determine whether the intake of AGEs was associated with cord sera cytokines/chemokines. Methods: Pregnant women ≥16 years were recruited in the Healthy Start study, a prospective pre-birth cohort from Colorado (N = 1410). The analysis included 962 dyads with adequate diet (≥2 recalls) and allergy outcome details. AGEs intake was estimated for each mother by matching intakes reported using 24-h dietary recalls during pregnancy to a reference database of commonly consumed foods' AGEs values. Child diagnoses of asthma and allergies up to 8 years were obtained from electronic medical records. Cord sera cytokines and chemokines were analysed in a subset (N = 462) of children. Results:The median [IQR] AGEs intake for the overall sample was 11,919 kU/day [8293,16,573]. Unadjusted analysis showed a positive association between maternal AGEs intake in pregnancy and rhinitis up to 8 years of age (HR = 1.03; 95% CI: 1.01, 1.06), but the association was attenuated and no longer significant in adjusted models (HR = 1.01; 95% CI: 0.98, 1.04). Both adjusted and unadjusted models showed no associations between AGEs intake in pregnancy and any of the other outcomes (p > .05). There were no significant associations between any cytokine or chemokine measured and AGEs intake or any of the outcomes studied (p > .05). Conclusion:The study showed that maternal AGEs intake was not associated with offspring asthma and allergy outcomes. AGEs exposure during pregnancy may not have the same impact on child development as postnatal exposure.

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Section: Discussionmentioning

confidence: 99%

Advanced glycation end product intake during pregnancy and offspring allergy outcomes: A Prospective cohort study

Venter

Pickett

Starling

et al. 2021

Clin Experimental Allergy

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“…Their isolation from tissues can cause undesirable chemical modifications and the formation of artefacts ( 44 ). Nevertheless, research on the content of AGEs in serum, in tissues and in food is very desirable, particularly for diagnostic and therapeutic purposes ( 14 , 21 , 38 , 41 , 45 , 46 ).…”

Section: Methodology For Determining Ages In Biological Materialsmentioning

confidence: 99%

“…A number of methods for determining AGEs in samples are available. Amongst the most frequently used are chromatographic methods coupled with mass spectroscopy ( 11 , 14 , 44 , 46 ). Equally popular are immunoenzymatic methods using antibodies ( 1 , 4 , 44 , 47 ); however, the specificity of the antibodies ( 11 , 14 ) or the low quantities of antigens in the sample can cause difficulties ( 1 ).…”

Section: Methodology For Determining Ages In Biological Materialsmentioning

confidence: 99%

Toxicity of advanced glycation end products (Review)

Kuzan

2021

Biomed Rep

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Advanced glycation end-products (AGEs) are proteins or lipids glycated nonenzymatically by glucose, or other reducing sugars and their derivatives, such as glyceraldehyde, glycolaldehyde, methyloglyoxal and acetaldehyde. There are three different means of AGE formation: i) Maillard reactions, the polyol pathway and lipid peroxidation. AGEs participate in the pathological mechanisms underlying the development of several diseases, such as diabetes and its complications, retinopathy or neuropathy, neurological disorders (for example, Parkinson's disease and Alzheimer's disease), atherosclerosis, hypertension and several types of cancer. AGE levels are increased in patients with hyperglycaemia, and is likely the result of the high concentration of glycation substrates circulating in the blood. The present review summarises the formation and nomenclature of advanced glycation end-products, with an emphasis on the role of AGEs in the development of diabetes, neurological disorders, as well as in cancer and other pathologies. A particular focus is placed on the functions of toxic AGEs. Additionally, studies which have shown the cytotoxicity of glycated albumin and other AGEs are also discussed. Finally, the diagnostic relevance of AGEs as well as for targeting in therapeutic strategies are highlighted.

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“…Significant amounts of MG-H1 and CEL have been quantified in a wide variety of bread and baked goods, fried eggs, cereal and cereal products, peanut butter, nuts and seeds, tofu, chocolate, salmon, and red and processed meats . Plasma levels of CEL were elevated in individuals without T2D consuming a diet high in red and processed meat and refined grains when compared to a group with a diet high in whole grain, dairy, nuts, and legumes …”

Section: Mg Forms Covalent Adducts On Dna and Proteinmentioning

confidence: 99%

Diet and Obesity-Induced Methylglyoxal Production and Links to Metabolic Disease

Hernandez-Castillo

Shuck

2021

Chem. Res. Toxicol.

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The obesity rate in the United States is 42.4% and has become a national epidemic. Obesity is a complex condition that is influenced by socioeconomic status, ethnicity, genetics, age, and diet. Increased consumption of a Western diet, one that is high in processed foods, red meat, and sugar content, is associated with elevated obesity rates. Factors that increase obesity risk, such as socioeconomic status, also increase consumption of a Western diet because of a limited access to healthier options and greater affordability of processed foods. Obesity is a public health threat because it increases the risk of several pathologies, including atherosclerosis, diabetes, and cancer. The molecular mechanisms linking obesity to disease onset and progression are not well understood, but a proposed mechanism is physiological changes caused by altered lipid peroxidation, glycolysis, and protein metabolism. These metabolic pathways give rise to reactive molecules such as the abundant electrophile methylglyoxal (MG), which covalently modifies nucleic acids and proteins. MG-adducts are associated with obesity-linked pathologies and may have potential for biomonitoring to determine the risk of disease onset and progression. MG-adducts may also play a role in disease progression because they are mutagenic and directly impact protein stability and function. In this review, we discuss how obesity drives metabolic alterations, how these alterations lead to MG production, the association of MG-adducts with disease, and the potential impact of MG-adducts on cellular function.

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Differential Effects of Dietary Patterns on Advanced Glycation end Products: A Randomized Crossover Study

Cited by 26 publications

References 40 publications

Advanced glycation end product intake during pregnancy and offspring allergy outcomes: A Prospective cohort study

Advanced glycation end product intake during pregnancy and offspring allergy outcomes: A Prospective cohort study

Toxicity of advanced glycation end products (Review)

Diet and Obesity-Induced Methylglyoxal Production and Links to Metabolic Disease

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