Comprehensive Analyses of Carbohydrates, 1,2-Dicarbonyl Compounds, and Advanced Glycation End Products in Industrial Bread Making

2021 ◽  
Author(s):  
Tobias Jost ◽  
Christian Henning ◽  
Thomas Heymann ◽  
Marcus A. Glomb
Keyword(s):  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Bread Making ◽  
Dicarbonyl Compounds ◽  
Glycation End Products ◽  
End Products

scholarly journals Effect of fatty acids and triglycerides on the formation of lysine-derived advanced glycation end-products in model systems exposed to frying temperature

RSC Advances ◽  
2019 ◽  
Vol 9 (27) ◽  
pp. 15162-15170 ◽  
Author(s):  
Yuting Wang ◽  
Huiyu Hu ◽  
David Julian McClements ◽  
Shaoping Nie ◽  
Mingyue Shen ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Advanced Glycation End Products ◽  
Model Systems ◽  
Advanced Glycation ◽  
Frying Temperature ◽  
Dicarbonyl Compounds ◽  
Amadori Products ◽  
Glycation End Products ◽  
End Products

Fatty acids and triglycerides impact lysine-derived AGE formation through modulating the formation of α-dicarbonyl compounds and Amadori products.

Induction of 1,2-Dicarbonyl Compounds, Intermediates in the Formation of Advanced Glycation End-Products, during Heat-Sterilization of Glucose-Based Peritoneal Dialysis Fluids

1999 ◽  
Vol 19 (4) ◽  
pp. 325-333 ◽  
Author(s):  
Casper G. Schalkwijk ◽  
Nynke Posthuma ◽  
Herman J. Ten Brink ◽  
Pieter M. Ter Wee ◽  
Tom Teerlink
Keyword(s):  
Peritoneal Dialysis ◽  
Advanced Glycation End Products ◽  
Dwell Time ◽  
Advanced Glycation ◽  
Fluorescence Excitation ◽  
Dicarbonyl Compounds ◽  
Glycation End Products ◽  
End Products

Objective To study the presence of 1,2-dicarbonyl compounds in peritoneal dialysis (PD) fluids, their concentration in effluents with increasing dwell time, and their role in the formation of advanced glycation end-products (AGEs). Measurements Dicarbonyl compounds in heat- and filter-sterilized PD fluids were quantified by reverse-phase high performance liquid chromatography (HPLC) after derivatization to dimethoxyquinoxaline derivatives. Kinetics of the in vitro formation of AGEs upon incubation of 1,2-dicarbonyl compounds or PD fluids with albumin, with or without aminoguanidine, were measured by AGE fluorescence (excitation/emission wavelengths of 350 nm/430 nm). Patients AGEs and dicarbonyl compounds were measured in effluents collected from standardized 4-hour dwells from 8 continuous cycling peritoneal dialysis patients. Results In PD fluids, 3-deoxyglucosone (3-DG) has been identified as the major dicarbonyl compound formed during the process of heat sterilization. The process also formed glyoxal (GO) and methylglyoxal (MGO), with the amount of 3-DG being approximately 25 – 60 times higher than GO and MGO. When incubated with albumin, the identified 1,2-dicarbonyl compounds rapidly formed AGEs. The formation of AGEs was more pronounced in conventional heat-sterilized PD fluids compared with filter-sterilized PD fluids, and was completely inhibited by aminoguanidine. In effluents, the concentration of MGO, GO, and 3-DG decreased with increasing dwell time, with a concomitant increase in AGE fluorescence. Conclusions The dicarbonyl compounds 3-DG, MGO, and GO are potent promoters of AGE formation. The presence of these and possibly other dicarbonyl compounds formed during heat sterilization of glucose-based PD fluids is, to a large extent, responsible for the in vitro AGE formation by these fluids, as evidenced by the speed of AGE formation in PD fluids and the complete inhibition by aminoguanidine. Because 3-DG, MGO, and GO are rapidly cleared from PD fluids during dialysis, these compounds may contribute to the in vivo AGE formation in PD patients.

scholarly journals In Vitro Evaluation of the Toxicological Profile and Oxidative Stress of Relevant Diet-Related Advanced Glycation End Products and Related 1,2-Dicarbonyls

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Vanesa Cepas ◽  
Friederike Manig ◽  
Juan C. Mayo ◽  
Michael Hellwig ◽  
Debora Collotta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amino Acids ◽  
Cell Death ◽  
Advanced Glycation End Products ◽  
Intracellular Signaling ◽  
Nuclear Translocation ◽  
Advanced Glycation ◽  
Dicarbonyl Compounds ◽  
Glycation End Products ◽  
End Products

During food processing and storage, and in tissues and fluids under physiological conditions, the Maillard reaction occurs. During this reaction, reactive 1,2-dicarbonyl compounds arise as intermediates that undergo further reactions to form advanced glycation end products (AGEs). Diet is the primary source of exogenous AGEs. Endogenously formed AGEs have been proposed as a risk factor in the pathogenesis of diet-related diseases such as diabetes, insulin resistance, cardiovascular diseases, or chronic disease. AGEs may differently contribute to the diet-related exacerbation of oxidative stress, inflammation, and protein modifications. Here, to understand the contribution of each compound, we tested individually, for the first time, the effect of five 1,2-dicarbonyl compounds 3-deoxyglucosone (3-DG), 3-deoxygalactosone (3-DGal), 3,4-dideoxyglucosone-3-ene (3,4-DGE), glyoxal (GO), and methylglyoxal (MGO) and four different glycated amino acids N-ε-(carboxyethyl)lysine (CEL), N- ε -(carboxymethyl)lysine (CML), methylglyoxal-derived hydroimidazolone-1 (MG-H1), and pyrraline (Pyrr) in a cell line of human keratinocytes (HaCaT). We found that most of the glycated amino acids, i.e., CEL, CML, and MG-H1, did not show any cytotoxicity. At the same time, 1,2-dicarbonyl compounds 3-DGal, 3,4-DGE, GO, and MGO increased the production of reactive oxygen species and induced cell death. MGO induced cell death by apoptosis, whereas 3-DGal and 3,4-DGE induced nuclear translocation of the proinflammatory NF-κB transcription pathway, and the activation of the pyroptosis-related NLRP3 inflammasome cascade. Overall, these results demonstrate the higher toxic impact of 1,2-dicarbonyl compounds on mucosal epithelial cells when compared to glycated amino acids and the selective activation of intracellular signaling pathways involved in the crosstalk mechanisms linking oxidative stress to excessive inflammation.

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