Dietary advanced glycation end products modify gut microbial composition and partially increase colon permeability in rats

2017 ◽  
Vol 61 (10) ◽  
pp. 1700118 ◽  
Author(s):  
Wanting Qu ◽  
Xiaojin Yuan ◽  
Jinsong Zhao ◽  
Yingxiao Zhang ◽  
Jing Hu ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Microbial Composition ◽  
Glycation End Products ◽  
End Products

scholarly journals Effects of Exogenous Dietary Advanced Glycation End Products on the Cross-Talk Mechanisms Linking Microbiota to Metabolic Inflammation

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2497
Author(s):  
Raffaella Mastrocola ◽  
Debora Collotta ◽  
Giulia Gaudioso ◽  
Marie Le Berre ◽  
Alessia Sofia Cento ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Protein Glycosylation ◽  
Advanced Glycation ◽  
Microbial Composition ◽  
Glycosylation Profile ◽  
Metabolic Inflammation ◽  
Altered Glucose ◽  
Glycation End Products ◽  
End Products ◽  
The Impact

Heat-processed diets contain high amounts of advanced glycation end products (AGEs). Here we explore the impact of an AGE-enriched diet on markers of metabolic and inflammatory disorders as well as on gut microbiota composition and plasma proteins glycosylation pattern. C57BL/6 mice were allocated into control diet (CD, n = 15) and AGE-enriched diet (AGE-D, n = 15) for 22 weeks. AGE-D was prepared replacing casein by methylglyoxal hydroimidazolone-modified casein. AGE-D evoked increased insulin and a significant reduction of GIP/GLP-1 incretins and ghrelin plasma levels, altered glucose tolerance, and impaired insulin signaling transduction in the skeletal muscle. Moreover, AGE-D modified the systemic glycosylation profile, as analyzed by lectin microarray, and increased Nε-carboxymethyllysine immunoreactivity and AGEs receptor levels in ileum and submandibular glands. These effects were associated to increased systemic levels of cytokines and impaired gut microbial composition and homeostasis. Significant correlations were recorded between changes in bacterial population and in incretins and inflammatory markers levels. Overall, our data indicates that chronic exposure to dietary AGEs lead to a significant unbalance in incretins axis, markers of metabolic inflammation, and a reshape of both the intestinal microbiota and plasma protein glycosylation profile, suggesting intriguing pathological mechanisms underlying AGEs-induced metabolic derangements.

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