The advanced glycation end product Nϵ‐carboxymethyllysine and its precursor glyoxal increase serotonin release from Caco‐2 cells

Advanced glycation end products (AGEs), comprising a highly diverse class of Maillard reaction compounds formed in vivo and during heating processes of foods, have been described in the progression of several degenerative conditions such as Alzheimer's disease and diabetes mellitus. Nϵ‐Carboxym...

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Published in:Journal of cellular biochemistry 2018-03, Vol.119 (3), p.2731-2741
Main Authors: Holik, Ann‐Katrin, Lieder, Barbara, Kretschy, Nicole, Somoza, Mark M., Ley, Jakob P., Hans, Joachim, Somoza, Veronika
Format: Article
Language:English
Subjects:
Advanced glycosylation end products
Alzheimer's disease
caco‐2 cells
Carboxymethyllysine
Diabetes mellitus
DNA microarrays
Enterocytes
Fatty acids
Food
Food processing
Gene expression
Gene regulation
Genomes
Glucose
glucose uptake
Glycosylation
glyoxal
Intestinal motility
Intestine
Maillard reaction
Neurodegenerative diseases
Nϵ‐carboxymethyllysine
Serotonin
serotonin release
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container_title Journal of cellular biochemistry
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Somoza, Veronika
description Advanced glycation end products (AGEs), comprising a highly diverse class of Maillard reaction compounds formed in vivo and during heating processes of foods, have been described in the progression of several degenerative conditions such as Alzheimer's disease and diabetes mellitus. Nϵ‐Carboxymethyllysine (CML) represents a well‐characterized AGE, which is frequently encountered in a Western diet and is known to mediate its cellular effects through binding to the receptor for AGEs (RAGE). As very little is known about the impact of exogenous CML and its precursor, glyoxal, on intestinal cells, a genome‐wide screening using a customized microarray was conducted in fully differentiated Caco‐2 cells. After verification of gene regulation by qPCR, functional assays on fatty acid uptake, glucose uptake, and serotonin release were performed. While only treatment with glyoxal showed a slight impact on fatty acid uptake (P 
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Nϵ‐Carboxymethyllysine (CML) represents a well‐characterized AGE, which is frequently encountered in a Western diet and is known to mediate its cellular effects through binding to the receptor for AGEs (RAGE). As very little is known about the impact of exogenous CML and its precursor, glyoxal, on intestinal cells, a genome‐wide screening using a customized microarray was conducted in fully differentiated Caco‐2 cells. After verification of gene regulation by qPCR, functional assays on fatty acid uptake, glucose uptake, and serotonin release were performed. While only treatment with glyoxal showed a slight impact on fatty acid uptake (P &lt; 0.05), both compounds reduced glucose uptake significantly, leading to values of 81.3% ± 22.8% (500 μM CML, control set to 100%) and 68.3% ± 20.9% (0.3 μM glyoxal). Treatment with 500 μM CML or 0.3 μM glyoxal increased serotonin release (P &lt; 0.05) to 236% ± 111% and 264% ± 66%, respectively. Co‐incubation with the RAGE antagonist FPS‐ZM1 reduced CML‐induced serotonin release by 34%, suggesting a RAGE‐mediated mechanism. Similarly, co‐incubation with the SGLT‐1 inhibitor phloridzin attenuated serotonin release after CML treatment by 32%, hinting at a connection between CML‐stimulated serotonin release and glucose uptake. Future studies need to elucidate whether the CML/glyoxal‐induced serotonin release in enterocytes might stimulate serotonin‐mediated intestinal motility. Nepsilon‐Carboxymethyllysine (CML), which represents a well‐characterized Maillard reaction product that is frequently encountered in a Western diet, and its precursor glyoxal induce serotonin release in fully differentiated Caco‐2 cells. 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Nϵ‐Carboxymethyllysine (CML) represents a well‐characterized AGE, which is frequently encountered in a Western diet and is known to mediate its cellular effects through binding to the receptor for AGEs (RAGE). As very little is known about the impact of exogenous CML and its precursor, glyoxal, on intestinal cells, a genome‐wide screening using a customized microarray was conducted in fully differentiated Caco‐2 cells. After verification of gene regulation by qPCR, functional assays on fatty acid uptake, glucose uptake, and serotonin release were performed. While only treatment with glyoxal showed a slight impact on fatty acid uptake (P &lt; 0.05), both compounds reduced glucose uptake significantly, leading to values of 81.3% ± 22.8% (500 μM CML, control set to 100%) and 68.3% ± 20.9% (0.3 μM glyoxal). Treatment with 500 μM CML or 0.3 μM glyoxal increased serotonin release (P &lt; 0.05) to 236% ± 111% and 264% ± 66%, respectively. Co‐incubation with the RAGE antagonist FPS‐ZM1 reduced CML‐induced serotonin release by 34%, suggesting a RAGE‐mediated mechanism. Similarly, co‐incubation with the SGLT‐1 inhibitor phloridzin attenuated serotonin release after CML treatment by 32%, hinting at a connection between CML‐stimulated serotonin release and glucose uptake. Future studies need to elucidate whether the CML/glyoxal‐induced serotonin release in enterocytes might stimulate serotonin‐mediated intestinal motility. Nepsilon‐Carboxymethyllysine (CML), which represents a well‐characterized Maillard reaction product that is frequently encountered in a Western diet, and its precursor glyoxal induce serotonin release in fully differentiated Caco‐2 cells. 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Co‐incubation with the RAGE antagonist FPS‐ZM1 reduced CML‐induced serotonin release by 34%, suggesting a RAGE‐mediated mechanism. Similarly, co‐incubation with the SGLT‐1 inhibitor phloridzin attenuated serotonin release after CML treatment by 32%, hinting at a connection between CML‐stimulated serotonin release and glucose uptake. Future studies need to elucidate whether the CML/glyoxal‐induced serotonin release in enterocytes might stimulate serotonin‐mediated intestinal motility. Nepsilon‐Carboxymethyllysine (CML), which represents a well‐characterized Maillard reaction product that is frequently encountered in a Western diet, and its precursor glyoxal induce serotonin release in fully differentiated Caco‐2 cells. 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subjects Advanced glycosylation end products
Alzheimer's disease
caco‐2 cells
Carboxymethyllysine
Diabetes mellitus
DNA microarrays
Enterocytes
Fatty acids
Food
Food processing
Gene expression
Gene regulation
Genomes
Glucose
glucose uptake
Glycosylation
glyoxal
Intestinal motility
Intestine
Maillard reaction
Neurodegenerative diseases
Nϵ‐carboxymethyllysine
Serotonin
serotonin release
title The advanced glycation end product Nϵ‐carboxymethyllysine and its precursor glyoxal increase serotonin release from Caco‐2 cells
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