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Open AccessArticle

Dietary Advanced Glycation Endproducts Decrease Glucocorticoid Sensitivity In Vitro

1
Department of Pharmacology and Toxicology, Faculty of Health, Medicine, and Life Sciences, Maastricht University, 6200 MD Maastricht, The Netherlands
2
Faculty of Science and Engineering, Campus Venlo, Maastricht University, 5911 AA Venlo, The Netherlands
3
Office for Risk Assessment and Research (BuRO), Dutch Food and Consumer Safety Authority (NVWA), 3540 AA Utrecht, The Netherlands
*
Author to whom correspondence should be addressed.
Nutrients 2020, 12(2), 441; https://doi.org/10.3390/nu12020441
Received: 8 January 2020 / Revised: 31 January 2020 / Accepted: 6 February 2020 / Published: 10 February 2020
(This article belongs to the Special Issue Drug-Nutrition Interactions)
Glucocorticoids are very effective anti-inflammatory drugs and widely used for inflammatory bowel disease (IBD) patients. However, approximately 20% of IBD patients do not respond to glucocorticoids and the reason for this is largely unknown. Dietary advanced glycation endproducts (AGEs) are formed via the Maillard reaction during the thermal processing of food products and can induce a pro-inflammatory reaction in human cells. To investigate whether this pro-inflammatory response could be mitigated by glucocorticoids, human macrophage-like cells were exposed to both LPS and AGEs to induce interleukin-8 (IL8) secretion. This pro-inflammatory response was then modulated by adding pharmacological compounds interfering in different steps of the anti-inflammatory mechanism of glucocorticoids: rapamycin, quercetin, and theophylline. Additionally, intracellular reactive oxygen species (ROS) were measured and the glucocorticoid receptor phosphorylation state was assessed. The results show that AGEs induced glucocorticoid resistance, which could be mitigated by quercetin and rapamycin. No change in the phosphorylation state of the glucocorticoid receptor was observed. Additionally, intracellular ROS formation was induced by AGEs, which was mitigated by quercetin. This suggests that AGE-induced ROS is an underlying mechanism to AGE-induced glucocorticoid resistance. This study shows for the first time the phenomenon of dietary AGE-induced glucocorticoid resistance due to the formation of ROS. Our findings indicate that food products with a high inflammatory potential can induce glucocorticoid resistance; these results may be of great importance to IBD patients suffering from glucocorticoid resistance.
Keywords: dietary advanced glycation endproducts; glucocorticoid resistance; inflammatory bowel diseases; inflammation; reactive oxygen species dietary advanced glycation endproducts; glucocorticoid resistance; inflammatory bowel diseases; inflammation; reactive oxygen species
MDPI and ACS Style

van der Lugt, T.; Weseler, A.R.; Vrolijk, M.F.; Opperhuizen, A.; Bast, A. Dietary Advanced Glycation Endproducts Decrease Glucocorticoid Sensitivity In Vitro. Nutrients 2020, 12, 441.

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