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α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
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Dietary Advanced Glycation Endproducts Decrease Glucocorticoid Sensitivity In Vitro.

Timme van der Lugt1, Antje R Weseler1, Misha F Vrolijk1,2

  • 1Department of Pharmacology and Toxicology, Faculty of Health, Medicine, and Life Sciences, Maastricht University, 6200 MD Maastricht, The Netherlands.

Nutrients
|February 14, 2020
PubMed
Summary

Dietary advanced glycation endproducts (AGEs) can cause resistance to glucocorticoid therapy in inflammatory bowel disease (IBD) patients by increasing reactive oxygen species (ROS). Quercetin and rapamycin can mitigate this AGE-induced glucocorticoid resistance.

Keywords:
dietary advanced glycation endproductsglucocorticoid resistanceinflammationinflammatory bowel diseasesreactive oxygen species

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Area of Science:

  • Gastroenterology
  • Immunology
  • Pharmacology

Background:

  • Glucocorticoids are primary anti-inflammatory drugs for inflammatory bowel disease (IBD).
  • A significant portion of IBD patients exhibit resistance to glucocorticoids, with underlying mechanisms often unclear.
  • Dietary advanced glycation endproducts (AGEs), formed during food processing, can trigger pro-inflammatory responses.

Purpose of the Study:

  • To investigate if dietary AGEs induce resistance to glucocorticoid anti-inflammatory effects.
  • To explore the role of reactive oxygen species (ROS) in AGE-induced glucocorticoid resistance.
  • To identify potential therapeutic agents that can overcome this resistance.

Main Methods:

  • Human macrophage-like cells were stimulated with lipopolysaccharide (LPS) and AGEs to induce interleukin-8 (IL8) secretion.
  • Cells were treated with glucocorticoids and modulators like rapamycin, quercetin, and theophylline.
  • Intracellular ROS levels and glucocorticoid receptor phosphorylation were measured.

Main Results:

  • AGEs induced resistance to glucocorticoid-mediated suppression of IL8 secretion.
  • Quercetin and rapamycin effectively mitigated AGE-induced glucocorticoid resistance.
  • AGEs significantly increased intracellular ROS production, which was reduced by quercetin.
  • No alterations in glucocorticoid receptor phosphorylation were observed.

Conclusions:

  • Dietary AGEs can induce glucocorticoid resistance in inflammatory cells, mediated by increased ROS production.
  • Quercetin and rapamycin show potential in overcoming AGE-induced glucocorticoid resistance.
  • These findings highlight the impact of dietary factors on IBD treatment efficacy and suggest therapeutic strategies for glucocorticoid-resistant patients.