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Fructose causes endothelial cell damage via activation of advanced glycation end products-receptor system

Ami Sotokawauchi1, Takanori Matsui1, Yuichiro Higashimoto2

  • 1Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume, Japan.

Diabetes & Vascular Disease Research
|August 4, 2019
PubMed
Abstract

Insights

Fructose consumption may harm endothelial cells by activating the advanced glycation end product-receptor for advanced glycation end product (AGE-RAGE) pathway. This study demonstrates fructose-induced oxidative stress and inflammation in endothelial cells.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Metabolic Research

Background:

  • Advanced glycation end products (AGEs) and their receptor (RAGE) are implicated in metabolic disorders.
  • The role of fructose in endothelial cell damage via AGE-RAGE activation is not fully understood.

Purpose of the Study:

  • To investigate whether fructose can induce endothelial cell damage through the activation of the AGE-RAGE axis.
  • To explore the mechanisms of fructose-induced endothelial dysfunction.

Main Methods:

  • Preparation of fructose-derived AGEs (Fruc-AGEs).
  • Evaluation of intracellular AGEs, reactive oxygen species (ROS) generation, and vascular cell adhesion molecule-1 (VCAM-1) gene expression in human umbilical vein endothelial cells (HUVECs).
  • Measurement of binding affinities using quartz crystal microbalance and aptamer inhibition assays.

Main Results:

  • Fructose increased intracellular AGEs and ROS generation in HUVECs.
  • Fructose exposure led to increased VCAM-1 gene expression.
  • A specific aptamer (Fruc-AGE-aptamer) inhibited Fruc-AGE binding to RAGE and prevented fructose-induced ROS and VCAM-1 upregulation.

Conclusions:

  • Fructose may contribute to endothelial cell damage by activating the AGE-RAGE pathway.
  • Fructose-induced oxidative stress and inflammation in endothelial cells are partly mediated by AGE-RAGE signaling.
Keywords:
Advanced glycation end productsRAGEcardiovascular diseaseendothelial cellsfructose

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