AGEs and chronic subclinical inflammation in diabetes: disorders of immune system

Diabetes Metab Res Rev. 2015 Feb;31(2):127-37. doi: 10.1002/dmrr.2560.

Abstract

Chronic subclinical inflammation represents a risk factor of type 2 diabetes and several diabetes complications, including neuropathy and atherosclerosis including macro-vasculopathy and micro-vasculopathy. However, the inflammatory response in the diabetic wound was shown to be remarkably hypocellular, unregulated and ineffective. Advanced glycation end products (AGEs) and one of its receptors, RAGE, were involved in inducing chronic immune imbalance in diabetic patients. Such interactions attracts immune cell into diffused glycated tissue and activates these cells to induce inflammatory damage, but disturbs the normal immune rhythm in diabetic wound. Traditional measurements of AGEs are high-performance liquid chromatography and immunohistochemistry staining, but their application faces the limitations including complexity, cost and lack of reproducibility. A new noninvasive method emerged in 2004, using skin autofluorescence as indicator for AGEs accumulation. It had been reported to be informative in evaluating the chronic risk of diabetic patients. Studies have indicated therapeutic potentials of anti-AGE recipes. These recipes can reduce AGE absorption/de novo formation, block AGE-RAGE interaction and arrest downstream signaling after RAGE activation.

Keywords: advanced glycation endproducts; chronic inflammation; diabetes.

Publication types

  • Review

MeSH terms

  • Animals
  • Diabetes Mellitus, Type 2 / complications
  • Diabetes Mellitus, Type 2 / immunology
  • Diabetes Mellitus, Type 2 / metabolism*
  • Glycation End Products, Advanced / metabolism*
  • Humans
  • Immune System Diseases / complications
  • Immune System Diseases / immunology
  • Immune System Diseases / metabolism*
  • Immune System Diseases / physiopathology
  • Models, Biological*
  • Oxidative Stress
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic / agonists
  • Receptors, Immunologic / metabolism
  • Severity of Illness Index
  • Signal Transduction

Substances

  • Glycation End Products, Advanced
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic