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Negative consequences of glycation.

M Brownlee1

  • 1Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

Metabolism: Clinical and Experimental
|February 29, 2000
PubMed
Summary
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High blood sugar (hyperglycemia) drives diabetic complications like retinopathy and neuropathy. Advanced glycation end products and reactive oxygen species are key contributors to these damaging effects.

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Molecular Biology

Background:

  • The Diabetes Control and Complications Trial (DCCT) linked hyperglycemia to diabetic complications.
  • Diabetic complications include retinopathy, nephropathy, and neuropathy.
  • The mechanisms by which hyperglycemia causes these complications are under investigation.

Purpose of the Study:

  • To explore the role of hyperglycemia in the development of diabetic complications.
  • To investigate the involvement of advanced glycation end products (AGEs) and reactive oxygen species (ROS) in these processes.

Main Methods:

  • Review of existing evidence on hyperglycemia, AGEs, and ROS in diabetes.
  • Analysis of the formation and cellular effects of AGEs.
  • Examination of the role of ROS in AGE formation and AGE-induced gene expression changes.

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Main Results:

  • Hyperglycemia is strongly associated with the incidence and progression of diabetic complications.
  • Advanced glycation end products (AGEs) form as a function of glucose concentration and play a major role.
  • Reactive oxygen species (ROS) are implicated in both AGE formation and AGE-induced pathological gene expression alterations.

Conclusions:

  • AGEs are central mediators of hyperglycemia-induced diabetic complications.
  • ROS play a critical role in AGE formation and subsequent cellular damage.
  • Inhibiting ROS may be a therapeutic strategy for preventing diabetic complications, as suggested by animal models.