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Oxidative stress, insulin signaling, and diabetes

Free Radic Biol Med. 2011 Mar 1;50(5):567-75. doi: 10.1016/j.freeradbiomed.2010.12.006. Epub 2010 Dec 13.

Abstract

Oxidative stress has been implicated as a contributor to both the onset and the progression of diabetes and its associated complications. Some of the consequences of an oxidative environment are the development of insulin resistance, β-cell dysfunction, impaired glucose tolerance, and mitochondrial dysfunction, which can lead ultimately to the diabetic disease state. Experimental and clinical data suggest an inverse association between insulin sensitivity and ROS levels. Oxidative stress can arise from a number of different sources, whether disease state or lifestyle, including episodes of ketosis, sleep restriction, and excessive nutrient intake. Oxidative stress activates a series of stress pathways involving a family of serine/threonine kinases, which in turn have a negative effect on insulin signaling. More experimental evidence is needed to pinpoint the mechanisms contributing to insulin resistance in both type 1 diabetics and nondiabetic individuals. Oxidative stress can be reduced by controlling hyperglycemia and calorie intake. Overall, this review outlines various mechanisms that lead to the development of oxidative stress. Intervention and therapy that alter or disrupt these mechanisms may serve to reduce the risk of insulin resistance and the development of diabetes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Amino Acids / metabolism
  • Antioxidants / therapeutic use
  • Chromium / metabolism
  • Diabetes Mellitus / etiology*
  • Diabetes Mellitus / metabolism*
  • Diabetic Ketoacidosis / metabolism
  • Energy Intake / physiology
  • Humans
  • Hyperglycemia / metabolism
  • Insulin / genetics
  • Insulin / metabolism*
  • Insulin Resistance*
  • Mitochondria / physiology
  • Nicotinic Acids / metabolism
  • Oxidative Stress / physiology*
  • PTEN Phosphohydrolase / genetics
  • PTEN Phosphohydrolase / metabolism
  • Protein Serine-Threonine Kinases / metabolism
  • Protein Serine-Threonine Kinases / physiology
  • Reactive Oxygen Species / metabolism
  • Signal Transduction / genetics
  • Signal Transduction / physiology

Substances

  • Amino Acids
  • Antioxidants
  • Insulin
  • Nicotinic Acids
  • Reactive Oxygen Species
  • glucose tolerance factor
  • Chromium
  • Protein Serine-Threonine Kinases
  • PTEN Phosphohydrolase
  • PTEN protein, human