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Glutathione depletion prevents diet-induced obesity and enhances insulin sensitivity

Hannes M Findeisen1, Florence Gizard, Yue Zhao

  • 1Saha Cardiovascular Research Center, University of Kentucky College of Medicine, Lexington, Kentucky, USA.

Obesity (Silver Spring, Md.)
|October 1, 2011
PubMed

Insights

Reducing antioxidant glutathione in mice prevented obesity and improved insulin sensitivity, suggesting reactive oxygen species (ROS) play a beneficial role in glucose homeostasis and energy balance.

Area of Science:

  • Biochemistry
  • Metabolic diseases
  • Cellular signaling

Background:

  • Reactive oxygen species (ROS) accumulation in adipose tissue is linked to insulin resistance and type 2 diabetes.
  • Emerging evidence suggests physiological roles for ROS in cellular signaling and insulin sensitivity.

Purpose of the Study:

  • To investigate the role of antioxidant glutathione depletion in metabolic regulation.
  • To determine the impact of ROS modulation on diet-induced obesity and insulin sensitivity.

Main Methods:

  • Pharmacologic depletion of glutathione in a mouse model.
  • Assessment of body weight, energy expenditure, locomotor activity, and insulin sensitivity.

Main Results:

  • Glutathione depletion prevented diet-induced obesity in mice.
  • Increased energy expenditure and locomotor activity were observed.
  • Enhanced insulin sensitivity was noted following glutathione depletion.

Conclusions:

  • Modulation of ROS levels through glutathione depletion has beneficial effects on metabolic health.
  • ROS may play a positive role in regulating glucose homeostasis and energy balance.
  • Further research is warranted to explore ROS regulation of metabolism.

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