Related Experiment Videos
Adipose tissue proadipogenic redox changes in obesity.
Anne Galinier1, Audrey Carrière, Yvette Fernandez
1Unite Mixte de Recherche 5018 CNRS, Université Paul Sabatier, Institut Fedératif Recherche 31, Institut Louis Bugnard, BP 84225, 31432 Toulouse Cedex 4, France.
The Journal of Biological Chemistry
|December 27, 2005
Summary
Obesity is linked to a reduced cellular redox state, not oxidative stress, promoting fat accumulation. Antioxidant interventions further enhance this effect, suggesting a novel mechanism in obesity development.
Area of Science:
- Biochemistry
- Metabolic disorders
- Obesity research
Background:
- The interplay between inflammation, oxidative stress, and obesity remains debated.
- Understanding redox metabolism is crucial for metabolic disorder research.
Purpose of the Study:
- To investigate redox metabolism in obese Zucker rats, a non-diabetic obesity model.
- To compare antioxidant status in adipose tissue, blood, and liver of obese versus lean rats.
Main Methods:
- Assessed antioxidant enzyme activities and lipophilic/hydrophilic antioxidant levels (alpha-tocopherol, coenzymes Q, glutathione, vitamin C).
- Determined the redox state (% oxidized form) of antioxidants in inguinal white fat.
- Utilized lipopolysaccharide-induced oxidative stress and in vitro preadipocyte models.
Main Results:
- Obese rats exhibited higher hydrophilic antioxidants in a reduced redox state and lower lipid peroxidation in adipose tissue compared to lean rats.
- Systemic oxidative stress decreased glutathione content and increased its oxidized form in adipose tissue.
- In vitro, increased glutathione and reduced redox state promoted triglyceride accumulation in preadipocytes.
Conclusions:
- Obesity is associated with a reduced intracellular redox state in adipose tissue, contrary to the prevailing view.
- This reduced redox state may intrinsically drive a pro-adipogenic process.
- Oxidative stress and obesity exert opposing effects on adipose tissue redox state.