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Related Concept Videos

Anorexia Nervosa01:28

Anorexia Nervosa

Anorexia nervosa is a complex and severe eating disorder characterized by an intense fear of weight gain, an unrelenting pursuit of thinness, and a distorted body image. It often leads to dangerously low body weight relative to an individual's age and height. This disorder is marked by significant physical and psychological consequences, making it one of the most life-threatening psychiatric illnesses.
Symptoms and Physical Effects
Individuals with anorexia nervosa commonly exhibit extreme...

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Assessing Activity-based Anorexia in Mice
08:26

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Published on: May 14, 2018

Hypothalamic mitochondrial dysfunction associated with anorexia in the anx/anx mouse.

Charlotte Lindfors1, Ida A K Nilsson, Pablo M Garcia-Roves

  • 1Department of Molecular Medicine and Surgery, Karolinska Institutet, 171 76 Stockholm, Sweden.

Proceedings of the National Academy of Sciences of the United States of America
|October 26, 2011
PubMed
Summary

Mitochondrial complex I dysfunction causes anorexia and neurodegeneration in the anx/anx mouse hypothalamus. This study links defects in oxidative phosphorylation (OXPHOS) to these feeding behavior and brain health issues.

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Area of Science:

  • Neuroscience
  • Mitochondrial Biology
  • Genetics

Background:

  • Anorexia and neurodegeneration in infants are linked to mitochondrial oxidative phosphorylation (OXPHOS) system dysfunction.
  • The anorectic anx/anx mouse model displays hypothalamic neurodegeneration and disturbed feeding behavior.

Purpose of the Study:

  • To investigate the potential role of mitochondrial OXPHOS defects in the pathogenesis of anorexia and neurodegeneration in the anx/anx mouse.
  • To explore the specific involvement of OXPHOS complex I in the observed phenotypes.

Main Methods:

  • Analysis of OXPHOS complex I assembly and activity in the hypothalamus of anx/anx mice.
  • Assessment of oxidative stress markers in the anx/anx hypothalamus.
  • Genetic mapping of the Ndufaf1 gene and its expression levels in anx/anx mice.

Main Results:

  • Reduced efficiency and assembly of hypothalamic OXPHOS complex I were observed in anx/anx mice.
  • Evidence of increased oxidative stress in the hypothalamus of anx/anx mice.
  • The Ndufaf1 gene, a complex I assembly factor, was mapped to the anx interval and found to be downregulated.

Conclusions:

  • Dysfunction of mitochondrial complex I is associated with anorexia and hypothalamic neurodegeneration in the anx/anx mouse.
  • These findings suggest a link between OXPHOS defects and feeding behavior disorders with neurological implications.