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Updated: Jul 23, 2025

Using the Activity-based Anorexia Rodent Model to Study the Neurobiological Basis of Anorexia Nervosa
07:46

Using the Activity-based Anorexia Rodent Model to Study the Neurobiological Basis of Anorexia Nervosa

Published on: October 22, 2015

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Anaplastic Lymphoma Kinase Receptor: Possible Involvement in Anorexia Nervosa

Simona Dedoni1, Maria Scherma1, Chiara Camoglio1

  • 1Section of Neuroscience and Clinical Pharmacology, Department of Biomedical Science, University of Cagliari, 09124 Cagliari, Italy.

Nutrients
|July 11, 2023
PubMed

Insights

Anaplastic lymphoma kinase (ALK) receptor expression decreases in rats with activity-based anorexia, suggesting its role in anorexia nervosa pathophysiology and potentially influencing weight regulation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Endocrinology

Background:

  • The pathophysiology of Anorexia Nervosa (AN) remains incompletely understood.
  • Anaplastic lymphoma kinase (ALK) is a protein-tyrosine kinase primarily recognized for its oncogenic role.
  • Recent studies suggest ALK influences energy expenditure and obesity resistance, hinting at a role in thinness regulation.

Purpose of the Study:

  • To investigate the expression of ALK and its downstream signaling pathways in a rat model of activity-based anorexia (ABA).
  • To explore the potential involvement of ALK in the mechanisms underlying AN.

Main Methods:

  • Utilized the activity-based anorexia (ABA) rat model, which mimics key features of human AN.
  • Analyzed hypothalamic tissue lysates from ABA rats to assess ALK receptor expression and phosphorylation of downstream kinases Akt and ERK1/2.
  • Examined changes in ALK expression during ABA induction and subsequent recovery.

Main Results:

  • ABA rats exhibited reduced hypothalamic ALK receptor expression and decreased Akt phosphorylation compared to controls.
  • Extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) phosphorylation levels remained unchanged.
  • Following recovery from weight loss, ALK expression normalized, but decreased again upon re-induction of ABA.

Conclusions:

  • Evidence suggests a potential role for the ALK receptor in the pathophysiology of Anorexia Nervosa.
  • ALK may be implicated in the stabilization, resistance, or exacerbation of AN.
  • Further research into ALK signaling could reveal novel therapeutic targets for AN.
Keywords:
Anorexia Nervosaactivity-based anorexia modelanaplastic lymphoma kinase receptorhypothalamus

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