Chronic administration of olanzapine affects Behavioral Satiety Sequence and feeding behavior in female mice

R Coccurello1, F R D'Amato, A Moles

  • 1Institute of Neuroscience, National Research Council (C.N.R.), 00143 Rome, Italy.

Insights

Chronic olanzapine (Ola) administration in female mice delayed satiety and increased food intake, suggesting altered hunger-satiety regulation contributes to weight gain from atypical antipsychotics (AAPs).

Area of Science:

  • Neuroscience
  • Pharmacology
  • Behavioral Science

Background:

  • Atypical antipsychotics (AAPs) improve schizophrenia management but are linked to metabolic issues like obesity.
  • Olanzapine (Ola) is a notable AAP associated with significant weight gain.
  • Understanding the mechanisms behind AAP-induced weight gain is crucial for patient health.

Purpose of the Study:

  • To investigate the effects of chronic olanzapine administration on feeding behavior in female mice.
  • To analyze the Behavioral Satiety Sequence (BSS) following olanzapine treatment.
  • To explore potential mechanisms linking olanzapine to weight gain via appetite regulation.

Main Methods:

  • Female mice received chronic oral administration of olanzapine (0.75, 1.5, 3 mg/kg) for 36 days.
  • A palatable wet mash diet was used to assess feeding behavior.
  • The Behavioral Satiety Sequence (BSS) was analyzed to measure satiation onset.

Main Results:

  • The highest dose of olanzapine (3 mg/kg) significantly postponed satiation onset, indicated by a rightward shift in the BSS.
  • Olanzapine (3 mg/kg) administration led to a confirmed increase in actual food intake.
  • These findings suggest olanzapine alters the regulation of hunger and satiety.

Conclusions:

  • Chronic olanzapine administration can disrupt hunger-satiety regulation in female mice.
  • Altered food intake and reduced sensitivity to satiety signals may contribute to olanzapine-induced weight gain.
  • These results support the hypothesis that impaired appetite regulation is a key factor in metabolic dysregulation associated with AAPs.