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Fat Preference: A Novel Model of Eating Behavior in Rats
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Published on: June 27, 2014

NF-κB knockdown can modulate amphetamine-mediated feeding response.

Dong-Yih Kuo1, Pei-Ni Chen, Meng-Hsien Kuo

  • 1Department of Physiology, Chung Shan Medical University and Chung Shan Medical University Hospital, Taichung City 40201, Taiwan, ROC. dykuo@csmu.edu.tw

Neuropharmacology
|December 21, 2011
PubMed
Summary
This summary is machine-generated.

Transcription factor NF-κB (nuclear factor kappa B) plays a key role in amphetamine-mediated appetite suppression. This study shows NF-κB modulates neuropeptide Y and proopiomelanocortin expression, impacting feeding behavior.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Amphetamine (AMPH) is known to affect feeding behavior.
  • The precise molecular mechanisms underlying AMPH-mediated appetite suppression are not fully understood.
  • Transcription factors and hypothalamic neuropeptides are potential mediators of these effects.

Purpose of the Study:

  • To investigate the involvement of transcription factor NF-κB (nuclear factor kappa B) in AMPH-mediated feeding responses.
  • To explore the roles of hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) in this process.
  • To elucidate the relationship between NF-κB, NPY, and POMC expression during AMPH treatment.

Main Methods:

  • Daily administration of AMPH to rats for four days.
  • Assessment and comparison of NF-κB, NPY, and POMC gene expression levels.
  • Measurement of NF-κB DNA binding ability.
  • Intracerebroventricular infusion of NF-κB antisense oligonucleotide before AMPH dosing to assess knockdown effects.

Main Results:

  • AMPH treatment led to down-regulation of NPY and up-regulation of NF-κB and POMC gene expression, with maximal effects on Day 2.
  • NF-κB DNA binding ability and expression increased, mirroring POMC expression patterns.
  • NF-κB knockdown significantly altered AMPH-induced anorexia and the expression of NPY and POMC.

Conclusions:

  • Cerebral NF-κB is implicated in the appetite suppression caused by AMPH.
  • NF-κB likely modulates NPY and POMC expression to mediate AMPH's effects on appetite.
  • These findings offer potential therapeutic insights for AMPH and related anti-obesity drug development.