Mediation of insulin hyperphagia by specific central opiate receptor antagonists

Iwona W. Beczkowska, Richard J. Bodnar

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

The hyperphagic properties of insulin (10 U/kg, s.c.) were transiently (2 h) and dose-dependently inhibited (30%) by central pretreatment with naltrexone (20-50 μg, i.c.v.). The irreversible μ opioid antagonist, β-funaltrexamine (B-FNA, 20 μg, i.c.v.) significantly inhibited insulin hyperphagia by 28-54% over the 6-h time course. In contrast, insulin hyperphagia was only transiently (2 h) inhibited (27-30%) by either the irreversible μ1 antagonist, naloxonazine (50 μg, i.c.v.) or the selective κ antagonist, nor-binaltorphamine (NorBNI, 20 μg, i.c.v.). The δ-antagonistic actions of [d-Ala2, Leu5, Cys6]-enkephalin (DALCE, 40 μg, i.c.v.) failed to affect insulin hyperphagia. These data suggest that the μ2 opioid receptor subtype modulates insulin hyperphagia.

Original languageEnglish
Pages (from-to)315-318
Number of pages4
JournalBrain Research
Volume547
Issue number2
DOIs
StatePublished - 3 May 1991
Externally publishedYes

Keywords

  • Insulin hyperphagia
  • Naloxonazine
  • Naltrexone
  • Nor-binaltorphamine
  • Opioid receptor subtype
  • [d-Ala, Leu, Cys]-Enkephalin
  • β-Funaltrexamine

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