Suppression of peptide YY-induced hyperphagia by terbutaline

Pharmacol Biochem Behav. 1993 Nov;46(3):679-81. doi: 10.1016/0091-3057(93)90561-7.

Abstract

Central administrations of neuropeptide Y and peptide YY (PYY) produce robust increases in food intake, and this response may be contingent upon the availability of insulin. In contrast, beta 2-adrenergic agonists decrease food intake, and this effect also appears to be dependent on circulating insulin. To investigate a possible interaction between PYY and beta 2-adrenergic function, rats were given systemic injections of terbutaline, a beta 2 agonist, at doses of 0, 5, 10, and 50 mg/kg prior to injections of 0.57 nmol PYY in the paraventricular nucleus of the hypothalamus. Terbutaline pretreatment significantly decreased feeding elicited by PYY in a dose-dependent fashion. This suggests that beta 2-adrenoreceptor activity is involved in PYY-induced feeding.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adrenergic beta-Agonists / pharmacology
  • Animals
  • Dose-Response Relationship, Drug
  • Eating / drug effects
  • Female
  • Gastrointestinal Hormones / administration & dosage
  • Gastrointestinal Hormones / antagonists & inhibitors*
  • Gastrointestinal Hormones / pharmacology
  • Hyperphagia / chemically induced
  • Hyperphagia / prevention & control*
  • Injections
  • Paraventricular Hypothalamic Nucleus
  • Peptide YY
  • Peptides / administration & dosage
  • Peptides / antagonists & inhibitors*
  • Peptides / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Adrenergic, beta-2 / drug effects
  • Receptors, Adrenergic, beta-2 / physiology
  • Terbutaline / pharmacology*

Substances

  • Adrenergic beta-Agonists
  • Gastrointestinal Hormones
  • Peptides
  • Receptors, Adrenergic, beta-2
  • Peptide YY
  • Terbutaline