Peptides that regulate food intake: norepinephrine is not required for reduction of feeding induced by cholecystokinin

Am J Physiol Regul Integr Comp Physiol. 2003 Jun;284(6):R1384-8. doi: 10.1152/ajpregu.00689.2002.

Abstract

CCK octapeptide (CCK-8) is released by the gut in response to a meal and acts via CCK(A) receptors on vagal afferents to induce satiety. However, the central neural pathways by which peripheral CCK-8 affects feeding are poorly understood. In the present study, we tested the hypothesis that norepinephrine (NE) is necessary for satiety induced by peripheral CCK-8 by using mice lacking dopamine beta-hydroxylase (Dbh(-/-)), the enzyme responsible for synthesizing NE and epinephrine from dopamine. We found that Dbh(-/-) mice are as responsive to the satiating effects of CCK-8 as their normal littermates.

MeSH terms

  • Animals
  • Cholecystokinin / pharmacology*
  • Dopamine beta-Hydroxylase / genetics
  • Dopamine beta-Hydroxylase / metabolism
  • Dose-Response Relationship, Drug
  • Feeding Behavior / drug effects*
  • Feeding Behavior / physiology
  • Female
  • Food Deprivation
  • Gene Deletion
  • Male
  • Mice
  • Mice, Knockout
  • Norepinephrine / biosynthesis
  • Norepinephrine / metabolism*
  • Peptide Fragments / pharmacology*
  • Satiety Response / drug effects*
  • Satiety Response / physiology*
  • Weight Gain / drug effects
  • Weight Gain / physiology
  • Weight Loss / drug effects
  • Weight Loss / physiology

Substances

  • Peptide Fragments
  • cholecystokinin 8
  • Cholecystokinin
  • Dopamine beta-Hydroxylase
  • Norepinephrine