Globular adiponectin inhibits GnRH secretion from GT1-7 hypothalamic GnRH neurons by induction of hyperpolarization of membrane potential

Biochem Biophys Res Commun. 2008 Jul 11;371(4):756-61. doi: 10.1016/j.bbrc.2008.04.146. Epub 2008 May 6.

Abstract

Reproduction is accurately regulated by metabolic states in mammals. Adiponectin regulates luteinizing hormone (LH) secretion in the pituitary and energy homeostasis in the hypothalamus. We further investigated the gonadotropin-releasing hormone (GnRH) secretion regulation by adiponectin and its related molecular and electrophysiological mechanisms. The results showed that adiponectin receptors (AdipR1 and 2) were expressed in GT1-7 cells derived from hypothalamus neurons. GnRH secretion was inhibited via activation of AMP-activated protein kinase (AMPK). Moreover, we revealed that hyperpolarization of plasma membrane potentials and reduction of calcium influx was also caused by adiponectin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • AMP-Activated Protein Kinase Kinases
  • Adiponectin / pharmacology
  • Adiponectin / physiology*
  • Animals
  • Calcium / metabolism
  • Cell Line
  • Enzyme Activation
  • Gonadotropin-Releasing Hormone / antagonists & inhibitors
  • Gonadotropin-Releasing Hormone / metabolism*
  • Hypothalamus / cytology
  • Hypothalamus / drug effects
  • Hypothalamus / metabolism*
  • Membrane Potentials* / drug effects
  • Mice
  • Neurons / drug effects
  • Neurons / metabolism
  • Protein Kinases / metabolism
  • Receptors, Adiponectin / metabolism

Substances

  • Adiponectin
  • Receptors, Adiponectin
  • adiponectin receptor 1, mouse
  • adiponectin receptor 2, mouse
  • Gonadotropin-Releasing Hormone
  • Protein Kinases
  • AMP-Activated Protein Kinase Kinases
  • Calcium