Insulin Activates ATP-sensitive K+ Channels in Hypothalamic Neurons of Lean, but Not Obese Rats

Nat Neurosci. 2000 Aug;3(8):757-8. doi: 10.1038/77660.

Abstract

Insulin and leptin receptors are present in hypothalamic regions that control energy homeostasis, and these hormones reduce food intake and body weight in lean, but not obese, Zucker rats. Here we demonstrate that insulin, like leptin, hyperpolarizes lean rat hypothalamic glucose-responsive (GR) neurons by opening KATP channels. These findings suggest hypothalamic K ATP channel function is crucial to physiological regulation of food intake and body weight.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / pharmacology*
  • Animals
  • Arcuate Nucleus of Hypothalamus / physiology
  • Glucose / pharmacology
  • Hypothalamus / physiology*
  • Hypothalamus / physiopathology
  • In Vitro Techniques
  • Insulin / pharmacology*
  • Leptin / pharmacology
  • Membrane Potentials / drug effects
  • Neurons / physiology*
  • Obesity / genetics
  • Obesity / physiopathology*
  • Patch-Clamp Techniques
  • Phosphatidylinositol 3-Kinases / metabolism
  • Potassium Channels / drug effects
  • Potassium Channels / physiology*
  • Rats
  • Rats, Zucker
  • Thinness
  • Tolbutamide / pharmacology

Substances

  • Insulin
  • Leptin
  • Potassium Channels
  • Adenosine Triphosphate
  • Tolbutamide
  • Phosphatidylinositol 3-Kinases
  • Glucose