Shedding light on the intricate puzzle of ghrelin's effects on appetite regulation

J Endocrinol. 2009 Aug;202(2):191-8. doi: 10.1677/JOE-09-0056. Epub 2009 Mar 20.

Abstract

Ghrelin, a hormone primarily produced by the stomach, has a wide range of metabolic and non-metabolic effects. It also stimulates food intake through activation of various hypothalamic and brain stem neurons. A series of recent studies have explored the intracellular mechanisms of the appetite-inducing effect of ghrelin in the hypothalamus, shedding light on the intricate mechanisms of appetite regulation. AMP-activated protein kinase (AMPK) is a key metabolic enzyme involved in appetite regulation. Calmodulin kinase kinase 2 (CaMKK2) has been identified as an upstream kinase of AMPK and a key mediator in the effect of ghrelin on AMPK activity. The fatty acid pathway, hypothalamic mitochondrial respiration, and uncoupling protein 2 have been outlined as downstream targets of AMPK and mediators of ghrelin's appetite stimulating effect. This short overview summarises the present data in this field.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Appetite Regulation / physiology*
  • Calcium-Calmodulin-Dependent Protein Kinase Kinase / metabolism
  • Cannabinoids / metabolism
  • Cannabinoids / pharmacology
  • Drug Interactions
  • Fatty Acids / metabolism
  • Ghrelin / metabolism
  • Ghrelin / physiology*
  • Humans
  • Ion Channels / metabolism
  • Mitochondrial Proteins / metabolism
  • Uncoupling Protein 2

Substances

  • Cannabinoids
  • Fatty Acids
  • Ghrelin
  • Ion Channels
  • Mitochondrial Proteins
  • UCP2 protein, human
  • Ucp2 protein, mouse
  • Uncoupling Protein 2
  • Calcium-Calmodulin-Dependent Protein Kinase Kinase
  • Camkk2 protein, mouse