Ghrelin inhibits insulin secretion through the AMPK-UCP2 pathway in beta cells

FEBS Lett. 2010 Apr 16;584(8):1503-8. doi: 10.1016/j.febslet.2010.02.069. Epub 2010 Mar 3.

Abstract

Ghrelin inhibits insulin secretion partly via induction of IA-2beta. However, the orexigenic effect of ghrelin is mediated by the AMP-activated protein kinase (AMPK)-uncoupling protein 2 (UCP2) pathway. Here, we demonstrate that ghrelin's inhibitory effect on insulin secretion also occurs through the AMPK-UCP2 pathway. Ghrelin increased AMPK phosphorylation and UCP2 mRNA expression in MIN6 insulinoma cells. Overexpression or downregulation of UCP2 attenuated or enhanced insulin secretion, respectively. Furthermore, AMPK activator had a similar effect to ghrelin on UCP2 and insulin secretion in MIN6 cells. In conclusion, ghrelin's inhibitory effect on insulin secretion is partly mediated by the AMPK-UCP2 pathway, which is independent of the IA-2beta pathway.

MeSH terms

  • AMP-Activated Protein Kinases / metabolism*
  • Animals
  • Cell Line
  • Enzyme Activation / drug effects
  • Ghrelin / pharmacology*
  • Glucose / metabolism
  • Insulin / metabolism*
  • Insulin Secretion
  • Insulin-Secreting Cells / cytology
  • Insulin-Secreting Cells / drug effects*
  • Insulin-Secreting Cells / metabolism
  • Ion Channels / metabolism*
  • Mice
  • Mitochondrial Proteins / metabolism*
  • Receptor-Like Protein Tyrosine Phosphatases, Class 8 / metabolism
  • Signal Transduction / drug effects*
  • Uncoupling Protein 2
  • Up-Regulation / drug effects

Substances

  • Ghrelin
  • Insulin
  • Ion Channels
  • Mitochondrial Proteins
  • Ucp2 protein, mouse
  • Uncoupling Protein 2
  • AMP-Activated Protein Kinases
  • Ptprn protein, mouse
  • Receptor-Like Protein Tyrosine Phosphatases, Class 8
  • Glucose