Insulin-degrading enzyme antagonizes insulin-dependent tissue growth and Abeta-induced neurotoxicity in Drosophila

FEBS Lett. 2010 Jul 2;584(13):2916-20. doi: 10.1016/j.febslet.2010.05.010. Epub 2010 May 21.

Abstract

Insulin-degrading enzyme (IDE) is implicated in the pathogenesis of type 2 diabetes mellitus (DM2) and Alzheimer's disease (AD). Here we provide genetic evidence that Drosophila Ide (dIde) antagonizes the insulin signaling pathway and human Abeta-induced neurotoxicity in Drosophila. In this study, we also generated a dIde knockout mutant (dIde(KO)) by gene targeting, and found that loss of IDE increases the content of the major insect blood sugar, trehalose, thus suggesting a conserved role of IDE in sugar metabolism. Using dIde(KO) as a model, further investigations into the biological functions of IDE and its role in the pathogenesis of DM2 and AD can be made.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / metabolism
  • Amyloid beta-Peptides / genetics
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Animals, Genetically Modified
  • Body Weight
  • Disease Models, Animal
  • Drosophila
  • Female
  • Glucose / metabolism
  • Hemolymph / metabolism
  • Humans
  • Insulysin / genetics
  • Insulysin / metabolism*
  • Male
  • Neurons / metabolism*
  • Trehalose / metabolism

Substances

  • Amyloid beta-Peptides
  • Trehalose
  • Insulysin
  • Glucose