Identification of glucose-dependant insulin secretion targets in pancreatic beta cells by combining defined-mechanism compound library screening and siRNA gene silencing

J Biomol Screen. 2008 Feb;13(2):128-34. doi: 10.1177/1087057107313763. Epub 2008 Jan 23.

Abstract

Identification and validation of novel drug targets continues to be a major bottleneck in drug development, particularly for polygenic complex diseases such as type 2 diabetes. Here, the authors describe an approach that allows researchers to rapidly identify and validate potential drug targets by combining chemical tools and RNA interference technology. As a proof-of-concept study, the known mechanism Sigma LOPAC library was used to screen for glucose-dependent insulin secretion (GDIS) in INS-1 832/13 cells. In addition to several mechanisms that are known to regulate GDIS (such as cyclic adenosine monophosphate-specific phosphodiesterases, adrenoceptors, and Ca(2+) channels), the authors find that several of the dopamine receptor (DRD) antagonists significantly enhance GDIS, whereas DRD agonists profoundly inhibit GDIS. Subsequent siRNA studies in the same cell line indicate that knockdown of DRD2 enhanced GDIS. Furthermore, selective DRD2 antagonists and agonists also enhance or suppress, respectively, GDIS in isolated rat islets. The data support that the approach described here offers a rapid and effective way for target identification and validation.

Publication types

  • Validation Study

MeSH terms

  • Animals
  • Cells, Cultured
  • Dopamine Antagonists / pharmacology
  • Gene Library*
  • Gene Silencing* / physiology
  • Glucose / pharmacology*
  • Insulin / metabolism*
  • Insulin Secretion
  • Insulin-Secreting Cells / metabolism*
  • Metabolic Networks and Pathways / drug effects
  • Metabolic Networks and Pathways / genetics*
  • RNA, Messenger / metabolism
  • RNA, Small Interfering / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Dopamine / genetics
  • Receptors, Dopamine / metabolism

Substances

  • Dopamine Antagonists
  • Insulin
  • RNA, Messenger
  • RNA, Small Interfering
  • Receptors, Dopamine
  • Glucose