Adenosine kinase inhibition selectively promotes rodent and porcine islet β-cell replication

Proc Natl Acad Sci U S A. 2012 Mar 6;109(10):3915-20. doi: 10.1073/pnas.1201149109. Epub 2012 Feb 15.

Abstract

Diabetes is a pathological condition characterized by relative insulin deficiency, persistent hyperglycemia, and, consequently, diffuse micro- and macrovascular disease. One therapeutic strategy is to amplify insulin-secretion capacity by increasing the number of the insulin-producing β cells without triggering a generalized proliferative response. Here, we present the development of a small-molecule screening platform for the identification of molecules that increase β-cell replication. Using this platform, we identify a class of compounds [adenosine kinase inhibitors (ADK-Is)] that promote replication of primary β cells in three species (mouse, rat, and pig). Furthermore, the replication effect of ADK-Is is cell type-selective: treatment of islet cell cultures with ADK-Is increases replication of β cells but not that of α cells, PP cells, or fibroblasts. Short-term in vivo treatment with an ADK-I also increases β-cell replication but not exocrine cell or hepatocyte replication. Therefore, we propose ADK inhibition as a strategy for the treatment of diabetes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Kinase / pharmacology*
  • Animals
  • Female
  • Fibroblasts / metabolism
  • Gene Expression Regulation*
  • Glucagon-Like Peptide-1 Receptor
  • Glucose / metabolism
  • Hepatocytes / cytology
  • Insulin / metabolism
  • Insulin-Secreting Cells / cytology*
  • Islets of Langerhans / cytology
  • Mice
  • Mice, Inbred C57BL
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Glucagon / metabolism
  • Swine
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Glp1r protein, mouse
  • Glp1r protein, rat
  • Glucagon-Like Peptide-1 Receptor
  • Insulin
  • Receptors, Glucagon
  • Adenosine Kinase
  • TOR Serine-Threonine Kinases
  • Glucose