Intracellular signal transduction pathways that control pancreatic beta-cell proliferation

FEBS Lett. 1992 Oct 19;311(2):85-90. doi: 10.1016/0014-5793(92)81373-t.

Abstract

This review focuses on the factors that regulate the proliferation of pancreatic islet beta-cells in vitro, and in particular on the intracellular pathways that convey the mitogenic signal into a proliferative response. Substances as diverse as nutrients, polypeptides, cytokines, adrenergic agents, lithium, phorbol esters and cyclic AMP analogs are all able to stimulate or inhibit beta-cell proliferation in a time- and concentration-dependent manner. The evidence for involvement of cyclic AMP, cyclic GMP, protein kinase C, inositol polyphosphates, GTP-binding proteins, polyamines and oncogenes is reviewed.

Publication types

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

MeSH terms

  • Amino Acids / pharmacology
  • Animals
  • Cell Division / drug effects
  • Cells, Cultured
  • Cyclic AMP / physiology
  • GTP-Binding Proteins / physiology
  • Glucose / pharmacology
  • Inositol Phosphates / metabolism
  • Islets of Langerhans / cytology*
  • Islets of Langerhans / metabolism
  • Peptides / pharmacology
  • Polyamines / metabolism
  • Protein Kinase C / metabolism
  • Signal Transduction*

Substances

  • Amino Acids
  • Inositol Phosphates
  • Peptides
  • Polyamines
  • Cyclic AMP
  • Protein Kinase C
  • GTP-Binding Proteins
  • Glucose