The early phase of glucose-stimulated insulin secretion requires nitric oxide

Diabetologia. 1998 Mar;41(3):292-9. doi: 10.1007/s001250050906.


Nitric oxide (nitrogen monoxide, NO) acts as a signal transducer in a variety of cells. In the present study rat pancreatic islets were perifused with physiologically relevant glucose concentrations in the presence or absence of various NO-modulating agents. Perifusion in the presence of 0.1-1 mmol/l of the NO synthase inhibitor, NG-monomethyl-L-arginine or of 10 micromol/l of the NO-scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), resulted in an inhibition of the early phase of glucose-stimulated insulin secretion by 60-65% and 46%, respectively. Light- and electron-microscopic studies revealed that pancreatic islets constitutively express NO-synthase in alpha and delta cells, where it is confined to the secretory granules. Therefore, these data indicate that NO may be important in the signal transduction pathway of the early phase of glucose-stimulated insulin secretion.

MeSH terms

  • Animals
  • Endothelium, Vascular / enzymology
  • Endothelium, Vascular / ultrastructure
  • Glucose / pharmacology*
  • Immunohistochemistry
  • In Vitro Techniques
  • Insulin / metabolism*
  • Insulin Secretion
  • Islets of Langerhans / chemistry
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / metabolism
  • Nitric Oxide / physiology*
  • Nitric Oxide Synthase / analysis
  • Nitric Oxide Synthase / ultrastructure
  • Perfusion
  • Rats
  • Signal Transduction
  • Time Factors


  • Insulin
  • Nitric Oxide
  • Nitric Oxide Synthase
  • Glucose