Insulin-like growth factor I reverses interleukin-1beta inhibition of insulin secretion, induction of nitric oxide synthase and cytokine-mediated apoptosis in rat islets of Langerhans

FEBS Lett. 1997 Nov 10;417(2):235-8. doi: 10.1016/s0014-5793(97)01291-x.

Abstract

We have previously observed that treatment of rat islets of Langerhans with interleukin-1beta for 12 h results in nitric oxide-dependent inhibition of insulin secretion, while 48 h treatment increased rates of islet cell death by apoptosis. Here, we demonstrate that interleukin-1beta-mediated nitric oxide formation and inhibition of insulin secretion are significantly reduced by 24 h pretreatment of rat islets of Langerhans with insulin-like growth factor I (IGF-I). IGF-I decreased cytokine induction of nitric oxide synthase in islets. Use of an arginine analogue in culture or IGF-I pretreatment of islets were also effective in protecting islets against cytokine-mediated apoptotic cell death. We conclude that IGF-I antagonises inhibitory and cytotoxic effects of cytokines in rat islets.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Apoptosis / drug effects*
  • Enzyme Induction / drug effects
  • Female
  • Insulin / metabolism*
  • Insulin Secretion
  • Insulin-Like Growth Factor I / pharmacology*
  • Interleukin-1 / pharmacology*
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / metabolism*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase / biosynthesis*
  • Rats
  • Rats, Sprague-Dawley
  • Secretory Rate / drug effects
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Insulin
  • Interleukin-1
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Insulin-Like Growth Factor I
  • Nitric Oxide Synthase