Interleukin-1 inhibits glucose-induced Ca2+ uptake by islets of Langerhans

FEBS Lett. 1989 May 8;248(1-2):35-8. doi: 10.1016/0014-5793(89)80426-0.

Abstract

Recombinant interleukin-1 (rIL-1) is known to inhibit glucose-induced insulin secretion by islets of Langerhans, a novel target tissue of cytokine. We have investigated whether rIL-1 pretreatment affects biochemical mechanisms known to be involved in the regulation of Ca2+ homeostasis during glucose-induced insulin secretion. Glucose-induced Ca2+ uptake by intact islets through the plasma membrane was dramatically inhibited (96%) by rIL-1 (2 nM). rIL-1, however, did not affect Ca2+ uptake by, or Ins 1,4,5-P3-induced Ca2+ efflux from, the endoplasmic reticulum in digitonin-permeabilized islets, although glucose-induced accumulation of inositol trisphosphates was inhibited (38%). These results suggest that perturbation of intracellular Ca2+ homeostasis in islets is involved in inhibition of insulin secretion by rIL-1.

Publication types

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

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Cells, Cultured
  • Digitonin / pharmacology
  • Endoplasmic Reticulum / metabolism
  • Glucose / pharmacology*
  • Homeostasis
  • Inositol Phosphates / metabolism
  • Insulin / metabolism
  • Interleukin-1 / pharmacology*
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / metabolism*
  • Rats
  • Recombinant Proteins / pharmacology

Substances

  • Inositol Phosphates
  • Insulin
  • Interleukin-1
  • Recombinant Proteins
  • Glucose
  • Digitonin
  • Calcium