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

Bryan A. Wolf, Jonathan H. Hughes, Jon Florholmen, John Turk, Michael L. McDaniel

Research output: Contribution to journalArticle

24 Scopus citations

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.

Original languageEnglish
Pages (from-to)35-38
Number of pages4
JournalFEBS Letters
Volume248
Issue number1-2
DOIs
StatePublished - May 8 1989

Keywords

  • (Pancreatic islet)
  • Ca uptake
  • Glucose
  • Inositol phosphate
  • Interleukin-1

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