Interleukin-1 inhibits glucose-induced Ca2+ uptake by islets of Langerhans.
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.
Wolf
B A
BA
Department of Pathology, Washington University School of Medicine, Saint Louis, MO 63110.
Hughes
J H
JH
Florholmen
J
J
Turk
J
J
McDaniel
M L
ML
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D004072:Digitonin / Q000494:pharmacology; D004721:Endoplasmic Reticulum / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology*; D006706:Homeostasis; D007295:Inositol Phosphates / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D007375:Interleukin-1 / Q000494:pharmacology*; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D011994:Recombinant Proteins / Q000494:pharmacology
D007295:Inositol Phosphates; D007328:Insulin; D007375:Interleukin-1; D011994:Recombinant Proteins; D005947:Glucose; D004072:Digitonin; D002118:Calcium