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

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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. © 1989.

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APA

Wolf, B. A., Hughes, J. H., Florholmen, J., Turk, J., & McDaniel, M. L. (1989). Interleukin-1 inhibits glucose-induced Ca2+ uptake by islets of Langerhans. FEBS Letters, 248(1–2), 35–38. https://doi.org/10.1016/0014-5793(89)80426-0

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