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Interleukin‐1 inhibits glucose‐induced Ca 2+ uptake by islets of Langerhans
Author(s) -
Wolf Bryan A.,
Hughes Jonathan H.,
Florholmen Jon,
Turk John,
McDaniel Michael L.
Publication year - 1989
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(89)80426-0
Subject(s) - secretion , endoplasmic reticulum , medicine , glucose homeostasis , endocrinology , islet , homeostasis , insulin , intracellular , chemistry , digitonin , inositol , biology , biochemistry , receptor , membrane , insulin resistance
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 Ca 2+ homeostasis during glucose‐induced insulin secretion. Glucose‐induced Ca 2+ uptake by intact islets through the plasma membrane was dramatically inhibited (96%) by rIL‐1 (2 nM). rIL‐1, however, did not affect Ca 2+ uptake by, or Ins 1,4,5‐P 3 ‐induced Ca 2+ 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 Ca 2+ homeostasis in islets is involved in inhibition of insulin secretion by rIL‐1.