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Interleukin 1β Increases the Cytosolic Free Sodium Concentration in Isolated Rat Islets of Langerhans
Author(s) -
HELQVIST S.,
BOUCHELOUCHE P. N.,
JOHANNESEN J.,
NERUP J.
Publication year - 1990
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1990.tb02891.x
Subject(s) - islet , endocrinology , medicine , pancreatic islets , chemistry , sodium , amiloride , cytosol , extracellular , sodium–hydrogen antiporter , insulin , biology , biochemistry , organic chemistry , enzyme
Interleukin l (1L‐I) exerts both stimulatory and inhibitor) (cytotoxic) effects on insulin producing βcells in isolated pancreatic islets. Since alteration in ion fluxes is crucial for endocrine cell activation and is a denominator of cell death, and since IL‐1 was recently shown to increase the total sodium content in a murine pre‐B‐lymphocyte cell line, we investigated the effect of recombinant human IL‐lβ (rhIL‐1β) on the cytosolic tree sodium concentration (Na + ) in rat islets, furthermore, long‐term rhIL‐1βeffects on islet cell function were studied during exposure of islets to amiloride. a blocker of the plasma membrane Na + /H + exchange. One hour of islet exposure to 60 U/ml of rhIL‐lβ caused a threefold increase in I Na + . in islet cells, and this effect was abolished by deplelion of extracellular sodium. Blockade of Na + /H + exchange with amiloride abolished the inhibitory effect of rhIL‐1β Son insulin release. In conclusion. rhIL‐lβwas found to increase sodium influx in pancreatic islet cells. This might underlie the widespread effects of rhIL‐lβ on β‐cell function and morphology, possibly related to IL‐l‐mediated toxic free radical formation.