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Insulin‐secreting β‐cells possess specific receptors for interleukin‐1β
Author(s) -
Hammonds Peter,
Beggs Mark,
Beresford Guy,
Espinal Joseph,
Clarke Jennifer,
Mertz Robert J.
Publication year - 1990
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(90)80645-y
Subject(s) - secretagogue , insulin , endocrinology , beta (programming language) , medicine , receptor , beta cell , cytokine , secretion , chemistry , biology , islet , computer science , programming language
The effect of the cytokine interleukin‐1β on the insulin secretory responsiveness of single β‐cells (HIT‐T15) was investigated. In the short‐term, IL‐1β induced a dosage‐dependent stimulation of insulin release. In contrast, in the long‐term, IL‐1β, inhibited both basal and secretagogue‐stimulated insulin secretion. We also demonstrate the simultaneous presence of specific high and low affinity binding sites for IL‐1β on β‐cells. IL‐1β, which has been implicated in the pathogenesis of insulin‐dependent diabetes, may therefore mediate its opposing effects on β‐cells through a specific plasma membrane receptor.

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