Insulin‐secreting β‐cells possess specific receptors for interleukin‐1β

Abstract

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.