Prostaglandins inhibit pancreatic β-cell replication and long-term insulin secretion by pertussis toxin-insensitive mechanisms but do not mediate the actions of interleukin-1 β

The effects of exogenous prostaglandins, inflammatory mediators known to be increased in pancreatic beta-cells by IL-1 beta, on the replication and long-term insulin secretion by beta-cells were investigated. Prostaglandins E1, E2, and F2 alpha suppressed beta-cell proliferation and long-term insulin secretion, thus mimicking the effects of IL-1 beta. The actions of prostaglandins were not prevented by pertussis toxin pretreatment. Additionally, the cyclooxygenase inhibitor indomethacin could not prevent the effects of IL-1 beta. It is concluded that prostaglandins suppress beta-cell growth and long-term insulin secretion without participation of pertussis-toxin sensitive GTP-binding proteins. In addition, although their synthesis is increased by IL-1 beta, prostaglandins seemingly do not convey the inhibitory actions of this cytokine in the beta-cell.