A role for endogenous prostaglandin E in biphasic pattern of insulin release in humans

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Abstract
Studies were undertaken to evaluate in humans the possible physiological role of prostaglandins of the E series (PGE) in modulating insulin release and to assess whether endogenous PGE synthesis may account for the biphasic pattern of insulin secretion. A square-wave glucose stimulation previously determined to give maximal biphasic insulin release was used. Infusion of lysine acetylsalicylate to block the synthesis of endogenous PGE increased by 2-fold total insulin response to glucose and also converted insulin release to a multiphasic pattern. The infusion of exogenous PGE1 (0.2 .mu.g .cntdot. kg-1 .cntdot. min-1) or PGE2 (10 .mu.g/min) in addition to lysine acetylsalicylate restored the typical biphasic pattern of insulin release and also decreased total insulin release to values similar to those of control studies. Infusion of either PGE1 or PGE2 in the absence of lysine acetylsalicylate reset insulin secretion to a lower level without altering the kinetics of release. Endogenous PGE released in response to glucose stimulation may exert an inhibiting effect on insulin release that becomes biphasic in appearance.