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Mechanism of action of insulin on acetylcholine‐evoked amylase secretion in the mouse pancreas.
Author(s) -
Singh J
Publication year - 1985
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1985.sp015562
Subject(s) - medicine , endocrinology , acetylcholine , insulin , depolarization , amylase , chemistry , adenosine , secretion , efflux , membrane potential , hyperpolarization (physics) , biology , biochemistry , enzyme , organic chemistry , nuclear magnetic resonance spectroscopy
The effects of insulin and acetylcholine (ACh) on amylase secretion, transmembrane movement of 45Ca2+ and K+, membrane potential and cyclic nucleotide levels in the isolated mouse pancreas were investigated. Insulin alone had no effect on either amylase secretion or 45Ca2+ fractional efflux but it markedly potentiated the ACh‐evoked amylase secretion and significantly reduced the ACh‐induced 45Ca2+ fractional efflux. These effects were dose related. Insulin evoked a small membrane hyperpolarization and an increase in K+ efflux. The islet hormone had virtually no effect on ACh‐induced membrane depolarization but it markedly enhanced the ACh‐elicited K+ efflux. Both insulin and ACh had marked time‐dependent effects on the metabolism of adenosine 3',5'‐cyclic monophosphate (cyclic AMP). Insulin increased and ACh decreased cyclic AMP concentration when applied separately. However, when added together, insulin and ACh caused a rapid and sustained elevation of cyclic AMP levels. Superfusion of mouse pancreatic fragments with an exogenous lipid‐soluble derivative of cyclic AMP (dibutyryl adenosine 3',5'‐cyclic monophosphate) caused dose‐dependent increases in amylase secretion. Dibutyryl cyclic AMP also markedly enhanced, in a dose‐dependent manner, the ACh‐evoked amylase secretion. It is concluded that insulin may exert its potentiating action on ACh‐evoked amylase output in the mouse pancreatic acinar cells by elevating both cytoplasmic Ca2+ and cyclic AMP levels.