Relative contribution of Ca2+-dependent and Ca2+-independent mechanisms to the regulation of insulin secretion by glucose.
(1998) FEBS Letters — Vol. 421, n° 2, p. 115-119 (1998)
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- Although insulin secretion is usually regarded as a Ca2+-dependent mechanism, recent studies have suggested the existence of a Ca2+-independent pathway of regulation by glucose. Here, mouse islets were used to compare the contribution of Ca2+-dependent and -independent pathways. Glucose increased insulin release in a concentration-dependent manner both in a control medium, when it depolarizes beta cells and raises [Ca2+]i (triggering signal), and in the presence of 30 mM K+ and diazoxide, when it does not further raise [Ca2+]i but increases its efficacy on exocytosis. Both Ca2+-dependent responses were amplified by glucagon-like peptide-1+acetylcholine, and were strongly potentiated by forskolin+PMA. Under conditions of mild or stringent Ca2+ deprivation, glucose had no effect either alone or with GLP-1 and acetylcholine, and was poorly effective even during pharmacological activation of protein kinases A and C. Similar results were obtained with rat islets. It is concluded that physiological regulation of insulin release by glucose is essentially achieved through the two Ca2+-dependent pathways without significant contribution of a Ca2+-independent mechanism.
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Sato, Y., Nenquin, M., & Henquin, J.-C. (1998). Relative contribution of Ca2+-dependent and Ca2+-independent mechanisms to the regulation of insulin secretion by glucose. FEBS Letters, 421(2), 115-119. https://doi.org/10.1016/S0014-5793(97)01547-0 (Original work published 1998)