NDLI: Islet Oxygen Consumption and Insulin Secretion Tightly Coupled to Calcium Derived from L-type Calcium Channels but Not from the Endoplasmic Reticulum

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Islet Oxygen Consumption and Insulin Secretion Tightly Coupled to Calcium Derived from L-type Calcium Channels but Not from the Endoplasmic Reticulum

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sweet, Ian R. Jung, Seung-ryoung Reed, Benjamin J. Gilbert, Merle
Description	Author Affiliation: Gilbert M ( Department of Medicine, University of Washington, Seattle, Washington 98195, USA.)
Abstract	The aim of the study was to test whether the source of intracellular calcium (Ca2+) is a determinant of beta cell function. We hypothesized that elevations in cytosolic Ca2+ caused by the release of Ca2+ from the endoplasmic reticulum (ER) have little physiologic impact on oxygen consumption and insulin secretion. Ca2+ release from the ER was induced in isolated rat islets by acetylcholine and response of oxygen consumption rate (OCR), NAD(P)H, cytosolic Ca2+, and insulin secretory rate (ISR) were measured. Glucose increased all four parameters, and thereafter acetylcholine further increased cytosolic Ca2+, OCR, and ISR. To assess the contribution of Ca2+ release from the ER in mediating the effects of acetylcholine, ER Ca2+ stores were first emptied by inhibiting the sarcoendoplasmic reticulum Ca2+-ATPase, which subsequently reduced the effect of acetylcholine on cytosolic Ca2+ but not its effects on OCR or ISR. As predicted, OCR and ISR were acutely sensitive to changes in L-type Ca2+ channel activity; nimodipine completely inhibited glucose-stimulated ISR and suppressed OCR by 36%, despite only inhibiting cytosolic Ca2+ by 46%. Moreover, in the presence of nimodipine and high glucose, acetylcholine still elevated cytosolic Ca2+ levels above those observed in the presence of high glucose alone but did not significantly stimulate ISR. In conclusion, Ca2+ flux through L-type Ca2+ channels was tightly coupled to changes in OCR and ISR. In contrast, the results obtained support the notion that Ca2+ release from the ER has little or no access to the intracellular machinery that regulates OCR and ISR.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	36
Volume Number	283
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2008-09-05
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Calcium Channels, L-Type Metabolism Calcium Insulin Secretion Islets Of Langerhans Oxygen Consumption Physiology Acetylcholine Pharmacology Animals Calcium Channel Blockers Cholinergic Agents Endoplasmic Reticulum Glucose Nimodipine Rats, Inbred BB Tissue Culture Techniques Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S. Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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