NDLI: Vasopressin potentiates corticotropin-releasing hormone-induced insulin release from mouse pancreatic beta-cells.

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Vasopressin potentiates corticotropin-releasing hormone-induced insulin release from mouse pancreatic beta-cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	O'Carroll, Anne-Marie Howell, Gillian M. Roberts, Emma M. Lolait, Stephen J.
Description	Country affiliation: United kingdom Author Affiliation: O'Carroll AM ( Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology (LINE), University of Bristol, Dorothy Hodgkin Building, Whitson Street, Bristol BS1 3NY, UK. a.m.ocarroll@bristol.ac.uk)
Abstract	Arginine vasopressin (AVP) and corticotropin-releasing hormone (CRH) have both been implicated in modulating insulin secretion from pancreatic beta-cells. In the present study, we investigated the insulin-secreting activities of AVP and CRH in wild-type and AVP VIb receptor knockout mice. Both neuropeptides stimulated insulin secretion from isolated mouse pancreatic islets. The response of islets to CRH was increased fourfold by concomitant incubation with a subthreshold dose of AVP that alone did not stimulate insulin secretion. Activation of the endogenously expressed M3 receptor by the cholinergic agonist carbachol also potentiated CRH-induced insulin secretion, indicating that the phenomenon may be pathway specific (i.e. Ca2+-phospholipase C) rather than agonist specific. The protein kinase C (PKC) inhibitors Ro-31-8425 and bisindolylmaleimide I attenuated the potentiating effect of AVP on CRH-stimulated insulin secretion and blocked AVP-stimulated insulin secretion. A possible interaction between the PKC and protein kinase A pathways was also investigated. The phorbol ester phorbol myristate acetate (PMA) stimulated insulin secretion, while the addition of both PMA and CRH enhanced insulin secretion over that measured with either PMA or CRH alone. Additionally, no AVP potentiation of CRH-stimulated insulin secretion was observed upon incubation in Ca2+-free Krebs-Ringer buffer. Taken together, the present study suggests a possible synergism between AVP and CRH to release insulin from pancreatic beta-cells that relies at least in part on activation of the PKC signaling pathway and is dependent on extracellular Ca2+. This is the first example of a possible interplay between the AVP and CRH systems outside of the hypothalamic-pituitary-adrenal axis.
File Format	HTM / HTML
ISSN	00220795
e-ISSN	14796805
DOI	10.1677/JOE-07-0645
Journal	Journal of Endocrinology
Issue Number	2
Volume Number	197
Language	English
Publisher	BioScientifica
Publisher Date	2008-05-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Endocrinology Arginine Vasopressin Pharmacology Corticotropin-releasing Hormone Insulin-secreting Cells Drug Effects Insulin Secretion Animals Calcium Metabolism Carbachol Dose-response Relationship, Drug Drug Synergism Indoles Maleimides Mice Mice, Inbred C57bl Protein Kinase C Physiology Receptors, Vasopressin Tetradecanoylphorbol Acetate Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Endocrinology, Diabetes and Metabolism Endocrinology

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Vasopressin potentiates corticotropin-releasing hormone-induced insulin release from mouse pancreatic β-cells

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