Abstract
VIP and PACAP stimulate insulin release by interaction with the VIP-2/PACAP-3 receptor on the beta cell. Activation of the receptor results in Gs-mediated stimulation of adenylyl cyclase and increased cellular cyclic AMP levels. Increased cyclic AMP results in a small and transient increase in [Ca2+]i, which is likely to have only a small and transient effect on the secretion rate. Cyclic AMP also potentiates insulin secretion by an as yet unknown action at a distal site. A third action of VIP and PACAP is responsible for the continued stimulation of insulin secretion after the levels of cyclic AMP and [Ca2+]i have returned to basal values. This third pathway, which is identified at present only by its sensitivity to low concentrations of wortmannin, plays a major role in the prolonged stimulation of insulin release by VIP and PACAP.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
