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Sökning: onr:fp4f3g2fczq7kfj0 > Studies of cAMP and...

Studies of cAMP and Ca 2+  signaling in pancreatic islet cells [Elektronisk resurs]

Shuai, Hongyan (författare)
Tengholm, Anders, 1971- (preses)
Gylfe, Erik, 1947- (preses)
Barg, Sebastian, 1969- (preses)
Salehi, Albert (opponent)
Uppsala universitet Medicinska och farmaceutiska vetenskapsområdet (utgivare)
Publicerad: Uppsala : Acta Universitatis Upsaliensis, 2018
Engelska 53
Serie: Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, 1651-6206 1651-6206
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  • E-bokAvhandling(Diss. (sammanfattning) Uppsala : Uppsala universitet, 2018)
Sammanfattning Ämnesord
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  • The blood glucose-lowering and -elevating hormones insulin and glucagon are released from the pancreatic islet β- and α-cells, respectively. The intracellular messengers Ca 2+ and cAMP have central roles in controlling the secretion of both hormones, but the underlying mechanisms are incompletely understood. A powerful approach to gain further insight is to study the messengers in individual cells within pancreatic islets, provided that each cell can be identified. To facilitate such studies, adenoviral vectors were generated for expression of fluorescent proteins controlled by the insulin and preproglucagon promoters, as well as the somatostatin and pancreatic polypeptide promoters that identify the other two major islet cell types, δ- and PP-cells. Recordings of cAMP and Ca 2+ concentration changes with fluorescent reporters demonstrated that cells expressing identification markers responded as expected to well-known stimuli and modulators of the two messengers. Glucose-induced Ca 2+ oscillations in β-cells were found to be synchronized with those in δ-cells, and two subpopulations of α-cells with different Ca 2+ regulation by glucose were identified. Mouse and human β-cells responded to the insulinotropic hormones glucagon, GIP and GLP-1 with elevations of cAMP. Most α-cells reacted similarly to GIP, whereas only a subpopulation – larger among human than mouse α-cells - responded to glucagon and GLP-1. The GLP-1-receptor antagonist exendin-(9-39) suppressed both GLP-1- and glucagon-induced cAMP elevations in β-cells. Since exendin-(9-39) did not antagonize glucagon receptors, glucagon apparently activates GLP-1 receptors in β-cells. Even in the absence of glucagon/GLP-1, exendin-(9-39) reduced cAMP increases obtained by glucose stimulation or elevation of Ca 2+ . This effect was attributable to constitutive GLP-1-receptor activity rather than paracrine effects. Exendin-(9-39) also inhibited glucose-induced insulin release, highlighting the importance of cAMP formation in nutrient-stimulated secretion. Simultaneous recordings of cAMP and Ca 2+ showed a complex and variable interrelationship between the messengers and the cAMP precursor ATP in β-cells. Depolarization-induced Ca 2+ increases inhibited forskolin-, IBMX- and GLP-1-induced cAMP elevations. This cAMP lowering in part reflected suppression of the Ca 2+ -sensitive activity of adenylyl cyclases AC5 and 6, but also autocrine signaling induced by Ca 2+ -triggered exocytosis of insulin and adenine nucleotides, whose receptors activate phosphodiesterases and inhibit adenylyl cyclases, respectively. 

Ämnesord

Medical and Health Sciences  (hsv)
Basic Medicine  (hsv)
Cell and Molecular Biology  (hsv)
Medicin och hälsovetenskap  (hsv)
Medicinska och farmaceutiska grundvetenskaper  (hsv)
Cell- och molekylärbiologi  (hsv)

Genre

government publication  (marcgt)

Indexterm och SAB-rubrik

pancreatic islet
insulin
glucagon
somatostatin
pancreatic polypeptide
exendin-(9-39)
GLP-1
GIP
ATP
adenosine
cAMP
Ca2
β-cell
α-cell
δ-cell
PP-cell
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