WFRF:(Tengholm Anders)
Search: WFRF:(Tengholm Anders) > (2020-2024) > Glucose-induced cAM...
- 6 of 12
- Previous record
- Next record
- To hitlist
Glucose-induced cAMP elevation in β-cells involves amplification of constitutive and glucagon-activated GLP-1 receptor signalling
-
- Shuai, Hongyan (author)
- Uppsala universitet,Institutionen för medicinsk cellbiologi,School of Basic Medicine Sciences, Dali University, Yunnan, China
-
- Xu, Yunjian (author)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
-
- Ahooghalandari, Parvin (author)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
- show more...
- show less...
- (creator_code:org_t)
- 2021-01-09
- 2021
- English.
- In: Acta Physiologica. - : John Wiley & Sons. - 1748-1708 .- 1748-1716. ; 231:4
- Journal article (peer-reviewed)
Abstract
Subject headings
Close
- AIM: cAMP typically signals downstream of Gs -coupled receptors and regulates numerous cell functions. In β-cells, cAMP amplifies Ca2+ -triggered exocytosis of insulin granules. Glucose-induced insulin secretion is associated with Ca2+ - and metabolism-dependent increases of the sub-plasma-membrane cAMP concentration ([cAMP]pm ) in β-cells, but potential links to canonical receptor signalling are unclear. The aim of this study was to clarify the role of glucagon-like peptide-1 receptors (GLP1Rs) for glucose-induced cAMP signalling in β-cells.METHODS: Total internal reflection microscopy and fluorescent reporters were used to monitor changes in cAMP, Ca2+ and ATP concentrations as well as insulin secretion in MIN6 cells and mouse and human β-cells. Insulin release from mouse and human islets was also measured with ELISA.RESULTS: The GLP1R antagonist exendin-(9-39) (ex-9) prevented both GLP1- and glucagon-induced elevations of [cAMP]pm , consistent with GLP1Rs being involved in the action of glucagon. This conclusion was supported by lack of unspecific effects of the antagonist in a reporter cell-line. Ex-9 also suppressed IBMX- and glucose-induced [cAMP]pm elevations. Depolarization with K+ triggered Ca2+ -dependent [cAMP]pm elevation, an effect that was amplified by high glucose. Ex-9 inhibited both the Ca2+ and glucose-metabolism-dependent actions on [cAMP]pm . The drug remained effective after minimizing paracrine signalling by dispersing the islets and it reduced basal [cAMP]pm in a cell-line heterologously expressing GLP1Rs, indicating that there is constitutive GLP1R signalling. The ex-9-induced reduction of [cAMP]pm in glucose-stimulated β-cells was paralleled by suppression of insulin secretion.CONCLUSION: Agonist-independent and glucagon-stimulated GLP1R signalling in β-cells contributes to basal and glucose-induced cAMP production and insulin secretion.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
Keyword
- adenylyl cyclase
- exendin-(9-39)
- glucagon
- glucagon-like peptide-1
- insulin secretion
- pancreatic islets
Publication and Content Type
- ref (subject category)
- art (subject category)
Find in a library
- Acta Physiologica (Search for host publication in LIBRIS)
To the university's database
- 6 of 12
- Previous record
- Next record
- To hitlist
Find more in SwePub
- By the author/editor
- Shuai, Hongyan
- Xu, Yunjian
- Ahooghalandari, ...
- Tengholm, Anders ...
- About the subject
-
- MEDICAL AND HEALTH SCIENCES
- MEDICAL AND HEAL ...
- and Basic Medicine
- and Cell and Molecul ...
- Articles in the publication
- Acta Physiologic ...
- By the university
- Uppsala University
Search outside SwePub
- Extend your search to:
- Google Book Search
- Google Scholar
Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.
- Copyright © LIBRIS - National Library Systems
- LIBRIS.kb.se
