Sökning: id:"swepub:oai:lup.lub.lu.se:91686c85-3d91-452d-96c7-22f543ef24cc" >
Glucagon receptor k...
-
Sorensen, Heidi
(författare)
Glucagon receptor knockout mice display increased insulin sensitivity and impaired beta-cell function
- Artikel/kapitelEngelska2006
Förlag, utgivningsår, omfång ...
-
American Diabetes Association,2006
Nummerbeteckningar
-
LIBRIS-ID:oai:lup.lub.lu.se:91686c85-3d91-452d-96c7-22f543ef24cc
-
https://lup.lub.lu.se/record/685271URI
-
https://doi.org/10.2337/db06-0307DOI
Kompletterande språkuppgifter
-
Språk:engelska
-
Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
-
Ämneskategori:art swepub-publicationtype
-
Ämneskategori:ref swepub-contenttype
Anmärkningar
-
In previous studies, glucagon receptor knockout mice (Gcgr(-/-)) display reduced blood glucose and increased glucose tolerance, with hyperglucagonemia and increased levels of glucagon-like peptide (GLP)-1. However, the role of glucagon receptor signaling for the regulation of islet function and insulin sensitivity is unknown. We therefore explored P-cell function and insulin sensitivity in Gcgr(-/-) and wild-type mice. The steady-state glucose infusion rate during hyperinsulinemic-euglycemic clamp was elevated in Gcgr(-/-) mice, indicating enhanced insulin sensitivity. Furthermore, the acute insulin response (AIR) to intravenous glucose was higher in Gcgr(-/-) mice. The augmented AIR to glucose was blunted by the GLP-1 receptor antagonist, exendin-3. In contrast, AIR to intravenous administration of other secretagogues was either not affected (carbachol) or significantly reduced (arginine, cholecystokinin octapeptide) in Gcgr(-/-) mice. In islets isolated from Gcgr(-/-) mice, the insulin responses to glucose and several insulin secretagogues were all significantly blunted compared with wild-type mice. Furthermore, glucose oxidation was reduced in islets from Gcgr(-/-) mice. In conclusion, the present study shows that glucagon signaling is required for normal P-cell function and that insulin action is improved when disrupting the signal. In vivo, augmented GLP-1 levels compensate for the impaired beta-cell function in Gcgr(-/-) mice.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
-
Sörhede Winzell, MariaLund University,Lunds universitet,Medicin, Lund,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Medicine, Lund,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)medk-msw
(författare)
-
Brand, Christian L.
(författare)
-
Fosgerau, Keld
(författare)
-
Gelling, Richard W.
(författare)
-
Nishimura, Erica
(författare)
-
Ahrén, BoLund University,Lunds universitet,Medicin, Lund,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Medicine, Lund,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)med-bah
(författare)
-
Medicin, LundSektion II
(creator_code:org_t)
Sammanhörande titlar
-
Ingår i:Diabetes: American Diabetes Association55:12, s. 3463-34691939-327X0012-1797
Internetlänk
Hitta via bibliotek
-
Diabetes
(Sök värdpublikationen i LIBRIS)
Till lärosätets databas