Sökning: onr:"swepub:oai:prod.swepub.kib.ki.se:1940780" >
Impaired gene and p...
-
Ostenson, CGKarolinska Institutet
(författare)
Impaired gene and protein expression of exocytotic soluble N-ethylmaleimide attachment protein receptor complex proteins in pancreatic islets of type 2 diabetic patients
- Artikel/kapitelEngelska2006
Förlag, utgivningsår, omfång ...
-
American Diabetes Association,2006
Nummerbeteckningar
-
LIBRIS-ID:oai:prod.swepub.kib.ki.se:1940780
-
http://kipublications.ki.se/Default.aspx?queryparsed=id:1940780URI
-
https://doi.org/10.2337/diabetes.55.02.06.db04-1575DOI
Kompletterande språkuppgifter
-
Språk:engelska
-
Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
-
Ämneskategori:ref swepub-contenttype
-
Ämneskategori:art swepub-publicationtype
Anmärkningar
-
Exocytosis of insulin is dependent on the soluble N-ethylmaleimide attachment protein receptor (SNARE) complex proteins in the B-cells. We assessed insulin release as well as gene and protein expression of SNARE complex protein in isolated pancreatic islets of type 2 diabetic patients (n = 4) and nondiabetic control subjects (n = 4). In islets from the diabetic patients, insulin responses to 8.3 and 16.7 mmol/l glucose were markedly reduced compared with control islets (4.7 ± 0.3 and 8.4 ± 1.8 vs. 17.5 ± 0.1 and 24.3 ± 1.2 μU · islet−1 · h−1, respectively; P < 0.001). Western blot analysis revealed decreased amounts of islet SNARE complex and SNARE-modulating proteins in diabetes: syntaxin-1A (21 ± 5% of control levels), SNAP-25 (12 ± 4%), VAMP-2 (7 ± 4%), nSec1 (Munc 18; 34 ± 13%), Munc 13-1 (27 ± 4%), and synaptophysin (64 ± 7%). Microarray gene chip analysis, confirmed by quantitative PCR, showed that gene expression was decreased in diabetes islets: syntaxin-1A (27 ± 2% of control levels), SNAP-25 (31 ± 7%), VAMP-2 (18 ± 3%), nSec1 (27 ± 5%), synaptotagmin V (24 ± 2%), and synaptophysin (12 ± 2%). In conclusion, these data support the view that decreased islet RNA and protein expression of SNARE and SNARE-modulating proteins plays a role in impaired insulin secretion in type 2 diabetic patients. It remains unclear, however, to which extent this defect is primary or secondary to, e.g., glucotoxicity.
Biuppslag (personer, institutioner, konferenser, titlar ...)
-
Gaisano, H
(författare)
-
Sheu, L
(författare)
-
Tibell, AKarolinska Institutet
(författare)
-
Bartfai, T
(författare)
-
Karolinska Institutet
(creator_code:org_t)
Sammanhörande titlar
-
Ingår i:Diabetes: American Diabetes Association55:2, s. 435-4400012-17971939-327X
Internetlänk
Hitta via bibliotek
-
Diabetes
(Sök värdpublikationen i LIBRIS)
Till lärosätets databas