Glucose-induced Ca2+ (i) abnormalities in human pancreatic islets - Important role of overstimulation

↓ Direkt till sidans innehåll
↓ Direkt till sidans sekundära innehåll (sidomenyn)

Tyck till om SwePub Sök här!

Sökning: L773:0012 1797 OR L773:1939 327X > (2000-2004) > Glucose-induced Ca2...

Bjorklund, A.Karolinska Institutet (författare)

Glucose-induced Ca2+ (i) abnormalities in human pancreatic islets - Important role of overstimulation

Artikel/kapitelEngelska2000

Förlag, utgivningsår, omfång ...

American Diabetes Association,2000
printrdacarrier

Nummerbeteckningar

LIBRIS-ID:oai:DiVA.org:kth-20144
https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-20144URI
https://doi.org/10.2337/diabetes.49.11.1840DOI
http://kipublications.ki.se/Default.aspx?queryparsed=id:1942973URI

Kompletterande språkuppgifter

Språk:engelska
Sammanfattning på:engelska

Ingår i deldatabas

SwePubSwePub

Klassifikation

Ämneskategori:ref swepub-contenttype
Ämneskategori:art swepub-publicationtype

Anmärkningar

QC 20100525
Chronic hyperglycemia desensitizes beta -cells to glucose. To further define the mechanisms behind desensitization and the role of overstimulation, we tested human pancreatic islets for the effects of long-term elevated glucose levels on cytoplasmic free Ca2+ concentration ([Ca2+](i)) and its relationship to overstimulation. Islets were cultured for 48 h with 5.5 or 27 mmol/l glucose. Culture with 27 mmol/l glucose obliterated postculture insulin responses to 27 mmol/l glucose. This desensitization was specific for glucose versus arginine, Desensitization was accompanied by three major [Ca2+](i) abnormalities: 1) elevated basal [Ca2+](i),) loss of a glucose-induced rise in [Ca2+](i) and 3) perturbations of oscillatory activity with a decrease in glucose-induced slow oscillations (0.2-0.5 min(-1)). Coculture with 0.3 mmol/l diazoxide was performed to probe the role of overstimulation. Neither glucose nor diazoxide affected islet glucose utilization or oxidation, Coculture with diazoxide and 27 mmol/l glucose significantly (P < 0.05) restored postculture insulin responses to glucose and lowered basal [Ca2+](i) and normalized glucose-induced oscillatory activity. However, diazoxide completely failed to revive an increase in [Ca2+](i) during postculture glucose stimulation. In conclusion, desensitization of glucose-induced insulin secretion in human pancreatic islets is induced in parallel with major glucose-specific [Ca2+](i) abnormalities. Overstimulation is an important but not exclusive factor behind [Ca2+](i) abnormalities.

Ämnesord och genrebeteckningar

beta-cells
insulin release
cytoplasmic ca2+
b-cell
calcium-concentration
induced oscillations
prolonged exposure
glucagon-secretion
mouse
diazoxide

Biuppslag (personer, institutioner, konferenser, titlar ...)

Lansner, AndersKTH,Numerisk analys och datalogi, NADA(Swepub:kth)u12s8cr8 (författare)
Grill, V. E. (författare)
Karolinska InstitutetNumerisk analys och datalogi, NADA (creator_code:org_t)

Sammanhörande titlar

Ingår i:Diabetes: American Diabetes Association49:11, s. 1840-18480012-17971939-327X

Internetlänk

Hitta via bibliotek

Diabetes (Sök värdpublikationen i LIBRIS)

Till lärosätets databas

Hitta mer i SwePub

Av författaren/redakt...: Bjorklund, A.; Lansner, Anders; Grill, V. E.

Artiklar i publikationen: Diabetes

Av lärosätet: Kungliga Tekniska Högskolan; Karolinska Institutet

Sök utanför SwePub

Sök vidare i:: Google; 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.

LIBRIS.kb.se