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Glucose-induced Ca2...
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Bjorklund, A.Karolinska Institutet
(författare)
Glucose-induced Ca2+ (i) abnormalities in human pancreatic islets - Important role of overstimulation
- Artikel/kapitelEngelska2000
Förlag, utgivningsår, omfång ...
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American Diabetes Association,2000
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printrdacarrier
Nummerbeteckningar
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LIBRIS-ID:oai:DiVA.org:kth-20144
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https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-20144URI
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https://doi.org/10.2337/diabetes.49.11.1840DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:1942973URI
Kompletterande språkuppgifter
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Språk:engelska
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Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
Anmärkningar
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QC 20100525
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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
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beta-cells
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insulin release
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cytoplasmic ca2+
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b-cell
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calcium-concentration
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induced oscillations
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prolonged exposure
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glucagon-secretion
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mouse
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diazoxide
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Lansner, AndersKTH,Numerisk analys och datalogi, NADA(Swepub:kth)u12s8cr8
(författare)
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Grill, V. E.
(författare)
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Karolinska InstitutetNumerisk analys och datalogi, NADA
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Diabetes: American Diabetes Association49:11, s. 1840-18480012-17971939-327X
Internetlänk
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Diabetes
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