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Submembrane ATP and...
Submembrane ATP and Ca2+ kinetics in alpha-cells : unexpected signaling for glucagon secretion
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- Li, Jia (author)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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- Yu, Qian (author)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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- Ahooghalandari, Parvin (author)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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- Gribble, Fiona M. (author)
- Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge, United Kingdom
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- Reimann, Frank (author)
- Cambridge Institute for Medical Research, Addenbrooke’s Hospital, Cambridge, United Kingdom
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- Tengholm, Anders (author)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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- Gylfe, Erik (author)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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(creator_code:org_t)
- Wiley, 2015
- 2015
- English.
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In: The FASEB Journal. - : Wiley. - 0892-6638 .- 1530-6860. ; 29:8, s. 3379-3388
- Related links:
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https://europepmc.or...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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https://urn.kb.se/re...
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Abstract
Subject headings
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- Cytoplasmic ATP and Ca2+ are implicated in current models of glucose's control of glucagon and insulin secretion from pancreatic alpha- and beta-cells, respectively, but little is known about ATP and its relation to Ca2+ in alpha-cells. We therefore expressed the fluorescent ATP biosensor Perceval in mouse pancreatic islets and loaded them with a Ca2+ indicator. With total internal reflection fluorescence microscopy, we recorded subplasma membrane concentrations of Ca2+ and ATP ([Ca2+](pm); [ATP](pm)) in superficial alpha- and beta-cells of intact islets and related signaling to glucagon and insulin secretion by immunoassay. Consistent with ATP's controlling glucagon and insulin secretion during hypo- and hyperglycemia, respectively, the dose-response relationship for glucoseinduced [ATP](pm) generation was left shifted in alpha-cells compared to beta-cells. Both cell types showed [Ca2+](pm) and [ATP](pm) oscillations in opposite phase, probably reflecting energy-consuming Ca2+ transport. Although pulsatile insulin and glucagon release are in opposite phase, [Ca2+](pm) synchronized in the same phase between alpha- and beta-cells. This paradox can be explained by the overriding of Ca2+ stimulation by paracrine inhibition, because somatostatin receptor blockade potently stimulated glucagon release with little effect on Ca2+. The data indicate that an alpha-cell-intrinsic mechanism controls glucagon in hypoglycemia and that paracrine factors shape pulsatile secretion in hyperglycemia.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinsk bioteknologi -- Medicinsk bioteknologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Medical Biotechnology -- Medical Biotechnology (hsv//eng)
- 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
- oscillations
- islet of Langerhans
- signal transduction
- paracrine
Publication and Content Type
- ref (subject category)
- art (subject category)
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