| Naslov: | ATP regulates sodium channel kinetics in pancreatic islet beta cells |
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| Avtorji: | ID Zou, Na (Avtor)
ID Rupnik, Marjan (Avtor) |
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| Datoteke: |  http://link.springer.com/content/pdf/10.1007%2Fs00232-012-9506-7.pdf
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| Jezik: | Angleški jezik |
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| Vrsta gradiva: | Delo ni kategorizirano |
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| Tipologija: | 1.01 - Izvirni znanstveni članek |
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| Organizacija: | MF - Medicinska fakulteta
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| Opis: | Pancreatic beta cells act as glucose sensors, in which intracellular ATP ([ATP](i)) are altered with glucose concentration change. The characterization of voltage-gated sodium channels under different [ATP](i) remains unclear. Here, we demonstrated that increasing [ATP](i) within a certain range of concentrations (2-8 mM) significantly enhanced the voltage-gated sodium channel currents, compared with 2 mM cytosolic ATP. This enhancement was attenuated by even high intracellular ATP (12 mM). Furthermore, elevated ATP modulated the sodium channel kinetics in a dose-dependent manner. Increased [ATP](i) shifted both the current-voltage curve and the voltage-dependent inactivation curve of sodium channel to the right. Finally, the sodium channel recovery from inactivation was significantly faster when the intracellular ATP level was increased, especially in 8 mM [ATP](i), which is an attainable concentration by the high glucose stimulation. In summary, our data suggested that elevated cytosolic ATP enhanced the activity of Na(+) channels, which may play essential roles in modulating cell excitability and insulin release when blood glucose concentration increases. |
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| Ključne besede: | Langerhansovi otočki, trebušna slinavka |
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| Leto izida: | 2013 |
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| Št. strani: | str. 101-107 |
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| Številčenje: | Vol. 246, iss. 2 |
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| PID: | 20.500.12556/DKUM-50505  |
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| UDK: | 612.349.7 |
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| COBISS.SI-ID: | 512288568 |
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| ISSN pri članku: | 0022-2631 |
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| NUK URN: | URN:SI:UM:DK:8YJ0HDMY |
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| Datum objave v DKUM: | 10.07.2015 |
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| Število ogledov: | 2519 |
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| Število prenosov: | 283 |
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| Metapodatki: |    |
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| Področja: | Ostalo
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