期刊
SIAM JOURNAL ON APPLIED DYNAMICAL SYSTEMS
卷 13, 期 2, 页码 683-703出版社
SIAM PUBLICATIONS
DOI: 10.1137/130920198
关键词
oscillations; calcium; pancreatic beta-cells; dual oscillator model; metabolic
资金
- NIH/NIDDK Intramural Research Program
- Simons Foundation
- Starr Cancer Consortium [I3-A123]
- National Institutes of Health [F32-DK085960, R01-DK46409, DK080714]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK046409, K01DK101683, ZIADK013027] Funding Source: NIH RePORTER
Pancreatic islets exhibit bursting oscillations in response to elevated blood glucose. These oscillations are accompanied by oscillations in the free cytosolic Ca2+ concentration (Ca-c), which drives pulses of insulin secretion. Both islet Ca2+ and metabolism oscillate, but there is some debate about their interrelationship. Recent experimental data show that metabolic oscillations in some cases persist after the addition of diazoxide (Dz), which opens K(ATP) channels, hyperpolarizing beta-cells and preventing Ca2+ entry and Ca2+ oscillations. Further, in some islets in which metabolic oscillations were eliminated with Dz, increasing the cytosolic Ca2+ concentration by the addition of KCl could restart the metabolic oscillations. Here we address why metabolic oscillations persist in some islets but not others, and why raising Cac restarts oscillations in some islets but not others. We answer these questions using the dual oscillator model (DOM) for pancreatic islets. The DOM can reproduce the experimental data and shows that the model supports two different mechanisms for slow metabolic oscillations, one that requires calcium oscillations and one that does not.
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