Islet Model for Pancreatic Beta, Alpha and Delta Cells
This is supplementary material for:
M. Watts, O. Kimchi, and A. Sherman. 2016.
Paracrine Regulation of Glucagon Secretion: The β-α-δ Model.
Am. J. Physiol. (Endocrinol. Metab.), in press.
Source files by figure:
[Note: some of these simulations are very slow, requiring tens of minutes]
- Figures 3 - 5 (Response to glucose of the three cell types)
- Figure6 (Glucose response of alpha cells persists in somatostatin knockout)
- Figure7 (Glucose response of alpha cells persists with both somatostatin and KATP channels knocked out because of store operated channels (SOC))
- Figure8 (In diabetes, inadequate glucagon secretion at high glucose, excessive secretion at low glucose)
- Figures 9 - 11 (Anti-synchronous oscillations of insulin and glucagon, synchrony between insulin and somatostatin)
- Figure12 (Asynchronous slow oscillations of glucagon without paracrine effeffects, synchrony with paracrine effects)
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