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. [PubMed]

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)
• Figure 6 (Glucose response of alpha cells persists in somatostatin knockout)
• Figure 7 (Glucose response of alpha cells persists with both somatostatin and KATP channels knocked out because of store operated channels (SOC))
• Figure 8 (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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