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Mechanism of glucose dependent insulin release

CORRECTION: I think that the potassium channel allows potassium out of rather than into the cell as drawn, which is why inhibition by ATP (or the antidiabetic sulphonylurea drugs) causes depolarisation.


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COMMENT ON CORRECTION: I believe the image is accurately drawn. I would think that under steady-state the cell is continuously experiencing leakage of K+ out of the cell (as well as NA+ in). When the increase of the ATP:ADP ratio closes/deactivates the ATP-dependent K+ channel, it's not available to bring the K+ back in and reestablish resting membrane potential.

Comment of Correction: The image does justice to its meaning. If K+ was unable to leave the cell the influx of Na+ would cause depolarisation because there would be no subsequent outflow of K+ and compensation.However, K+ leaving the cell and Na+ entering is a passive process and therefore, would be unaffected by increase of the ATP: ADP ratio. The diagram shows K+ in a state in which it is not allowed to reenter, thus none is available to leave. Keeping the Na+ process constant, this results in a constant depolarised state.

Comment on Current K-transporter debate: There seems to some confusion on insulin release. Ca is the primary component in B-cells depolarization and release of insulin and not K. Potassium Efflux permeability is increased by several ways: Voltage-K Channels, Ca-Activated Channels, and new evidence has lead to ATP affecting K current as well (Both increasing and decreasing K permeability). Potassium current keeps Ca passive flux inward and in this model, deals nothing with Na. The constant depolarized state is the cause of K dissipating the charge buildup of Ca coming in and keeping the intracell Ca concentration at a much higher level. So while the picture is technically correct, it does not convey the correct idea and the comments so far to explain it seems a bit sketchy. Hope this help.

Reference: Giugliano,Michele, Marco Bove, and Massimo Grattarola 2000, "Insulin Release at the Molecular Level: Metabolic-Electrophysiological Modeling of the Pancreatic Beta-Cells" IEEE Transactions on Biomedical Engineering. 47:611-623.

COMMENT ON K-channels: I disagree with this picture being totally technically correct. Usually pictures like this one are drawn only with K leaving the cell. Well again this would be simplified. Actually when a resting membran potential is established equal amounts of K are leaving the cell through the K channel as well as entering it. So an arrow in both directions would be the totally right way to draw it. Anyway.
So the K-channel (if not closed by ATP) lets K in and out of the cell! This causes the resting membrane potential to establish. But when it's closed, the mechanism which is reliable for the resting membran potential crashes and so does the membrane potential. Still this has nothing to do with Na!(for a detailed description on this read: [ (furthermore do I doubt that the cell depolarization is caused by Ca influx - These Ca-channels are voltage gated which means that they are opened by cell-depolarization rather than causing it.)

Reference: Harrison's Internal Medicine > Part 14. Endocrinology and Metabolism > Section 1. Endocrinology > Chapter 323. Diabetes Mellitus > Insulin Biosynthesis, Secretion, and Action > Secretion

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