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Comment
. 2010 Nov;59(11):2735-6.
doi: 10.2337/db10-1238.

The welcome resurgence of the α-cell: a pro glucagon commentary

Affiliations
Comment

The welcome resurgence of the α-cell: a pro glucagon commentary

R Paul Robertson. Diabetes. 2010 Nov.
No abstract available

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Figures

FIG. 1.
FIG. 1.
Regulation of glucagon secretion by zinc. Left panel: α-cell electrical and hormonal status in states of physiological and elevated glucose conditions. β-cells release zinc and insulin hexamers into the intraislet periportal circulation. Zinc dissociates from insulin and reaches downstream α-cells where it binds to and opens the KATP channels. K+ ions leave the cell and hyperpolarize the α-cell, thus preventing voltage-dependent calcium channels from opening. Glucagon granules are not mobilized and remain stored inside the cell. Right panel: When blood glucose levels decrease in response to exogenous insulin, β-cell insulin and zinc secretion decrease as well. KATP channels on α-cells close, K+ remains in the cell, and the α-cell depolarizes, which induces calcium channels to open, and calcium enters the cell. Intracellular calcium rises, which induces glucagon exocytotic granules to migrate to the plasma membrane where they fuse and release glucagon into the portal venous system. (Reproduced from Slucca et al. [6]).

Comment on

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