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Plos Biology : a Katp Channel-dependent Pathway Within a Cells Regulates Glucagon Release from Both Rodent and Human Islets of Langerhans, Volume 5

By Vidal-puig, Antonio J.

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Book Id: WPLBN0003926868
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos Biology : a Katp Channel-dependent Pathway Within a Cells Regulates Glucagon Release from Both Rodent and Human Islets of Langerhans, Volume 5  
Author: Vidal-puig, Antonio J.
Volume: Volume 5
Language: English
Subject: Journals, Science, Biology
Collections: Periodicals: Journal and Magazine Collection, PLoS Biology
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Publisher: Plos

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Vidal-Puig, A. J. (n.d.). Plos Biology : a Katp Channel-dependent Pathway Within a Cells Regulates Glucagon Release from Both Rodent and Human Islets of Langerhans, Volume 5. Retrieved from http://netlibrary.net/


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Description : Glucagon, secreted from pancreatic islet a cells, stimulates gluconeogenesis and liver glycogen breakdown. The mechanism regulating glucagon release is debated, and variously attributed to neuronal control, paracrine control by neighbouring b cells, or to an intrinsic glucose sensing by the a cells themselves. We examined hormone secretion and Ca2þ responses of a and b cells within intact rodent and human islets. Glucose-dependent suppression of glucagon release persisted when paracrine GABA or Zn2þ signalling was blocked, but was reversed by low concentrations (1–20 lM) of the ATP-sensitive Kþ (KATP) channel opener diazoxide, which had no effect on insulin release or b cell responses. This effect was prevented by the KATP channel blocker tolbutamide (100 lM). Higher diazoxide concentrations ( 30 lM) decreased glucagon and insulin secretion, and a- and b-cell Ca2þ responses, in parallel. In the absence of glucose, tolbutamide at low concentrations (,1 lM) stimulated glucagon secretion, whereas high concentrations (.10 lM) were inhibitory. In the presence of a maximally inhibitory concentration of tolbutamide (0.5 mM), glucose had no additional suppressive effect. Downstream of the KATP channel, inhibition of voltage-gated Naþ (TTX) and N-type Ca2þ channels (x-conotoxin), but not L-type Ca2þ channels (nifedipine), prevented glucagon secretion. Both the N-type Ca2þ channels and a-cell exocytosis were inactivated at depolarised membrane potentials. Rodent and human glucagon secretion is regulated by an a-cell KATP channel-dependent mechanism. We propose that elevated glucose reduces electrical activity and exocytosis via depolarisation-induced inactivation of ion channels involved in action potential firing and secretion.

 

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