Islets of Langerhans, 2. Ed. 2014
DOI: 10.1007/978-94-007-6884-0_37-2
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Physiological and Pathophysiological Control of Glucagon Secretion by Pancreatic α-Cells

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Cited by 3 publications
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“…Therefore, to fully define the interaction matrix K σσ , one needs to define the signs for the autocrine interactions of A αα , A ββ , and A δδ , as well as the previously defined six paracrine interactions (table 1). Glucagon and glutamate, secreted by α cells, potentiate glucagon synthesis and secretion [120][121][122][123], which implies a positive autocrine interaction ( A αα = 1). Similarly insulin, serotonin, GABA, and ATP, secreted by β cells, stimulate insulin secretion [126,127,129,130,137], which also implies a positive autocrine interaction (A ββ = 1).…”
Section: Intra-islet Networkmentioning
confidence: 99%
“…Therefore, to fully define the interaction matrix K σσ , one needs to define the signs for the autocrine interactions of A αα , A ββ , and A δδ , as well as the previously defined six paracrine interactions (table 1). Glucagon and glutamate, secreted by α cells, potentiate glucagon synthesis and secretion [120][121][122][123], which implies a positive autocrine interaction ( A αα = 1). Similarly insulin, serotonin, GABA, and ATP, secreted by β cells, stimulate insulin secretion [126,127,129,130,137], which also implies a positive autocrine interaction (A ββ = 1).…”
Section: Intra-islet Networkmentioning
confidence: 99%