Editing Alpha cell (section)

==Function==
Alpha cells function in the maintenance of blood glucose levels. Alpha cells are stimulated to produce glucagon in response to hypoglycemia, epinephrine, amino acids, other hormones, and neurotransmitters.<ref name=":3">{{Cite journal |last1=Yu |first1=Qian |last2=Shuai |first2=Hongyan |last3=Ahooghalandari |first3=Parvin |last4=Gylfe |first4=Erik |last5=Tengholm |first5=Anders |date=July 2019 |title=Glucose controls glucagon secretion by directly modulating cAMP in alpha cells |journal=Diabetologia |language=en |volume=62 |issue=7 |pages=1212–1224 |doi=10.1007/s00125-019-4857-6 |issn=0012-186X |pmc=6560012 |pmid=30953108}}</ref>

=== Glucagon Secretion and Control of Gluconeogenesis ===
Glucagon functions to signal the liver to begin [[gluconeogenesis]] which increases glucose levels in the blood.<ref name=":3" /> Glucagon will bind to the glucagon receptors on the plasma membranes of [[hepatocyte]]s (liver cells). This ligand binding causes the activation of [[Adenylyl cyclase|adenylate cyclase]], which causes the creation of [[Cyclic adenosine monophosphate|cyclic AMP]] (cAMP).<ref name=":4">{{Cite journal |last1=Janah |first1=Lina |last2=Kjeldsen |first2=Sasha |last3=Galsgaard |first3=Katrine D. |last4=Winther-Sørensen |first4=Marie |last5=Stojanovska |first5=Elena |last6=Pedersen |first6=Jens |last7=Knop |first7=Filip K. |last8=Holst |first8=Jens J. |last9=Wewer Albrechtsen |first9=Nicolai J. |date=January 2019 |title=Glucagon Receptor Signaling and Glucagon Resistance |journal=International Journal of Molecular Sciences |language=en |volume=20 |issue=13 |pages=3314 |doi=10.3390/ijms20133314 |issn=1422-0067 |pmc=6651628 |pmid=31284506|doi-access=free }}</ref> As the intracellular concentration of cAMP rises, [[protein kinase A]] (PKA) is activated and phosphorylates the transcription factor [[CREB|cAMP Response Element Binding]] (CREB) protein.<ref name=":4" /> CREB then induces transcription of [[Glucose 6-phosphatase|glucose-6-phosphatase]] and [[phosphoenolpyruvate carboxylase]] (PEPCK). These enzymes increase gluconeogenic activity.<ref name=":4" /> PKA also phosphorylates [[Phosphofructokinase 2|phospho-fructokinase 2]] (PFK2)/fructose 2,6-biphsophatase (FBPase2), inhibiting PFK2 and activating FBPase2.<ref name=":4" /> This inhibition decreases intracellular levels of [[Fructose 2,6-bisphosphate|fructose 2,6-biphosphate]] and increases intracellular levels of [[fructose 6-phosphate]] which decreases glycolytic activity and increases gluconeogenic activity.<ref name=":4" /> PKA also phosphorylates [[pyruvate kinase]] which causes an increase in intracellular levels of fructose 1,6-biphosphate and decreases intracellular levels of pyruvate, further decreasing glycolytic activity.<ref name=":4" /> The most important action of PKA in regulating gluconeogenesis is the phosphorylation of phosphorylase kinase which acts to initiate the [[glycogenolysis]] reaction, which is the conversion of [[glycogen]] to glucose, by converting glycogen to glucose 1-phosphate.<ref name=":4" />

Alpha cells also generate [[Glucagon-like peptide-1]] and may have protective and regenerative effect on [[beta cell]]s. They possibly can [[Transdifferentiation|transdifferentiate]] into beta cells to replace lost beta cells.<ref>{{Cite journal|last1=Stanojevic|first1=Violeta|last2=Habener|first2=Joel F.|date=2015-10-08|title=Evolving Function and Potential of Pancreatic Alpha Cells|journal=Best Practice & Research. Clinical Endocrinology & Metabolism|volume=29|issue=6|pages=859–871|doi=10.1016/j.beem.2015.10.002|issn=1521-690X|pmc=4690008|pmid=26696515}}</ref>