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| === Structure ===
| | See [[Glucagon]] |
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| Glucagon is a kind of peptide [[hormone|hormone]] with 29 amino acids in a linear structure. Glucagon is produced originally as a formation of [[proglucagon|proglucagon]] in the [[pancreas|pancreas]], which is then converted to glucagon as a functional state in [[alpha cells of the pancreas|alpha cells]] of the islets <ref>R.Bowen (1999), Glucagon, http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/pancreas/glucagon.html (last accessed 09.01.11)</ref>.
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| === Function ===
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| The primary role of glucagon played in the body is increasing the [[Blood|blood]] [[glucose|glucose]] concentrations, which is the opposite function of [[insulin|insulin]], secreted from [[beta cells of the pancreas|beta cells]] of the islets. To be specific, glucagon raises the [[blood|blood]] [[sugar|sugar]] levels through the breakdown of the glycogen in the [[liver|liver]] when the concentration of the blood glucose is low <ref>R.Bowen (1999), Glucagon, http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/pancreas/glucagon.html (last accessed 09.01.11)</ref>. This process is called [[glycogenolysis|glycogenolysis]], which is decomposition of [[glycogen|glycogen]] into [[glucose|glucose]] <ref>Berg J., Tymoczko J. and Stryer L. (2007) Biochemistry, 6th edition, New York: WH Freeman(p601-603).</ref>.<sup> </sup>Another function of glucagon is activating [[gluconeogenesis|gluconeogenesis]], which convert non-hexose, for instance, [[amino acids|amino acids]], to glucose also for increasing the blood sugar levels <ref>Berg J., Tymoczko J. and Stryer L. (2007) Biochemistry, 6th edition, New York: WH Freeman(p770-771).</ref>
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| === Disease ===
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| [[Glucagonomas|Glucagonomas]] is a result of excessive seglucagon excretion, which causes some harm effects,for example, skin lesions <ref>R.Bowen (1999), Glucagon, http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/pancreas/glucagon.html (last accessed 09.01.11)</ref>.<br>
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| === References''':''' ===
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| <references /><br>
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Latest revision as of 06:16, 19 October 2015