von Dr. Sankarganesh Jeyaraj
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| [1.] Sj/Fragment 003 01 - Diskussion Zuletzt bearbeitet: 2016-11-24 19:41:32 Schumann | Fragment, Gesichtet, Li 2004, SMWFragment, Schutzlevel sysop, Sj, Verschleierung |
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| In the triggering pathway, the facilitative glucose transporter GLUT2 transports the glucose into the β cell. It causes the rise in the ratio of ATP/ADP which leads ATP-sensitive K+ channels (KATP channels) in the plasma membrane to close. The decreased K+ permeability leads to membrane depolarization, opening of voltage-dependent Ca2+ channels, Ca2+ influx, and the eventual rise of the cytosolic Ca2+ concentration ([Ca2+]c) that triggers exocytosis of insulin containing vesicles. This pathway is also called KATP channel-dependent pathway. Please see Figure 1 for an illustration. The amplifying pathway which is a KATP channel-independent pathway, simply increases the efficiency of the Ca2+ on exocytosis when the concentration of Ca2+ has been elevated. | • Triggering Pathway The GLUT2 transports the glucose into the β cell. It causes the rise in the ratio of ATP/ADP which causes ATP-sensitive K+ channels (KATP channels) in the plasma membrane to close. The decreased K+ permeability leads to membrane depolarization, opening of voltage-dependent Ca2+ channels, Ca2+ influx, and the eventual rise of the cytosolic Ca2+ concentration ([Ca2+]c) that triggers exocytosis. This pathway is also called KATP channel-dependent pathway. See Figure 1.3.2 for an illustration.
• Amplifying Pathway The KATP channel-independent pathway simply increases the efficiency of the Ca2+ on exocytosis when the concentration of Ca2+ has been elevated. |
The two described figures are not identical. The source is not mentioned. |
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| [2.] Sj/Fragment 003 12 - Diskussion Zuletzt bearbeitet: 2016-11-25 19:31:57 WiseWoman | Fragment, Gesichtet, Li 2004, SMWFragment, Schutzlevel sysop, Sj, Verschleierung |
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| Figure 1. Pancreatic beta cells secrete insulin when glucose concentration levels are elevated.
The facilitated glucose transporter GLUT2 transports the glucose into the cell where it is phosphorylated by glucokinase. The glucose metabolism causes ATP-sensitive K+ channels to close, the membrane to depolarize and the Ca2+ channels to open. This triggers a cascade of protein phosphorylations leading to insulin exocytosis. The insulin receptor is a transmembrane glycoprotein that belongs to the large class of tyrosine kinase receptors. Two α subunits and two β subunits make up the insulin receptor. The β subunits pass through the cellular membrane and are linked by disulfide bonds (10) . 10. Ackermann,AM, Gannon,M: Molecular regulation of pancreatic beta-cell mass development, maintenance, and expansion. J.Mol.Endocrinol. 38:193-206, 2007 |
Figure 1.3.2. The β cells secrete insulin when glucose concentration level elevated
The facilitated GLUT2 transport the glucose into the β cell and the glucose is phosphorylated by glucokinase. The ratio of ATP:ADP is elevated. The glucose metabolism causes ATP-sensitive K+ channels to close, the membrane to depolarize and the Ca2+ channels to open. This triggers a cascade of protein phosphorylations and leads to insulin exocytosis [68]. (The figure is partially adapted from [68].) [page 13] 3.4. Insulin Receptors. In molecular biology, the insulin receptor is a transmembrane glycoprotein that is activated by insulin. It belongs to the large class of tyrosine kinase receptors. Two α subunits and two β subunits make up the insulin receptor. The β subunits pass through the cellular membrane and are linked by disulfide bonds ([90]). [68] V. Poitout, An integrated view of β-cell dysfunction in type-II diabetes, Annu. Rev. Med. 1996. 47:6983. [89] http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/pancreas/index.html |
The source is not given. The two figures with nearly identical captions are in fact quite different. |
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