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| [1.] Sj/Fragment 004 01 - Diskussion Zuletzt bearbeitet: 2016-11-25 19:44:13 WiseWoman | Fragment, Gesichtet, Li 2004, SMWFragment, Schutzlevel sysop, Sj, Verschleierung |
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| Untersuchte Arbeit: Seite: 4, Zeilen: 1-9, 10-12 |
Quelle: Li 2004 Seite(n): 13, 14, 15, Zeilen: 13: last paragraph; 14: 1ff; 15: 1ff |
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| The insulin receptors are embedded in the plasma membrane of myocytes and adipocytes (11). The binding of insulin to the receptors is the initial step in a signal transduction pathway, triggering the consumption and metabolism of glucose. Bound by insulin , the insulin receptor phosphorylates several proteins in the cytoplasm, including insulin receptor substrates (IRS-1 and IRS-2) that activate Phosphatidylinositol 3-kinase (PI-3-K) leading to an increase in the facilitative glucose transporters (GLUT4 and GLUT1) molecules in the outer membrane of muscle cells and adipocytes, and therefore to an increase in the uptake of glucose from blood into muscle and adipose tissue. Figure 2 elucidates this signaling pathway (12).
[FIGURE] Figure 2. Insulin signals cells to utilize glucose. Insulin binds to its receptors on the membrane of the cells and induces phosphorylation of several proteins in the cytoplasm, including insulin receptor substrates (IRS-1 and IRS-2) which activate Phosphatidylinositol 3-kinase (PI-3-K) thereby leading to an increase in glucose transporter (GLUT1 and GLUT4) molecules in the plasma membrane. GLUT1 and GLUT4 transport the glucose into the cells efficiently. The kinetics of insulin receptor binding is complex. The number of insulin receptors of each cell changes opposite to the circulating insulin concentration level. Increased insulin circulating level reduces the number of insulin receptors per cell and the decreased [circulating level of insulin triggers the number of receptors to increase (13).] 11. Sesti,G: Pathophysiology of insulin resistance. Best.Pract.Res.Clin.Endocrinol.Metab 20:665-679, 2006 12. Wardzala,LJ, Jeanrenaud,B: Potential mechanism of insulin action on glucose transport in the isolated rat diaphragm. Apparent translocation of intracellular transport units to the plasma membrane. J.Biol.Chem. 256:7090-7093, 1981 13. Grunberger,G, Ryan,J, Gorden,P: Sulfonylureas do not affect insulin binding or glycemic control in insulin-dependent diabetics. Diabetes 31:890-896, 1982 |
The insulin receptors are embedded in the plasma membrane of hepatocytes and myocytes. The binding of insulin to the receptors is the initial step in a signal
[page 14] transduction pathway, triggering the consumption and metabolism of glucose ([89], [86]). Bound by insulin, the insulin receptor phosphorylates from ATP to several proteins in the cytoplasm, including insulin receptor substrates (IRS-1 and IRS-2) containing signaling molecules, activates Phosphatidylinositol 3-kinase (PI-3-K) and leads to an increase in glucose transporter (GLUT4) molecules ([98]) in the outer membrane of muscle cells and adipocytes, and therefore to an increase in the uptake of glucose from blood into muscle and adipose tissue ([89]). GLUT4 will transport the glucose to the cells efficiently. Figure 1.3.3 elucidates this signaling pathway. [...] However, the kinetics of insulin receptor binding are complex. The number of insulin receptors of each cell changes opposite to the circulating insulin concentration level. Increased insulin circulating level reduces the number of insulin receptors per cell and the decreased circulating level of insulin triggers the number of receptors to increase. [page 15] [FIGURE] Figure 1.3.3. Insulin signals cells to utilize glucose Insulin binds to its receptors on the membrane of the cells and phosphorylates several proteins in the cytoplasm, including insulin receptor substrates (IRS-1 and IRS-2) containing signaling molecules, activates Phosphatidylinositol 3-kinase (PI-3-K) and leads to an increase in glucose transporter (GLUT4) molecules. This leads to an increase in glucose transporter (GLUT4) molecules. GLUT4 will transport the glucose to the cells efficiently. [86] S.Wanant and M. J. Quon, Insulin Receptor Binding Kinetics: Modeling and Simulation Studies, J. Theor. Bio., 205 (2000), 355-364. [89] http://arbl.cvmbs.colostate.edu/hbooks/ pathphys/endocrine/pancreas/index.html [98] E. Y. Skolnik, Insulin receptor signaling pathways, http://www.med.nyu.edu/research/skolne01.html |
The source is not given. The two figures are not identical. |
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