Stimulation of Glycogen Synthesis
Glycogen synthesis is also stimulated by the insulin receptor via IRS-1. In this case, it is the SH2 domain of PI-3 kinase (PI-3K) that binds the P-Tyr of IRS-1. Now activated, PI-3K can convert the membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP2) to phosphatidylinositol 3,4,5-triphosphate (PIP3). This indirectly activates a protein kinase, PKB (Akt), via phosphorylation. PKB then phosphorylates several target proteins, including glycogen synthase kinase 3 (GSK-3). GSK-3 is responsible for phosphorylating (and thus deactivating) glycogen synthase. When GSK-3 is phosphorylated, it is deactivated, and prevented from deactivating glycogen synthase. In this roundabout manner, insulin increases glycogen synthesis.
Read more about this topic: Insulin Receptor
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—Willard Van Orman Quine (b. 1908)
“The lore of our fathers is a fabric of sentences. In our hands it develops and changes, through more or less arbitrary and deliberate revisions and additions of our own, more or less directly occasioned by the continuing stimulation of our sense organs. It is a pale gray lore, black with fact and white with convention. But I have found no substantial reasons for concluding that there are any quite black threads in it, or any white ones.”
—Willard Van Orman Quine (b. 1908)
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—Andre Maurois (1885–1967)