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Created by alexlpeart
over 11 years ago
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Question | Answer |
Describe the mechanism for insulin causing the movement of GLUT4. | tyrosine in the presence of insulin autophosphotylates IRS1 to become phosphorylated-IRS1 which then activates PI3 kinase which catalyses the change of PIP2 to PIP3 which in turn activates PKD1. This activates PKC and PKB which causes GLUT4 to translocate to the cells membrain. |
Describe how obesity causes decreased GLUT 4 translocation as a result of insulin signalling. | Obesity increases Diacylglycerides and fatty acyl-CoA to be stored more in cells. These both cause PKC0 to increase which increases serine phosphorylation of the insulin receptor meaning less tyrosine phosphorylation can occur preventing the cascade taking place. Tumor necrosis factor also has the same effect as fats in the cell. Adipocytes also release resitin which inhibits the glucose uptake |
Is adiponectin good or bad for our health and what does it do? | Good for our health, it causes more FFA to be oxidized for energy by increasing insulin sensitivity. AMPK phosphorylated to AMPKp. This then phosphorylates ACC (acetyl-CoA carboxylase) so it becomes inactive meaning acetyl-CoA isn't turned into malonyl-CoA meaning CTP1 isn't inhibited. |
How does exercise affect TNF, Leptin and Adiponectin? | Decreases TNF and Leptin and increases adiponectin (so all good things) |
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