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Insulin
Question | Answer |
---|---|
What effect does insulin have on endothelial tissue? | Regulation of the secretion of the vasodilator nitric oxide and the vasoconstrictor Endothelin-1. Nitric oxide stimulates vasodilation and increased blood flow to the target tissues. It also inhibits pathways in the inflammation cascade |
What effect does insulin have on the liver? | It increases uptake of amino acid, activates glycogen synthase, inhibits GNG enzymes and decreases uptake of substrates. (Insulin also has no effect on the GLUT transporters in the liver) |
What effect does insulin have on adipose tissue? | It promotes leptin secretion, translocates GLUT 4, activates lipoprotein lipase, stores excess glucose as fat and inhibits lipolysis. |
What effect does insulin have on muscle tissue? | Activates glycogen synthase, increases uptake of BCAA, stimulates protein synthesis, translocates GLUT 4 and reduces loss of amino acids from muscle |
What happens in the endothelium without insulin? | Less vasodilation and slower movement of glucose to target tissues. CRP and the inflammation pathways both increase too |
What happens in the liver without insulin? | Amini acid uptake is decreased, glycogen is broken down (& glycogen synthase isn't activated), glucagon elevates and PEPCK expression is increased. GNG occurs. |
What happens in the adipose tissue without insulin? | Leptin is not secreted, GLUT 4 isn't translocated therefore glucose uptake & storage doesn't occur. LPL is not activated (lipoproteins are not broken down). There is also increased lipolysis and no lipogenesis. |
What happens in the muscle tissue without insulin? | Glycogen synthase is not activated (&and glycogen is not made). There is decreased uptake of BCAA, decreased protein synthesis, increased loss of amino acids and GLUT 4 is not translocated (Glucose is not take up) |
What are some factors that lead to insulin resistance? | Inflammatory mediators, overabundance of adipose tissue, lipid deposits in non-adipose tissue |
What is the effect of insulin resistance on the pancreas? | Hyperglycaemia is constantly stimulating cells to produce more insulin; this results in hyperinsulinaemia followed by insulin deficiency (as a result of beta-cell exhaustion) |
What are incretins? | Proteins/hormones released into circulation after minutes of eating and may continue to be released for up to 3 hours. They stimulate a decrease in blood glucose, slow the gastric emptying and inhibit glucagon release. |
What are the three stages of insulin release? | Cephalic, secretion 1 and secretion 2. |
What stage of insulin release is often inhibited in T2DM? | Secretion 2 |