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11 Cards in this Set
- Front
- Back
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In anerobic conditions, what happens and why?
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in non-yeast, you get lactate (2 mol for each glucose added) and the conversion of NADH to NAD+ (one of the ingredients found in glycolysis)
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In what steps of glycolysis is serious regulation happening? Regulation that could lead to glycolysis or gluconeogenesis?
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Steps 1, 3, and 10 (hexokinase, phospho fructokinase 1, and pyruvate kinase)
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Regulation of glycolysis can happen at the transport or at the enzyme level. Tell me about transport regulation.
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Glut 1: used at low glucose concentrations (1-2mM), present in all cells, works at lowest concentrations of glucose
Glut 2: present in LIVER and PANCREAS, work at highest Km (15-20 mM), good for removing excess glucose and for signaling the release of insulin Glut 4: present in Fat and Muscle cells, insuling dependent, used at medium glucose concentration (5 mM) Glut 5: present in small intestine, used at 10mM, for fructose transport |
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Where does the signal for insulin secretion come from?
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Glut 4 in pancreas and liver cells works at high glucose concentrations. Glucose transported into cell, undergoes glycolysis and releases ATP.
ATP works on ATP-sensitive K+ channels, closing them and depolarizing the cell. Depolarization leads to opening of Ca++ channels which releases Ca, this also releases insulin. Insulin can now float around and work on Glut4 transporters (on fat and muscle cells) |
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How does insulin act on the cell?
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Insulin activates the RTK pathway, which in turn activates PKB. PKB makes glut-4 containing vessicles travel up and bind to the plasma membrane, now allowing them to function and bring glucose into fat/muscle cells.
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In diabetes, what happens to the cells?
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without insulin, glut-4 receptors don't make it to the surface and don't get uptake of glucose into muscle and fat cells.
this decreases glycolysis and makes cells break down fats for energy this releases b-hydroxy butyrate and acetoacetate. also get decreased pH from ketoacidosis. |
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What two different hexokinases should we be familiar with, and what inhibits them?
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Hexokinase-1 is present in most cells (muscles, etc) and works at a low Km. Feed back and shut down happens from the 2nd product in glycolysis, glucose-6-phosphate.
Hexokinase IV (aka glucokinase) is in pancreas and liver cells, works at a higher Km. at low [glucose], hex IV is sequestered in the nucleus. at high [glucose], it's released to the cytosol and can go to work. note - it's IMMUNE to g-6-p, but can be shut down by Fructose-6-phosphate (it re-sequesters it in the nucleus. |
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PFK-1 and ATP - how is the enzyme affected?
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PFK-1 is down-regulated by excess ATP (if well-fed, don't need more ATP production via glycolysis).
Up regulated by ADP/AMP. |
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PFK-1 and its substrate - how does it affect the enzyme?
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PFK-1 is activated by its own substrate (F-6-P)
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What's the most important regulator of PFK-1?
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Fructose 2,6 bisphosphate.
F 2,6 BP activates PFK-1 somethin' fierce. |
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Biggest regulator of PFK-1 is F 2,6 BP. Where does it come from and what creates/destroys it?
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F 2,6 BP is formed from F-6-P (2nd step of glycolysis) in a separate reaction.
There's a bifunctional enzyme called: PFK-2/FBP-2. Note that PFK-2 catalyzes the creation of F 2,6BP. So: PFK-2 turns on F 2,6 BP which turns on PFK-1 which encourages glycolysis. PFK-2 is activated by phosphorylation, in response to insulin. The other half of the di-enzyme, PFK-2, breaks down F 2,6 BP and stops glycolysis. This is activated by glucagon. |
