so, until now i only managed to create this..
2. White muscles usually only perform aerobic glycolysis because postural maintainance movements hardly leads muscle to exhaustion. In addition to that, white muscles has a high fatique rate. In general, skeletal muscles are able to perform glycolysis even during anaerobic conditions. However the end product would be lactate. Why lactate? Due to the production of NADH2 during the 6th glyceraldehyde dehydrogenase reaction.Then it requires a place for NADH2 to be oxidised. In a normal senario we are able to send the NADH2 into respirative phosphorylation chain for oxidation. However, in anaerobic situation it is not possible. Thus, the lactate dehydrogenase[LDH] oxidises the NADH2 at reaction 11 of glycolysis.
inhibition of LDH would then result accumulation of NADH2. which probably will allosterically inhibit enzyme 6.
3.
4. glycogen phosphorylase of skeletal muscles has higher Vmax due to the requirement to induce a huge amount of glucose-6-phosphate release at the spur of the moment that muscle action is needed. The glycogen phosphorylase of liver has alot of time to slowly release glucose because there is no real dire need for glucose, it is just to maintain the body's blood glucose rate.
5. not very possible due to no ATP production from those processes.
6. treat bicarbonate as the CO2 that is required for the 1st reaction of pyruvate decarboxylase.
7.From the view of glycolysis:
A rising ATP conc means that AMP is yet to be present to activate PFK I complex. However, ATP will be used by PFK 2 to catalyse fructose2,6-bisphosphate. The F2,6-bp will then allosterically activate PFK 1 and change its conformation into a conformation rather similar if the AMP activates it. Now, why do AMP is the activator of PFK 1? This is due to AMP is the signal of used ATP, which is followed by the excessive usage of ATP in muscles, which in turn signify that muscle has been put to much work. Thus, F 2,6-biphos will help the degeneration of glycogen to provide glucose.
a rising AMP conc will allosterically activate PFK 1 complex.
From the view of gluconeogenesis:
ATP increase will activate gluconeogenesis and AMP increase will activate glycolysis
8.
10. 2 NADH2 molecules are formed. In the case of aerobic condition, NADH2 = 3 ATP. Thus 6 ATP is generated and outweights the ATP used in glucokinase and phosphofructokinase reactions. Net ATP = 4.
11. through oxidative phosphorylation pathway 3 ATP is generated of each NADH2. So 2 NADH2 will generate 6 ATP and the net ATP gain is 4 ATP.
12. Synthesis of glucose will increase due to
13.
14. could this substance be protein kinase c???
15.
16. This procedure saves the 1 ATP that is used by hexokinase aka glucokinase to add the phosphate back to glucose that results the formation of glucose 6- phosphate. This process is only possible due to sm glycolysis is used up at the time of release. Thus, saving the 1 single ATP does not affect the blood glucose levels unlike in liver.
17. glucose lvl blood drop , glycolysis drop, glycogen decomp drop, glycogen synthesis up.
18.
19.
1. Myocardium infaction = no oxygen. This results the anaerobic affinity of LDH to work [LDH4,5 which is at muscles]
2. Acute hepatitis = ???
20. glucose levels will go up due to glycolysis. Glycolysis by epineprine is possible to be activated by 2 receptors which have their own diff pathways.
1. Receptor alpha does the PIP2 CA2+ signal transduction method. [which ultilizes IP3 DAG + calcimodulin,it is an intracellular receptor pathway]
2. Receptor beta does the typical glucagon pathway. Which is cAMP signal transduction method [ intracellular, which requires adenylate cyclase]
21. insulin. For which test, maybe check ur biochem workbook.
22. its all about PFK 1. The increase in AMP due to continuous usage will result allosteric activation at PFK 1. [ATP]/[AMP] ratio will also decrease and the less ATP is a signal for PFK 2 to convert fructose 6 phosphate into fructose 2,6 phosphate that binds to the simillar purine allosteric site at PFK 1 and creates a change in conformation that resembles the allosteric activation of PFK1. In both bindings, rate of PFK 1 converting fructose 6 phosphate to glucose 2,6-phosphate with the usage of 1 ATP results in speeding up the glycolysis.
23.
No comments:
Post a Comment