Im sorry if this has already been asked but im new to the thread. I can't find the 2014 f214 paper anywhere. Does anyone have it or know what the big questions were?
After a prolonged period of fasting, glycogen levels in the liver are depleted. However the liver can still produce glucose by the process of gluconeogenesis. Describe one way in which this is done?
Anyone gonna try to answer that? I found it really difficult lol..
Protein can be converted to glucose in glucogenesis
Does cyclic and non-cyclic photophosphorylation occur at the same time? And if so, how does it work because in cyclic PSI electrons are returned to PSI, but in non-cyclic, PSI gets electrons from PSII?
Does cyclic and non-cyclic photophosphorylation occur at the same time? And if so, how does it work because in cyclic PSI electrons are returned to PSI, but in non-cyclic, PSI gets electrons from PSII?
In non-cyclic, water undergos photolysis to form H+ and electrons Photolysis is splitting of water using light
The electrons from water replace those lost from PSII
Please can someone give a detailed summary of selective reabsorption in the pct. I'm so confused by it :'(
Sodium/potassium ion pump actively removes Na+ from cells lining pct Na enter back the cell in association with glucose through cotransporter proteins Glucose diffuses back into the blood Water potential in filtrate increases H20 enters cells by osmosis
After a prolonged period of fasting, glycogen levels in the liver are depleted. However the liver can still produce glucose by the process of gluconeogenesis. Describe one way in which this is done?
Anyone gonna try to answer that? I found it really difficult lol..
Gluconeogenesis from fatty acids right? was this a PPQ?
Glucose isn't made by a reaction between amino acids and fats. It's fats and/or amino acids entering the krebs cycle and then doing glycolysis in reverse (bar a few reactions) to form glucose. The two don't bind together.
The vagus nerve (also know as the decelerator nerve) connects the medulla oblongata in the brain to the sinoatrial node (SAN) in the heart. Action potentials are sent down it to decrease the frequency of contractions of the heart muscle, reducing the heart rate. The opposite is the accelerator nerve which is the same except action potentials sent down it increase the frequency of contractions, raising heart rate.
Gluconeogenesis is the process of converting amino acids, fats and nucleic acids into glucose. Certain amino acids can be bled into the krebs cycle and then go through reverse glycolysis (bar a few reactions) and are turned back to glucose. Pyrimidines can do this as well (purines can not).
Thats what i thought. The answer however is... either deaminationof amino acids / removal of NH2 from amino acids ; pyruvate/ carbon skeleton / AW ; triosephosphate / TP ;condensation/ increasing number of carbon atoms ; or breakdownof, lipid / triglyceride ; glycerol; triosephosphate / TP ; condensation/ increasing number of carbon atoms ; max3
Im sorry if this has already been asked but im new to the thread. I can't find the 2014 f214 paper anywhere. Does anyone have it or know what the big questions were?
I'm going to assume the main point is that not all the water is lost in the descending limb. The water potential gradient is there, but by the time it's passed into the ascending limb some of it hasn't diffused out into the capillaries yet. That's why ADH can have an affect to vary it - not all of the water diffuses out of the collecting duct either, so aquaporins can help it along a bit more.
Can someone please explain all the G words for me please, getting a little confused :/ (like glycogenesis etc)
Glucose - a carbohydrate Glycogen - animal carbohydrate storage molecule Glucagon - hormone that increases blood glucose Glycolysis - Breaking down of glucose to form pyruvate, first stage of respiration Glycogenolysis - Breaking down of glycogen to glucose Glycogenesis - Glycogen synthesis from glucose Gluconeogenesis - Formation of new glucose from animo acids and fatty acids.