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About pegasus10

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  1. Hello, I was reading a scientific article which reported that oral administration of a mutated form of apolipoprotein A1 (ApoA-I) to mice fed with a high cholesterol diet significantly lowers the rate of formation of atherosclerotic plaques. But I can't understand how this is possible. I mean, if mice are given the protein by mouth, it is digested into single amino acids, isn't it? So, how can it reduce plaque formation in the circulatory system if it is broken down by the digestive system? Thanks in advance!
  2. ATP-ADP translocase mediates the exchange of ATP and ADP and this favored by the proton gradient across the inner mitochondrial membrane. But is this transport process an active process? I mean, are ATP and ADP transported against their concentration gradient or not? I don't understand if the function of the proton gradient is just to further favor an already-favorable process (passive transport) or to make possible an unfavorable process (active transport). Thanks in advance!
  3. Why are ketone bodies only produced in the liver? I guess because some enzymes involved in their synthesis are only present in this organ, but I wasn't able to find this information in my textbook. Can someone help me? Thanks in advance!
  4. Hello, talking about CO2 transport, we know that the T form of hemoglobin binds more CO2 as carbamate than does the R form, so when the concentration of CO2 is high, the T state is favored and hemoglobin releases its bound O2. This mechanism is pretty clear to me, but I can't understand a statement made by my textbook when explaining this concept: "Although the difference in CO2 binding between the T and R states of hemoglobin accounts for only 5% of the total blood CO2, it is responsible for around 50% the CO2 transported by the blood. This is because only 10% of the total blood CO2 is lost through the lungs in each circulatory cycle". Can someone explain this sentence in different words? Thanks in advance!
  5. No, unfortunately I wasn't able to find anything useful on PubMed. Thank you, by the way.
  6. Hello, is muscle glycogen phosphorylase sensitive to glucose? I mean, is glucose an allosteric effector for the muscle isoform of glycogen phosphorylase? My answer would be no, but going through Voet's Biochemistry book I found a diagram in which glucose is depicted as a negative allosteric effector for glycogen phosphorylase in general, without specifying muscle isoform / liver isoform. Thanks in advance!
  7. Hello, is it possible to draw the ring structure of a ketopentose, like for example D-ribulose? I've been browsing the web and some organic chemistry textbooks, but I haven't been able to find anything. Thanks in advance!
  8. Hello, the following equation is the short formula to calculate plasma osmolality (I found it on my physiology book as well as on Wikipedia): Calculated osmolality = 2 [Na] + [Glucose] + [Urea] My question is: why is the concentration of Na+ (sodium ions) multiplied by 2? Thanks in advance!
  9. Hello, in the sentence "insulin stimulates the activity of a phosphoprotein phosphatase that catalyzes removal of the phosphoryl group from the bifunctional protein PFK-2/FBPase-2", the word "stimulates" means that insulin enhances transcription and translation of the phosphoprotein phosphatase or that the signalling pathway activated by insulin stimulates a phosphoprotein phosphatase which is already present in the cytoplasm? Thanks in advance!
  10. Hello, is it formally correct to state that anaerobic glycolysis is the exact same thing as fermentation? For example, if I write "In human cells anaerobic glycolysis, starting from one molecule of glucose, gives two molecules of lactate", can I substitute "anaerobic glycolysis" with "lactic acid fermentation"? Thanks in advance!
  11. A table in the book "Medical Physiology" by Boron and Boulpaep. The chapter is the one dealing with the fluid compartments in the human body
  12. Hello, I read about an autosomal recessive disease called "essential fructosuria", in which the enzyme fructokinase is absent and dietary fructose is phosphorylated by hexokinase to give fructose 6-phosphate. But why is this compound excreted instead of entering the glycolytic pathway? I mean, the third step of glycolysis is the conversion of fructose 6-phosphate (deriving from glucose) into fructose 1,6-bisphosphate, so why can't fructose 6-phosphate deriving from fructose be processed in the same way?
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