Study questions for the third exam.

  1. What is the physiological rationale behind coordinated activation of gluconeogenesis and glycogen breakdown in the liver, vs. coordination of glycolysis and glycogen breakdown in muscle? What enzymes are at the crux of this difference in regulation?
  2. Write out the mechanism of alpha-ketoglutarate dehydrogenase.
  3. Why can glutamate be a source of net synthesis of glucose, whereas (in our cells) most fat cannot? Why is this fact consistent with the fact that radiolabel administered in fat can subsequently show up in glycogen?
  4. Why is glycogen more branched than starch?
  5. Describe the cascade leading from glucagon signaling to glycogen breakdown.
  6. Why must the reversal of a highly exergonic transformation be catalyzed by a different pathway than the forward reaction? Give an example.
  7. Give an example of regulation of glycolyis or the TCA cycle according to the energy charge of the cell.
  8. Speculate on why muscles don't do gluconeogenesis.
  9. Write out any two of the reactions of the TCA cycle, including all reactants, products, and enzymes.
  10. Explain the origin of the Pasteur effect, that yeast use much more sugar growing anaerobically than aerobically.
  11. Give two reasons why beer is made in an air-tight container.
  12. What is the driving force for the highly endergonic malate dehydrogenase reaction?
  13. Explain why G6PDH mutations have arisen and persisted in human populations.
  14. Can the pentose phosphate pathway (and other reactions that we know about) be used to metabolize glucose all the way to CO2? Does your answer change if gluconeogenesis is activated?
  15. Why is glycogen breakdown thermodynamically favorable in the cell even though we are forming a phosphate ester?
  16. Briefly describe four things a liver cell can do with glucose-6-phosphate.
  17. Why is citrate prochiral and succinate not?
  18. What are the functions we have seen for CoA and biotin?
  19. What is the average oxidation state of the carbons in each of the following compounds: glucose, octane, ethanol, pyruvate, and CO2?
  20. Why do obligate anaerobes still have many of the enzymes of the TCA cycle?
  21. What is the mechanism of PEPCK? What pathway is it used in? What is one function of the limited amount of PEPCK synthesized by adipose cells?
  22. Give an analogy explaining why electrons are transferred from NADH through several intermediates before arriving at oxygen.
  23. Several "terminal electron acceptors" other than oxygen are used by anaerobes. They include sulfate and nitrate. Estimate the maximum possible efficiency of ATP production for NADH reduction (ATP's produced per NADH oxidized) by O2, SO4(2-), and NO3(-1).
  24. Write out the mechanism of aconitase.