METABOLISM REVISION QUESTIONS
Q1. Describe the structure and function of the pyruvate dehydrogenase complex, including its
cofactors and regulatory mechanisms.
Q2. Explain how phosphofructokinase-1 is regulated by ATP, AMP, and citrate. Why is it
considered the key control point in glycolysis?
Q3. Outline the complete sequence of reactions in the citric acid cycle and indicate where NADH,
FADH₂, and GTP are produced.
Q4. Compare the metabolic fates of pyruvate under aerobic and anaerobic conditions in mammalian
cells.
Q5. Explain the chemiosmotic theory and how it accounts for ATP synthesis in mitochondria.
Q6. Describe how glycogen phosphorylase is regulated by both covalent modification and allosteric
effectors.
Q7. Explain how gluconeogenesis bypasses the irreversible steps of glycolysis. Include the enzymes
involved.
Q8. Describe the role of uncoupling agents in oxidative phosphorylation and their physiological
consequences.
Q9. Explain why the citric acid cycle is described as amphibolic, providing specific examples.
Q10. Compare the regulation of glycolysis and gluconeogenesis, highlighting how futile cycling is
prevented.
Q11. Describe the hormonal regulation of glycogen metabolism in liver cells, focusing on insulin
and glucagon signaling pathways.
Q12. Explain the role of NAD⁺ in glycolysis and why its regeneration is essential for continued
ATP production.
Q13. Describe how the electron transport chain is organized within the inner mitochondrial
membrane and the function of each complex.
Q14. Explain the differences in glycogen metabolism between liver and muscle tissues.
Q15. Describe the energy yield of glycolysis under aerobic conditions and explain how this yield is
achieved.
Q16. Explain how the activity of the pyruvate dehydrogenase complex is regulated by
phosphorylation.
Q17. Describe the role of citrate in linking glycolysis and the citric acid cycle.
Q18. Explain how AMP-activated protein kinase (AMPK) influences metabolic pathways under
low-energy conditions.
Q19. Describe the formation and significance of lactate during anaerobic metabolism.
Q20. Explain how proton motive force is generated and how it is used to drive ATP synthesis.
, Q21. A patient presents with severe lactic acidosis during mild exercise. Muscle biopsy shows
normal oxygen supply but impaired oxidative metabolism. Propose possible defects and explain the
biochemical basis.
Q22. In an experiment, cells are treated with oligomycin. Predict the effects on ATP production,
oxygen consumption, and NADH levels. Explain your reasoning.
Q23. A researcher knocks out phosphofructokinase-1 in cultured hepatocytes. Predict the metabolic
consequences on glycolysis, gluconeogenesis, and overall cellular energy balance.
Q24. During prolonged fasting, blood glucose remains stable despite depleted glycogen stores.
Explain the metabolic adaptations that allow this to occur.
Q25. A mutation reduces the activity of pyruvate dehydrogenase kinase (PDK). Predict how this
affects carbohydrate metabolism under fed and fasting conditions.
Q26. Cells are supplied with radiolabeled glucose ([¹⁴C]-glucose). Describe how you would trace
carbon atoms through glycolysis and the TCA cycle.
Q27. A toxin specifically inhibits Complex III of the electron transport chain. Predict the
downstream effects on ATP synthesis, NADH oxidation, and reactive oxygen species formation.
Q28. Compare the metabolic response of muscle tissue during intense sprinting versus prolonged
endurance exercise.
Q29. A liver-specific deficiency of glucose-6-phosphatase is observed. Explain the metabolic
consequences and expected clinical presentation.
Q30. In an experimental model, AMP levels are artificially increased. Describe how this alters
metabolic flux through glycolysis, fatty acid oxidation, and gluconeogenesis.
Q31. A patient has a mutation in glycogen phosphorylase in skeletal muscle. Predict how this
affects exercise tolerance and energy metabolism.
Q32. Describe how you would experimentally distinguish between substrate-level phosphorylation
and oxidative phosphorylation in isolated mitochondria.
Q33. A drug increases proton permeability across the inner mitochondrial membrane. Explain its
effect on metabolic rate and ATP yield.
Q34. During hypoxia, cells shift their metabolism. Explain the regulatory mechanisms that drive
this shift and the role of transcription factors.
Q35. A mutation causes citrate synthase to become insensitive to feedback inhibition. Predict the
consequences for TCA cycle flux and metabolic balance.
Q36. In a perfused liver experiment, high levels of glucagon are introduced. Predict the changes in
glycolysis, gluconeogenesis, and glycogen metabolism.
Q37. A researcher observes that ATP levels remain constant despite inhibition of the electron
transport chain. Provide possible explanations.
Q38. Describe how metabolic intermediates from the TCA cycle are replenished (anaplerosis)
during high biosynthetic demand.
Q1. Describe the structure and function of the pyruvate dehydrogenase complex, including its
cofactors and regulatory mechanisms.
Q2. Explain how phosphofructokinase-1 is regulated by ATP, AMP, and citrate. Why is it
considered the key control point in glycolysis?
Q3. Outline the complete sequence of reactions in the citric acid cycle and indicate where NADH,
FADH₂, and GTP are produced.
Q4. Compare the metabolic fates of pyruvate under aerobic and anaerobic conditions in mammalian
cells.
Q5. Explain the chemiosmotic theory and how it accounts for ATP synthesis in mitochondria.
Q6. Describe how glycogen phosphorylase is regulated by both covalent modification and allosteric
effectors.
Q7. Explain how gluconeogenesis bypasses the irreversible steps of glycolysis. Include the enzymes
involved.
Q8. Describe the role of uncoupling agents in oxidative phosphorylation and their physiological
consequences.
Q9. Explain why the citric acid cycle is described as amphibolic, providing specific examples.
Q10. Compare the regulation of glycolysis and gluconeogenesis, highlighting how futile cycling is
prevented.
Q11. Describe the hormonal regulation of glycogen metabolism in liver cells, focusing on insulin
and glucagon signaling pathways.
Q12. Explain the role of NAD⁺ in glycolysis and why its regeneration is essential for continued
ATP production.
Q13. Describe how the electron transport chain is organized within the inner mitochondrial
membrane and the function of each complex.
Q14. Explain the differences in glycogen metabolism between liver and muscle tissues.
Q15. Describe the energy yield of glycolysis under aerobic conditions and explain how this yield is
achieved.
Q16. Explain how the activity of the pyruvate dehydrogenase complex is regulated by
phosphorylation.
Q17. Describe the role of citrate in linking glycolysis and the citric acid cycle.
Q18. Explain how AMP-activated protein kinase (AMPK) influences metabolic pathways under
low-energy conditions.
Q19. Describe the formation and significance of lactate during anaerobic metabolism.
Q20. Explain how proton motive force is generated and how it is used to drive ATP synthesis.
, Q21. A patient presents with severe lactic acidosis during mild exercise. Muscle biopsy shows
normal oxygen supply but impaired oxidative metabolism. Propose possible defects and explain the
biochemical basis.
Q22. In an experiment, cells are treated with oligomycin. Predict the effects on ATP production,
oxygen consumption, and NADH levels. Explain your reasoning.
Q23. A researcher knocks out phosphofructokinase-1 in cultured hepatocytes. Predict the metabolic
consequences on glycolysis, gluconeogenesis, and overall cellular energy balance.
Q24. During prolonged fasting, blood glucose remains stable despite depleted glycogen stores.
Explain the metabolic adaptations that allow this to occur.
Q25. A mutation reduces the activity of pyruvate dehydrogenase kinase (PDK). Predict how this
affects carbohydrate metabolism under fed and fasting conditions.
Q26. Cells are supplied with radiolabeled glucose ([¹⁴C]-glucose). Describe how you would trace
carbon atoms through glycolysis and the TCA cycle.
Q27. A toxin specifically inhibits Complex III of the electron transport chain. Predict the
downstream effects on ATP synthesis, NADH oxidation, and reactive oxygen species formation.
Q28. Compare the metabolic response of muscle tissue during intense sprinting versus prolonged
endurance exercise.
Q29. A liver-specific deficiency of glucose-6-phosphatase is observed. Explain the metabolic
consequences and expected clinical presentation.
Q30. In an experimental model, AMP levels are artificially increased. Describe how this alters
metabolic flux through glycolysis, fatty acid oxidation, and gluconeogenesis.
Q31. A patient has a mutation in glycogen phosphorylase in skeletal muscle. Predict how this
affects exercise tolerance and energy metabolism.
Q32. Describe how you would experimentally distinguish between substrate-level phosphorylation
and oxidative phosphorylation in isolated mitochondria.
Q33. A drug increases proton permeability across the inner mitochondrial membrane. Explain its
effect on metabolic rate and ATP yield.
Q34. During hypoxia, cells shift their metabolism. Explain the regulatory mechanisms that drive
this shift and the role of transcription factors.
Q35. A mutation causes citrate synthase to become insensitive to feedback inhibition. Predict the
consequences for TCA cycle flux and metabolic balance.
Q36. In a perfused liver experiment, high levels of glucagon are introduced. Predict the changes in
glycolysis, gluconeogenesis, and glycogen metabolism.
Q37. A researcher observes that ATP levels remain constant despite inhibition of the electron
transport chain. Provide possible explanations.
Q38. Describe how metabolic intermediates from the TCA cycle are replenished (anaplerosis)
during high biosynthetic demand.
