1. Describe the pathway for the storage of glucose in the liver in the fed state? How is this pathway regulated? Are there any possible futile cycles prevented?
2. What pathway provides for the production of pyruvate to be used for fatty acid synthesis in the fed state? How is this pathway regulated?
3. During the conversion of glucose to fatty acid, how is pyruvate, produced from glycolysis, converted to citrate in the cytosol? In which compartment does each reaction take place?
4. What are the sources of the reducing agent used for the reductive biosynthesis of fatty acids?
5. Which enzyme controls the pathway for the synthesis of fatty acids from acetyl CoA in the cytosol? How is this pathway regulated? (ignore citrate)
6. What keeps newly formed free fatty acid from entering the mitochondria in the fed state?
7. What happens to the product of the fatty acid synthase complex before it is found in the blood?
8. Compare the Km for lipoprotein lipase in heart and adipose tissue. What implications dose this have for the usage of blood triacylglycerol in the fed and fasting state?
9. How does insulin affect the delivery and storage of free fatty acid into adipose cells in the fed state?
10. What are the pathways for the synthesis of triacylglycerol in adipose from glucose and free fatty acids? How is the production of glycerol phosphate regulated?
11. What happens to the glycerol released in the lipoprotein lipase reaction in the fed state?
12. What pathways provide blood glucose during fasting? Why are these pathways active?
13. Glycogen is not made in the liver during fasting. Why not?
14. Glycolysis does not function when gluconeogenesis is functioning. What factors turn on gluconeogenesis and turn off glycolysis?
15. What is the control enzyme for the release of free fatty acids during a fast and how is this enzyme regulated?
16. Why are ketone bodies produced during a fast?
17. Besides providing ATP, how does increased β-oxidation enable gluconeogenesis?

18. Explain how increased fatty acid oxidation and decreased insulin spares blood glucose by muscle in the fasting and resting state.
19. What is the effect of exercise upon the use of blood glucose by muscle in the fasting state? What is the mechanism?
20. Concerning Di Beatty, who has type I diabetes and has developed ketoacidosis: On a molecular level, explain why she has opalescent serum. Why does she have high blood glucose? Why does she have ketonemia?
21. Concerning Ann Sulin who has type II diabetes: On a molecular level, explain why she has high serum triacylglycerol. Why does she have high blood glucose? Would you expect ketoacidosis?


acetyl CoA, acetyl CoA carboxylase, AMP-dependent protein kinase, cAMP, carnitine:palmitoyltransferase I, chylomicron, citrate, , CPTI, dephosphorylation, dihydroxyacetone phosphate, epinephrine, fatty acid, fructose-1,6-bisphosphatase, fructose-2,6-bisphosphatase, fructose-2,6-bisphosphate, glucagon, glucose, glucose-6-phosphatase, glucose-6-phosphate dehydrogenase, glucose transporter, gluconeogenesis, glucokinase, GLUT4 transporters, glycogen, glycogen phosphorylase, glycogen synthase, glycogenolysis, hormone-sensitive lipase, hypertriglyceridemia, , insulin, insulin/glucagon, induction, , Km, lipoprotein lipase, malic enzyme, malonyl CoA, NADPH, NIDDM, palmitoyl CoA, pentose phosphate pathway, phosphatase, phosphoenolpyruvate carboxykinase, 6-phosphogluconate dehydrogenase, phosphofructokinase-1, phosphofructokinase-2, phosphorylase kinase, protein kinase A, pyruvate carboxylase, pyruvate dehydrogenase, pyruvate kinase, repression, substrate, triacylglycerol, type 1, type 2, VLDL.


Understand the meaning of the key words in the context of Chapter 36.

Examine Questions (Q:) and Answers (A:) in Chapter 36.

Work Review Questions 1, 2, 3, and 4 at the end of the Chapter 36 but not Questions 5.

Work the Practice Questions for Chapter 36 Objectives

Other Help:

No Other Help for Chapter 36