Objectives:

1. Describe the glycogen molecule.
2. What are the functions of glycogen in liver and skeletal muscle? Why must glucose-6-phosphate produced from glycogen in muscle enter glycolysis? Why does glucose produced from glycogen in liver usually enter the blood stream instead of glycolysis?
3. What effect does glucagon have upon glycogenolysis and gluconeogenesis in the liver?
4. Use the activation or inhibition of glycogen synthesis or glycogenolysis to explain the concept of a futile cycle and how a futile cycle is usually prevented.
5. Describe the pathway for glycogen synthesis from glucose in liver and muscle: Name, Function, Substrates, Products, Control Enzyme, Regulation, Compartment.
6. Describe the pathway for glycogen degradation to glucose or glucose-6-phosphate in liver and muscle: Name, Function, Substrates, Products, Control Enzyme, Regulation, Compartment.
7. Briefly, what is Von Gierke's disease? What is McArdle's disease?
8. What is the effect of a high carbohydrate meal, fasting, or stress upon the blood concentrations of insulin, glucagon, and epinephrine?
9. What is the effect of a high carbohydrate meal upon blood glucose and the glucose in liver cells?
10. What is the effect of changes in the insulin/glucagon ratio, blood glucose or epinephrine upon glycogen synthesis and glycogen degradation in the liver?
11. What is the effect of changes in the insulin, blood glucose or epinephrine upon glycogen synthesis or glycogen degradation in muscle? Error in fourth edition, Table 28.2: Exercise does not decrease either AMP or glycogen degradation in muscle cells.
12. In order of their activation, be able to name and give the reason for the activation of all the intermediates in the cAMP cascade in liver. Start with a decrease in the insulin/glucagon ratio or an increase in epinephrine and end with the change in activity of glycogen synthase, phosphorylase kinase and phosphorylase a? See Chapter 9>Othe Help>cAMP cascade.
13. What role does protein phosphatase have in the cAMP cascade? How is protein phosphatase activated or inhibited?
14. What is the effect of insulin upon the cAMP cascade?
15. Following the ingestion of carbohydrate, the glucose concentration in the cytosol of liver cells increases. What effect does this have upon phosphorylase a?

16. When the insulin to glucagon ratio is low as it usually is in both Type I and Type II diabetics, how is the storage of glucose in muscle and liver affected after a high carbohydrate meal? Why? What happens to blood glucose?
17. In order of their activation, be able to name and give the reason for the activation of the intermediates in the inositol trisphosphate and diacylglycerol cascade in liver. Start with epinephrine binding to an a1-receptor and finish with the change in activity of glycogen synthase and glycogen phosphorylase a? Limit the answer to the terms a1-receptor, Gq-protein, GTP, GDP, Gαq-subunit, phospholipase C, phosphatidylinositol bisphosphate, IP3, diacylglycerol, protein kinase C, calcium release from endoplasmic reticulum, Ca2+, calmodulin, Ca2+-calmodulin, phosphorylase kinase, phosphorylase b, phosphorylase a, glycogen synthase a, and glycogen synthase b.
18. What are the three major activators of phosphorylase in muscle?
19. Concerning Getta Carbo: Compare the relative concentrations of insulin, glucagon, and epinephrine before labor and after delivery. Why was her blood glucose low? Why is the oxidation of fatty acids by the liver important during the first five or six hours?
20. Concerning Jim Bodie: Jim injected insulin just before exercise. What were the affects upon the pathways and transport mechanisms of the liver and muscle that led to his hypoglycemic coma?

Keywords:

adenylate cyclase, AMP, α-agonist receptors, amylo-4:6-transferase, ATP, blood glucose, branched polymer, branching enzyme, Ca++, calmodulin, catalytic subunit, cAMP, cAMP-dependent protein kinase, debrancher enzyme, diacylglycerol, endoplasmic reticulum, epinephrine, futile cycle, G protein, glucagon, glucagon receptor, glucokinase, glucose, glucose-1-phosphate, glucose-6-phosphate, glucose-6-phosphatase, glucose transport, a-1,4-glucosidic bond, a 1,6-glucosidase, a-1,6-glucosidic bond, glycogen, glycogen phosphorylase a, glycogen phosphorylase b, glycogen storage diseases, glycogen synthase, glycogenolysis, glycogenin, hepatic protein phosphatase-1, hexokinase, hypoglycemia, inositol trisphosphate, insulin, McArdle's Disease, nonreducing end, phosphatidyl inositol bisphosphate, phosphoglucomutase, phospholipase C, phosphorylase a, phosphorylase b, phosphorylase kinase, protein kinase A, protein kinase C, protein phosphatase, pyrophosphate, a-receptors, beta receptor, reducing end, regulatory subunit, serum glucose, signal transduction system, transport, UDP-glucose, UDP-glucose pyrophosphorylase, Von Gierke's Disease.

Assignments:

Understand the meaning of the key words in the context of Chapter 28.

Examine Questions (Q:)and Answers(A:) in Chapter 28.

Work Review Questions 1- 5 at the end of the Chapter 28.

Work the Practice Questions for Chapter 28 Objectives

Other Help:

No Other Help for Chapter 28.