Objectives:

1. Why is insulin called the anabolic hormone?
2. Which counterregulatory hormones are mentioned in this chapter and why are they called counterregulatory hormones?
3. Which hormones are exerting a major effect upon fuel metabolism following a meal? After an overnight fast? During stress?
4. What is the effect of insulin upon the following metabolic pathways?
The storage of glucose in glycogen.
The mobilization of glucose from glycogen.
The synthesis of fatty acids from glucose in the liver.
The synthesis of triacylglycerols in liver and adipose tissue.
The mobilization of free fatty acids from adipose tissue.
The synthesis of proteins in most tissues.
The mobilization of amino acids from proteins for gluconeogenesis.
5. Would you expect this insulin effect after a high carbohydrate meal, after an overnight fast, during times of stress?
6. What is the effect of glucagon upon the following metabolic pathways?
The storage of glucose in glycogen.
The mobilization of glucose from glycogen.
The synthesis of fatty acids from glucose in the liver.
The synthesis of triacylglycerols in liver and adipose tissue.
The mobilization of free fatty acids from adipose tissue.
The mobilization of amino acids from muscle proteins for gluconeogenesis.
7. Would you expect this glucagon effect after a high carbohydrate meal, after an overnight fast, during times of stress?

8. What is the effect of stress hormones as a group upon the following metabolic pathways?
The storage of glucose in glycogen.
The mobilization of glucose from glycogen.
The synthesis of fatty acids from glucose in the liver.
The synthesis of triacylglycerols in liver and adipose tissue.
The mobilization of free fatty acids from adipose tissue.
The synthesis of proteins in most tissues.
The mobilization of amino acids from proteins for gluconeogenesis.
9. Know the important events in the synthesis of insulin from synthesis of the preprohormone to precipitation in storage granules. Include the terms: pancreas, beta cells, preprohormone, prohormone (proinsulin), intrachain disulfide bonds, proteases, interchain disulfide bond, C-peptide, A-chain, B-chain, insulin storage vesicle, and zinc precipitate
10. Describe the mechanism of release of insulin from beta cells in response to increased blood glucose. Include the terms: blood glucose, glucose transporter, glucokinase, glycolysis, ATP concentration, ATP sensitive K+ channel, membrane depolarization, calcium concentration, exocytotic vesicle, plasma membrane, fusion, insulin release
11. Explain how a mutation that caused an elevated Km for glucokinase could explain some types of MODY. Include rate of glycolysis, ATP concentration and the rate of insulin released at any blood glucose concentration between 80 and 300 mg/dL.
12. What is the effect of the following upon insulin release and what is the hormone or metabolite directly affecting the B-cells?:
(1) A high carbohydrate meal.
(2) A high protein meal.
(3) Starvation, trauma, or vigorous exercise.
13. What is the effect of the following upon glucagon release and what is the hormone or metabolite directly affecting the a-cells?
(1) A high carbohydrate meal.
(2) A high protein meal.
(3) Starvation, trauma, or vigorous exercise.
14. To the extent that it is known, explain the series of events following an increase in insulin that results in more glucose transporters in muscle and adipose tissue cell membranes. Refer to Figures 11.12, 11.13, 11.14, and 27.13 in your text and use the following terms: Insulin, insulin receptor, insulin-binding site, change in conformation, tyrosine kinase domains, auto-phosphorylation, IRS proteins, phosphorylation of IRS proteins, SH2 homology, activation of phosphatidylinositol 3' kinase, protein kinase B, and glut-4 (glucose-4-transporter).

15. To the extent that it is known, explain the effects of insulin upon cAMP cascade. How would insulin affect the concentration of cAMP? Name the enzyme. How would insulin affect the proteins phosphorylated as a result of the cAMP cascade? Name the type of enzymes.
16. Be able to list all the intermediates in the signal transduction of glucagon from the binding of the ligand to the activation of a protein by phosphorylation. Use the terms: glucagon, receptor, conformation, Gs protein complex, GDP, GTP, dissociation a subunit, bg subunit, adenylcyclase, cAMP, protein kinase A, regulatory subunit, catalytic subunit, phosphorylation, activation or inhibition of regulatory enzymes. Refer to Chapter 9 Other Help>cAMP cascade link.
17. One characteristic of a second messenger system is signal amplification! What does this statement mean?
18. When the glucagon concentration outside a liver cell is decreased suddenly, there is rapid change in the activation of many of the pathways influenced by glucagon. What is responsible for the rapid termination of signal?
19. What is the major second messenger systems associated with the a1-adrenergic receptor (Table 11.1: Gαq, activates phospholipase C)? How about the B1-, B2, and B3-adrenergic receptors?
20. Concerning Ann Sulin: She has type 2 diabetes and her blood insulin levels are within the normal range. Are her Β-cells secreting enough insulin? Are her muscle and adipose cells responding normally to insulin?
21. Concerning Ann Sulin who has type 2 diabetes: explain one way in which high blood glucose changes the conformation of many types of proteins and may cause vascular disease.
22. Concerning Ann Sulin who has type 2 diabetes: Explain how taking a sulfonylurea drug will increase insulin output by the Β-cells.
23. Concerning Ann Sulin who has type 2 diabetes: given a concentration of blood glucose, will she have a normal amount of insulin release? Will her blood insulin to glucose ratio be normal?
24. Concerning Ann Sulin who has type 2 diabetes: What does insulin resistance mean? Is glucose uptake by liver, adipose and muscle cells normal? Is the release of fatty acids from adipose tissue normal?
25. Concerning Ann Sulin who has type 2 diabetes: why does she have a higher than normal concentration of blood glucagon?
26. Concerning Bea Selmass: Explain why a patient with an insulinoma would have fasting hypoglycemia.
27. Concerning Bea Selmass, who has an insulinoma: What effect would the hyperinsulinemia alone to have upon the release of glucagon from a cells? What effect did the combined effect of hyperinsulinemia and hypoglycemia have upon the release of glucagon from the alpha-cells?

Keywords:

adenylylcyclase, alpha1-adrenergic receptor, b1-, b2, and b3-adrenergic receptors, adrenocorticotropic hormone (ACTH), amino acids, anabolic hormone, amplification, autonomous, autophosphorylation, C-peptide, Ca++ , cAMP, catalytic subunits, alpha cells, beta cells, a chain, b chain, conformation, cortisol, counterregulatory hormones, 3',5'-cyclic adenosine monophosphate (cAMP), epinephrine, G protein, Gs protein complex, glucagon, glucagon, receptor, glucose transporter-4 (glut-4), insulin receptor, IRS-1, insulin receptor substrate 1, insulin, insulin resistance, insulin storage vesicle, interchain disulfide bond, intrachain disulfide bond, IRS-1, Km, K+- channel, membrane depolarization, MODY, nonenzymatic glycosylation, nonketotic hyperosmolar coma, norepinephrine, phosphatidylinositol 3’ kinase, phosphodiesterase, phosphorylation, preprohormone, proinsulin, proteases, protein kinase A, protein kinase B, protein phosphatases, regulatory enzymes, regulatory subunit, SH2 domain, stress hormones, a-subunit, bg subunit, sulfonylurea, transduction, type 1 diabetes, type 2 diabetes, tyrosine kinase, tyrosine kinase domain, voltage-gated Ca2+ channel, zinc.

Assignments:

Understand the meaning of the key words in the context of Chapter 26.

Examine the Question (Q:) and Answer (A:) in Chapter 26.

Work Review Questions 2-5, but not 1, at the end of the Chapter 26.

Work the Practice Questions for Chapter 26 Objectives

Other Help:

Membrane potential and the ATP-sensitive potassium channels