Questions:

1. Insulin is called the anabolic hormone because it promotes all of the following EXCEPT
  1. The net synthesis of protein from amino acids
  2. The storage of glucose as glycogen
  3. The conversion of amino acids to glucose
  4. The conversion of glucose to fatty acids and triacylglycerol
  5. The storage of dietary and de novo fats
2. All of the following are called counter regulatory hormones because they counter the effects of insulin EXCEPT
  1. Glucagon
  2. Epinephrine
  3. Norepinephrine
  4. Cortisol
  5. Thyroid hormone
3. All of the following statements about hormones and when they exert their major effect are correct EXCEPT
  1. Glucagon, catecholamines, and cortisol exert a major effect during stress
  2. Glucagon, catecholamines, insulin, and cortisol exert a major effect during starvation (prolonged fasting)
  3. Insulin exerts a major effect in the fed state
  4. Glucagon exerts a major effect in the fasting state
  5. Catecholamines exerts a major effect during exercise
4. The hormone insulin will either greatly increase or is necessary for all of the following EXCEPT
  1. The incorporation of glucose into glycogen
  2. The synthesis of fatty acids from glucose
  3. The synthesis of triacylglycerols in liver and adipose tissue
  4. The mobilization of amino acids from proteins for gluconeogenesis
  5. The net synthesis of proteins
5. You would expect that the release of insulin would be the greatest
  1. When digging ditches for 4 hours
  2. When suffering from a bacterial or viral infection
  3. When running from a gorilla
  4. When eating a high carbohydrate
  5. When eating a high protein meal
6. All of the following actions of glucagon are true EXCEPT
  1. Glucagon will inhibit glycogen synthesis and activate glycogenolysis
  2. Glucagon will inhibit glycolysis in the liver and activate gluconeogenesis in the liver
  3. Glucagon will activate fatty acid mobilization (release) in adipose tissue
  4. Glucagon will activate triacylglycerol synthesis in liver and adipose
  5. Glucagon will remove amino acids for gluconeogenesis and thus increase the mobilization of amino acids from proteins
7. You would expect the release of glucagon to be least
  1. When eating a high protein meal
  2. When eating a high carbohydrate meal
  3. When pushing a car for 20 miles
  4. During hypoglycemia
  5. When fasting
8. As a group, you would expect the stress hormones to
  1. Increase the synthesis of fatty acids in the liver
  2. Increase triacylglycerol synthesis in liver and adipose tissue
  3. Increase the utilization of muscle protein for glucose synthesis
  4. Increase glycogen synthesis
  5. Increase net protein synthesis (Protein synthesis – Protein degradation)
9. All the following events regarding the synthesis of insulin are true EXCEPT
  1. Like all protein hormones, the preprohormone is synthesized on the rough endoplasmic reticulum
  2. Cleavage of the signal peptide in the endoplasmic reticulum converts the preprohormone to the prohormone
  3. Formation of disulfide bonds and cleavage of the C-peptide and a few amino acids by proteases converts the prohormone into insulin
  4. Insulin consists of an alpha-chain and a beta-chain linked by two interchain disulfide bonds
  5. Insulin precipitates with protamine in the storage vesicles of beta-cells of the pancreas
10. All of the following help to explain the mechanism for releasing insulin from Β-cells in response to the concentration of blood glucose EXCEPT
  1. The important regulator of glycolysis in beta cells is the concentration of glucose reacting with glucokinase
  2. ATP is made in proportion to the rate of glycolysis
  3. The rate of K+ leaving the cell through a potassium channel is a major determinant of the polarization of the cell membrane
  4. ATP inhibits the K+-channel, the more ATP, the less K+ leaving the cell, and the less polarized (more depolarized) the cell membrane
  5. Depolarization causes Ca++ to exit the cell and insulin leaves the cell through the insulin transporter
11. One form of diabetes known as MODY (maturity onset diabetes of the young) results from an elevated Km of glucokinase.  This would result in all of the following EXCEPT
  1. For any concentration of blood glucose, there would be less glucose converted to glucose-6-P
  2. Glycolysis and ATP production would be slower than normal for any given blood glucose
  3. Less inhibition of the K+ channel and less polarization of the membrane would occur
  4. There would be less Ca++ entering the cell through the voltage-gated calcium channel
  5. There would be less fusion of insulin vesicles with the cell membrane and less insulin released from the cell
12. All of the following are true EXCEPT.  The release of insulin from beta-cells
  1. Is decreased during fasting because of high concentrations of glucagon binding to receptors
  2. Is decreased during illness because of epinephrine and norepinephrine binding to receptors
  3. Is decreased following the initiation of exercise because of epinephrine and norepinephrine binding to receptors
  4. Is increased following a high protein diet in response to increased concentrations of amino acids
  5. Is increased following a high carbohydrate meal in response to increased concentrations of glucose
13. Concerning the release of glucagon from alpha-cells, all of the following are true EXCEPT
  1. A high carbohydrate meal will suppress the release of glucagon
  2. Insulin will bind to alpha-cells and increase the release of glucagon
  3. A high protein meal will increase the release of glucagon
  4. Hypoglycemia will increase the release of glucagon
  5. Trauma and other types of stress will increase the release of glucagon
14. When insulin increases, it binds to insulin receptors on muscle cells and all of the following result EXCEPT
  1. The receptor changes conformation and autophosphorylation of the insulin receptor occurs
  2. Before autophosphorylation, the insulin receptor phosphorylates seryl residues on the IRS protein
  3. Phosphatidylinositol 3' kinase binds to the phosphorylated IRS protein because it contains a SH2 domain
  4. A chain of reactions occur that eventually activate protein kinase B, a serine kinase
  5. Protein kinase B initiates a sequence of events that results in Glut-4 moving from storage vesicles to the membrane so that there is an increase in glucose transport
15. When a fasting person eats a high carbohydrate or mixed meal, the concentration of glucagon may decreases or remains the same, but the second messenger system of glucagon is wiped out.  All of the following would explain or help to explain how this happens EXCEPT
  1. Insulin reverses glucagon-stimulated phosphorylation
  2. Insulin inactivates cAMP phosphodiesterase, an enzyme that converts cAMP into AMP
  3. Insulin activates protein phosphatases that remove phosphate from proteins that were phosphorylated by protein kinase A
  4. Proteins like liver phosphofructokinase-2/fructose-2,6-bisphosphatase are dephosphorylated by protein phosphatases
  5. Proteins like pyruvate kinase are dephosphorylated by protein phosphatase
16. When glucagon binds to its receptor on the liver membrane, all of the following occur EXCEPT
  1. A change in conformation of the glucagon receptor results in binding to Gi protein and release of bound GTP
  2. The binding of GTP to Gs protein causes dissociation of the alpha subunit from beta-gamma subunit
  3. Until GTP is hydrolyzed, the G-alpha subunit will activate adenylate cyclase and cAMP will be produced
  4. cAMP will bind to and remove the regulatory subunit from protein kinase A
  5. Active protein kinase A will phosphorylate other proteins and the activity of regulatory enzymes will be changed
17. When one glucagon molecule binds to a receptor on a liver cell, thousands of protein kinase A enzymes are activated.  This is an example of
  1. Integration of metabolic response
  2. Antagonism of signal
  3. Augmentation of signal
  4. Amplification of signal
  5. Rapid signal termination
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. All of the following are partially responsible for the rapid termination of signal EXCEPT
  1. Without glucagon bound, receptors can no longer activate Gs protein
  2. The G-beta-gama subunit hydrolyzes GTP and is no longer active
  3. cAMP phosphodiesterase removes cAMP from the cell
  4. Protein phosphatases remove phosphate groups and cause some enzymes to be more active
  5. Protein phosphatases remove phosphate groups and cause some enzymes to be less active
19. When epinephrine is bound to the following receptors, all EXCEPT one will activate the cAMP cascade
  1. Alpha-1 adrenergic receptor
  2. Beta-1 adrenergic receptor
  3. Beta-2 adrenergic receptor
  4. Beta-3 adrenergic receptor
20. Concerning Ann Sulin, who has type 2 diabetes and her blood insulin levels are within the normal range
  1. Her pancreas is responding normally to a meal containing carbohydrate
  2. Her pancreas is putting out the normal amount of insulin for her blood sugar
  3. Her liver cells are responding normally to the insulin bound
  4. Her muscle cells are responding normally to the insulin bound
  5. None of her cells are responding normally to glucose or insulin
21. Which statement is FALSE?  There is some evidence that much of the pathology of diabetes
  1. Due to the nonenzymatic reactions between protein and glucose
  2. Results from glucose forming a covalent and irreversible bond with many proteins
  3. Results because glycosylation of protein often changes its function
  4. Results because glycosylation makes it harder for the cell to get rid of old proteins
  5. Can be prevented if Hemoglobin A1C can be kept above 8%
22. Your patient Ann Sulin has type 2 diabetes.  When she takes a sulfonylurea drug, all of the following will occur EXCEPT
  1. The drug will act on the K+ATP channels on the surface of the pancreatic beta-cells
  2. The binding of the drug to these channels closes K+ATP channels
  3. The ATP level of the beta-cell cytosol will be increased
  4. The voltage gated Ca++-channel will let more Ca++ into the cell
  5. More insulin will be released from the Β-cells
23. Concerning Ann Sulin who has type 2 diabetes:
  1. Following a meal, insulin will increase more slowly than normal for a given amount of sugar intake
  2. Following a meal, insulin will rise as high as it should based upon the sugar intake
  3. In the fasting state, insulin will be as high as it should be considering the high blood sugar concentration
  4. As Ann gets older, the release of sugar from her pancreas will improve
  5. If Ann fasts for two days, her blood insulin to blood glucose ratio will be normal
24. Which of the following statements about insulin resistance is FALSE
  1. Insulin resistance in found in type 2 diabetics
  2. Insulin resistance is defined clinically as the inability of a known quantity insulin to increase glucose uptake and utilization in an individual as much as it does in a normal population
  3. Insulin resistance is a subnormal response of target cells to both endogenous and exogenous insulin
  4. With insulin resistance, the binding of insulin at receptors does not elicit most of the normal intracellular effects
  5. With insulin resistance, glucose uptake and disposal will be less than normal but the release of free fatty acids from adipose and other non-carbohydrate functions will be normal
25. Which of the following statements is FALSE?  Your patient Ann Sulin has type 2 diabetes and a higher than normal blood concentration of glucagon
  1. In the fed state but not the fasting state
  2. Because insulin inhibition of glucagon release is less than normal
  3. Because the normal mechanism of inhibition of glucagon release by blood sugar is impaired
  4. Because less insulin secretion results in more glucagon release
  5. Because insulin resistance results in more glucagon release for any concentration of insulin
26. Your patient Bea Selmass has an insulinoma and suffers from fasting hypoglycemia.  All of the following would help explain why the abnormally high insulin levels would cause fasting hypoglycemia EXCEPT
  1. Insulin is signaling cells to remove and use or store glucose, thus lowering the blood glucose
  2. Insulin is inhibiting the breakdown of liver glycogen so blood glucose cannot be renewed from this source
  3. Insulin is inhibiting gluconeogenesis so blood glucose cannot be renewed from this source
  4. Insulin is inhibiting glycolysis in muscle so even more glucose is used to maintain normal levels of ATP
  5. Insulin is inhibiting the release of free fatty acids from adipose so even more glucose is needed to maintain the ATP of most cell types
27. Your patient Bea Selmass has an insulinoma and suffers from fasting hypoglycemia.  All of the following statements would be true EXCEPT
  1. One effect of hypoglycemia is to increase the release of epinephrine and glucagon
  2. Both glucagon and epinephrine normally increase the release of glucose from liver
  3. The liver normally releases enough glucose to maintain normal blood glucose levels
  4. The high insulin to glucagon ratio of insulinoma prevents sufficient release of glucose from liver
  5. C-peptide would be low in your patients blood
28. The hormone insulin will greatly increase or is necessary for the
  1. net synthesis of proteins
  2. release of glucose from glycogen
  3. mobilization of free fatty acids
  4. entry of fatty acyl CoA into the mitochondria
  5. mobilization of amino acids from proteins for gluconeogenesis
29. The hormone glucagon will greatly increase or is necessary for the
  1. mobilization of amino acids from proteins for gluconeogenesis
  2. storage of free fatty acids in adipose tissue
  3. storage of glucose in glycogen
  4. synthesis of fatty acids from glucose in the liver
  5. synthesis of triacylglycerols in liver and adipose tissue
30. When the glucose concentration is increased, all of the following occur in Β-cells of the pancreas EXCEPT
  1. Increased ATP inhibits the ATP sensitive K+ channels
  2. More K+ leaves the cell
  3. The membrane potential drops from a negative value toward zero
  4. Calcium channels are opened
  5. The calcium concentration inside the cell increases dramatically
31. One form of diabetes known as MODY (maturity onset diabetes of the young) results from an elevated Km of glucokinase. This would result in all of the following EXCEPT
  1. Less glucose converted to glucose-6-P at any given concentration of glucose
  2. Less inhibition of the ATP-sensitive potassium channels
  3. More potassium leaving the cell through the ATP-sensitive potassium channels
  4. Less negative membrane potential
  5. Less activation of calcium channels
32. Following an increase in insulin, a series of events occur that results in more glucose transporters in muscle and adipose tissue cell membranes. All of the following are true, EXCEPT
  1. The insulin binds to the insulin receptor at the insulin binding site but the conformation of the receptor does not change
  2. Tryosine kinase domains are activated and autophosphorylation take place
  3. The IRS binds to the phosphorylated insulin receptor and is phosphorylated on tyrosyl residues
  4. The SH2 domain of Phosphatidylinositol 3' kinase binds to the IRS and is activated
  5. A chain of events follows that includes activation of Protein kinase B and results in Glut-4 moving from storage vesicles to the membrane so that there is an increase in glucose transport
33. This enzyme is found in the a1-adrenergic signal transduction pathway
  1. Phospholipase C
  2. Adenylylcyclase
  3. Phosphodiesterase
  4. Phosphatidylinositol 3’ kinase
  5. Protein kinase B
34. Concerning Ann Sulin, who has type 2 diabetes and her blood insulin levels are within the normal range
  1. Glycolysis in the liver is probably controlled in a normal manner
  2. Glycolysis in muscle is probably controlled in a normal manner
  3. Fatty acid mobilization is probably controlled in a normal manner
  4. Fatty acid utilization by muscle cells is probably controlled in a normal manner
  5. Because of insulin resistance, none of her pathways are controlled in a normal manner
35. Your patient Ann Sulin has type 2 diabetes. When she takes a sulfonylurea drug, the drug has the same effect on the B-cell as
  1. Raising the Km for glucokinase
  2. Raising the intracellular concentration of ATP
  3. Decreasing the intracellular Ca++ concentration
  4. Inhibiting phosphofructokinase-1
  5. Inhibiting pyruvate kinase
36. Your patient has Type 2 diabetes but for how long, you do not know. All of the following are probably true EXCEPT
  1. Her blood insulin may be above normal if she has recently been diagnosed
  2. Her blood insulin may be normal if she has had the disease for a few years
  3. Her blood insulin may be below normal if she has had the disease for a long time
  4. Measuring her blood insulin will be helpful
  5. Measuring her bold sugar and glycosylated hemoglobin will be helpful

Answers:

1. Answer: C. Chapter 26, Objective 1: Why is insulin called the anabolic hormone? Back to question 1.
2. Answer: E. Chapter 26, Objective 2: Which counterregulatory hormones are mentioned in this chapter and why are they called counterregulatory hormones? Back to question 2.
3. Answer: B. Chapter 26, Objective 3: Which hormones are exerting a major effect upon fuel metabolism following a meal? After an overnight fast? During stress? Back to question 3.
4. Answer: D. Chapter 26, Objective 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 Back to question 4.
5. Answer: D. Chapter 26, Objective 5: Would you expect this insulin effect after a high carbohydrate meal, after an overnight fast, during times of stress? Back to question 5.
6. Answer: D. Chapter 26, Objective 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 proteins for gluconeogenesis. Back to question 6.
7. Answer: B. Chapter 26, Objective 7: Would you expect this glucagon effect after a high carbohydrate meal, after an overnight fast, during times of stress? Back to question 7.
8. Answer: C. Chapter 26, Objective 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. Back to question 8.
9. Answer: E. Chapter 26, Objective 9: Know the important events in the synthesis of insulin from synthesis of the preprohormone to precipitation in storage granules. Back to question 9.
10. Answer: E. Chapter 26, Objective 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 Back to question 10.
11. Answer: C. Chapter 26, Objective 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. Back to question 11.
12. Answer: A. Chapter 26, Objective 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. Back to question 12.
13. Answer: B. Chapter 26, Objective 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. Back to question 13.
14. Answer: B. Chapter 26, Objective 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 11.13 and 11.14 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, glucose transporters (glut-4). Back to question 14.
15. Answer: B. Chapter 26, Objective 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 types of enzymes. Back to question 15.
16. Answer: A. Chapter 26, Objective 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. Back to question 16.
17. Answer: D. Chapter 26, Objective 17: One characteristic of a second messenger system is signal amplification! What does this statement mean? Back to question 17.
18. Answer: B. Chapter 26, Objective 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? Back to question 18.
19. Answer: A. Chapter 26, Objective 19: What is the major second messenger systems associated with the a1-adrenergic receptor? How about the B1-, B2, and B3-adrenergic receptors? Back to question 19.
20. Answer: E. Chapter 26, Objectives 20: Concerning Ann Sulin: She has type 2 and her blood insulin levels are within the normal range. Are her B-cells secreting enough insulin? Are her muscle and adipose cells responding normally to insulin? Back to question 20.
21. Answer: E. Chapter 26, Objectives 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. Back to question 21.
22. Answer: C. Chapter 26, Objective 22: Concerning Ann Sulin who has type 2 diabetes: Explain how taking a sulfonylurea drug will increase insulin output by the beta-cells. Back to question 22.
23. Answer: A. Chapter 26, Objective 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? Back to question 23.
24. Answer: E. Chapter 26, Objective 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? Back to question 24.
25. Answer: A. Chapter 26, Objective 25: Concerning Ann Sulin who has type 2 diabetes: why does she have a higher than normal concentration of blood glucagon? Back to question 25.
26. Answer: D. Chapter 26, Objective 26: Concerning Bea Selmass: Explain why a patient with an insulinoma would have fasting hypoglycemia. Back to question 26.
27. Answer: E. Chapter 26, Objective 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 a cells? Back to question 27.
28. Answer: A. Chapter 26, Objective 4:What is the effect of insulin upon the following metabolic pathways? 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.The storage of glucose in glycogen. Back to question 28.
29. Answer: A. Chapter 26, Objective 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 proteins for gluconeogenesis. Back to question 29.
30. Answer: B. Chapter 26, Objective 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 Back to question 30.
31. Answer: D. Chapter 26, Objective 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. Back to question 31.
32. Answer: A. Chapter 26, Objective 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 and 11.13 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). Back to question 32.
33. Answer: A. Chapter 26, Objective 19: What is the major second messenger systems associated with the a1-adrenergic receptor? How about the B1-, B2, and B3-adrenergic receptors? Back to question 33.
34. Answer: E. Chapter 26, Objective 20: Concerning Ann Sulin: She has type 2 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? Back to question 34.
35. Answer: B. Chapter 26, Objective 22: Concerning Ann Sulin who has type 2 diabetes: Explain how taking a sulfonylurea drug will increase insulin output by the Β-cells. Back to question 35.
36. Answer: D. Chapter 26, Objective 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? Back to question 36.