Chapter 24

1. Which cell type in the pancreatic islets is responsible for secreting insulin?

a) A cells
b) B cells
c) D cells
d) F cells
e) None of the above

2. What is the primary function of insulin in the regulation of metabolism?

a) Promotion of gluconeogenesis
b) Inhibition of glycogen synthesis
c) Stimulation of lipolysis
d) Facilitation of glucose uptake into cells
e) Suppression of protein synthesis

3. Which pancreatic cell type secretes somatostatin?

a) A cells
b) B cells
c) D cells
d) F cells
e) None of the above

4. What is the approximate volume percentage of β-islets in the human

pancreas?
a) 20%
b) 40%
c) 60%
d) 80%
e) 90%
5. Where is insulin synthesized within the pancreatic cells?
a) Rough endoplasmic reticulum
b) Golgi apparatus
c) Mitochondria
d) Nucleus
e) Cytoplasm

6. What cellular process is responsible for the expulsion of insulin-containing

granules from pancreatic cells?
a) Endocytosis
b) Phagocytosis
c) Exocytosis
d) Pinocytosis
e) Transcytosis

7. What is the approximate half-life of insulin in the circulation of humans?

a) 1 minute
b) 5 minutes
c) 15 minutes
d) 30 minutes
e) 45 minutes

8. How is insulin primarily destroyed after binding to insulin receptors?

a) Phagocytosis
b) Exocytosis
c) Endocytosis and subsequent degradation by proteases
d) Transcytosis
e) Apoptosis

9. Which of the following is NOT a physiological effect of insulin?

a) Increased fatty acid synthesis in adipose tissue
b) Inhibition of hormone-sensitive lipase
c) Decreased protein synthesis in ribosomes
 d) Increased glycogen synthesis in muscle
e) Stimulation of amino acid uptake in muscle

10.What effect does insulin have on glucose entry into adipose tissue?
a) Decreases glucose entry
b) Has no effect on glucose entry
c) Increases glucose entry
d) Converts glucose into fatty acids before entry
e) Enhances glucose oxidation

11.What is the primary action of insulin on muscle tissue?

a) Inhibits glucose entry
b) Promotes protein catabolism
c) Stimulates amino acid uptake
d) Decreases ketone uptake
e) Increases glycogenolysis

12.How does insulin affect glucose transport into muscle and adipose tissues?
a) Decreases the number of glucose transporters (GLUTs) in cell
membranes
b) Increases the activity of glucokinase in the cell membranes
c) Enhances glucose entry by increasing the number of GLUTs in cell
membranes
d) Inhibits secondary active transport of glucose with Na+
e) Induces phosphorylation of glucose outside the cell

13.Which of the following statements about GLUTs is true?

a) They decrease glucose entry into cells.
b) They are not involved in facilitated diffusion of glucose.
c) They are exclusively found in liver cells.
d) They are activated by insulin in liver cells.
e) They have their amino and carboxyl terminals outside the cell.
14.What is the primary mechanism by which insulin facilitates glucose entry
into liver cells?
a) Increasing the activity of hexokinase
b) Enhancing the activity of Na+/glucose cotransporters
c) Inducing the expression of GLUT-4 transporters
d) Stimulating phosphorylation of glucose by glucokinase
e) Inhibiting the breakdown of glycogen

15.In which tissues does glucose enter cells by secondary active transport with
Na+?
a) Liver and adipose tissue
b) Intestine and kidneys
c) Muscle and brain
d) Pancreas and spleen
e) Heart and lungs

16.What effect does insulin have on glucose output from the liver?
a) Increases gluconeogenesis
b) Decreases glycogen synthesis
c) Stimulates ketogenesis
d) Enhances glucose output
e) Decreases gluconeogenesis

17.What is the composition of the insulin receptor?

a) Tetramer made up of two β and two α glycoprotein subunits
b) Tetramer made up of two α and two β glycoprotein subunits
c) Dimer made up of two α and two β glycoprotein subunits
d) Dimer made up of two β and two α glycoprotein subunits
e) Monomer made up of one α and one β glycoprotein subunit

18.Which subunits of the insulin receptor bind insulin?

a) α subunits
b) β subunits
 c) γ subunits
d) δ subunits
e) ε subunits

19.How can insulin deficiency be induced in animals?

a) Administration of insulin-secreting drugs
b) Pancreatectomy
c) Administration of drugs that enhance insulin secretion
d) Administration of anti-insulin antibodies
e) Administration of toxins that selectively destroy α cells

20.What is the consequence of hyperglycemia in terms of blood osmolality?

a) Decreases blood osmolality
b) Causes no change in blood osmolality
c) Increases blood osmolality
d) Blood osmolality remains unaffected
e) Depends on the severity of hyperglycemia

21.How is HbA1c used clinically in diabetes management?

a) Measures acute changes in blood glucose levels
b) Provides a snapshot of current blood glucose levels
c) Reflects blood glucose levels over the past 24 hours
d) Represents integrated index of diabetic control over a 4- to 6-week
period
e) Measures fasting blood glucose levels

22.What effect does hyperglycemia have on protein metabolism in diabetes?

a) Decreased amino acid catabolism
b) Decreased gluconeogenesis
c) Increased protein synthesis in muscle
d) Increased amino acid catabolism to CO2 and H2O
e) Decreased blood amino acid levels
23.Which hormone inhibits hormone-sensitive lipase in adipose tissue?
a) Glucagon
b) Somatostatin
c) Insulin
d) Cortisol
e) Epinephrine

24.What is the principal abnormality of fat metabolism in diabetes?

a) Decreased lipid catabolism
b) Decreased formation of ketone bodies
c) Increased synthesis of fatty acids and triglycerides
d) Accelerated lipid catabolism and increased formation of ketone bodies
e) Increased synthesis of fatty acids but decreased synthesis of
triglycerides

25.Why does the plasma level of free fatty acids (FFA) increase in diabetes?
a) Increased insulin secretion
b) Increased activity of hormone-sensitive lipase
c) Decreased plasma glucose level
d) Decreased activity of lipoprotein lipase
e) Decreased triglyceride synthesis

26.What contributes to the elevated plasma cholesterol level in diabetes?

a) Decreased hepatic production of VLDL
b) Increased removal of VLDL and LDL from circulation
c) Decreased plasma concentration of VLDL
d) Increased plasma concentration of chylomicrons
e) Increased hepatic production of VLDL

27.How does glucose affect insulin secretion from pancreatic B cells?

a) By directly inhibiting insulin production
b) By increasing the expression of GLUT-4 transporters
c) By depolarizing the B cell membrane and increasing Ca2+ influx
 d) By reducing ATP production within the B cells
e) By promoting the release of inhibitory neurotransmitters

28.What is the biphasic response of insulin secretion to glucose?

a) A gradual increase followed by a rapid decrease
b) A rapid but short-lived increase followed by a prolonged increase
c) A steady increase that plateaus after a certain point
d) An initial decrease followed by a gradual increase
e) A single spike in secretion followed by a rapid decline

29.Which transporter is responsible for glucose entry into pancreatic B cells?

a) GLUT-1
b) GLUT-2
c) GLUT-3
d) GLUT-4
e) SGLT-1

30.What is the role of ATP in insulin secretion?

a) It inhibits K+ efflux from the B cell, leading to membrane
depolarization
b) It promotes the release of inhibitory neurotransmitters
c) It enhances the breakdown of secretory granules
d) It stimulates the expression of insulin receptors on target cells
e) It activates ATP-sensitive K+ channels, leading to hyperpolarization

31.How does the citric acid cycle contribute to insulin secretion?

a) By inhibiting mitochondrial respiration
b) By promoting the release of stored insulin from secretory granules
c) By increasing intracellular glutamate levels, which aid in the
mobilization of insulin-containing granules
d) By reducing Ca2+ influx into the B cell
e) By decreasing ATP production, leading to decreased insulin secretion
32.Which cells produce glucagon?
a) B cells of the pancreatic islets
b) D cells of the pancreatic islets
c) A cells of the pancreatic islets
d) F cells of the pancreatic islets
e) G cells of the gastric mucosa

33.What is the primary action of glucagon in the liver?

a) Inhibition of glycogenolysis
b) Promotion of glycogen synthesis
c) Stimulation of glycolysis
d) Activation of glycogenolysis
e) Inhibition of gluconeogenesis

34.How does glucagon affect ketone body formation?

a) By increasing malonyl-CoA levels in the liver
b) By inhibiting lipolysis
c) By decreasing intracellular cAMP levels
d) By reducing gluconeogenesis
e) By decreasing malonyl-CoA levels in the liver

35.What stimulates glucagon secretion?

a) High plasma glucose levels
b) Activation of parasympathetic nerves to the pancreas
c) Administration of insulin
d) Hypoglycemia
e) Inhibition of sympathetic nerves to the pancreas

36.Which hormones or substances inhibit glucagon secretion?

a) Cholecystokinin and gastrin
b) Insulin
c) Secretin
d) β-adrenergic receptor agonists
 e) Protein meals

37.Where is somatostatin primarily found?

a) A cells of pancreatic islets
b) B cells of pancreatic islets
c) D cells of pancreatic islets
d) F cells of pancreatic islets
e) G cells of the gastric mucosa

38.Which form of somatostatin is more active in inhibiting insulin secretion?

a) Somatostatin 14 (SS 14)
b) Somatostatin 28 (SS 28)
c) Both are equally active
d) Neither affects insulin secretion
e) Somatostatin has no effect on insulin secretion

39.What stimulates the secretion of pancreatic somatostatin?

a) High levels of insulin
b) High levels of glucagon
c) High levels of glucose
d) Amino acids
e) Cholecystokinin (CCK)

40.Which cells in the pancreatic islets produce pancreatic polypeptide?

a) A cells
b) B cells
c) D cells
d) F cells
e) G cells

41.What effect does pancreatic polypeptide have on food absorption?

a) It accelerates food absorption
 b) It has no effect on food absorption
c) It inhibits food absorption
d) It decreases gastric motility
e) It enhances nutrient breakdown

42.What are common symptoms of chronic mild hypoglycemia?

a) Excessive thirst and hunger
b) Slurred speech and incoordination
c) Weight gain and lethargy
d) Hyperglycemia and glycosuria
e) Increased urination and weight loss

43.Which of the following is NOT a characteristic symptom of diabetes

mellitus?
a) Polyuria
b) Hyperglycemia
c) Weight gain
d) Polyphagia
e) Glycosuria

44.What is the fundamental defect underlying most of the abnormalities in

diabetes mellitus?
a) Reduced entry of glucose into various "peripheral" tissues
b) Increased glucose uptake by peripheral tissues
c) Reduced glucose liberation from the liver
d) Increased insulin sensitivity
e) Increased glucose utilization in cells

45.Which of the following complications is NOT associated with long-standing

diabetes mellitus?
a) Diabetic retinopathy
b) Diabetic nephropathy
c) Diabetic neuropathy
 d) Diabetic ketoacidosis
e) Accelerated atherosclerosis

46.What is the primary cause of microvascular abnormalities in diabetes

mellitus?
a) Increased plasma LDL
b) Proliferative scarring of the retina
c) Increased release of insulin
d) Decreased blood pressure
e) Accelerated atherosclerosis

47.What is the relationship between obesity and insulin resistance?

a) Obesity decreases insulin resistance
b) Obesity has no effect on insulin resistance
c) Obesity increases insulin resistance
d) Obesity leads to insulin sensitivity
e) Obesity reduces insulin secretion

48.What effect does weight reduction have on insulin resistance?

a) Increases insulin resistance
b) Has no effect on insulin resistance
c) Decreases insulin resistance
d) Increases insulin secretion
e) Reduces insulin sensitivity

49.Which of the following is a characteristic of dyslipidemia associated with

obesity?
a) Low circulating triglycerides
b) High high-density lipoprotein (HDL) levels
c) Low-density lipoprotein (LDL) dominance
d) Low cholesterol levels
e) High circulating triglycerides and low HDL levels
50.What is the term commonly used to describe the combination of obesity,
insulin resistance, dyslipidemia, and accelerated development of
atherosclerosis?
a) Obesity syndrome
b) Atherosclerotic syndrome
c) Metabolic syndrome
d) Insulin syndrome
e) Dyslipidemic syndrome

51.What is the primary consequence of hyperinsulinemia associated with

obesity?
a) Decreased glucose uptake by cells
b) Increased lipolysis
c) Increased glycogenolysis
d) Increased glucose release from the liver
e) Reduced adipose tissue storage