,CHAPTER LIST
Chapter 1: Fuel Metabolism and Nutrition — Basic Principles
Chapter 2: Basic Aspects of Biochemistry — Organic
Chemistry, Acid–Base Chemistry, Amino Acids, Protein
Structure and Function, and Enzyme Kinetics
Chapter 3: Genome Maintenance (Replication), Gene
Expression (Transcription), Protein Synthesis (Translation),
and Regulation of Gene Expression
Chapter 4: Cell Biology, Signal Transduction, and the
Molecular Biology of Cancer
Chapter 5: Generation of ATP From Metabolic Fuels and
Oxygen Toxicity
Chapter 6: Carbohydrate Metabolism
Chapter 7: Lipid and Ethanol Metabolism
Chapter 8: Tissue Metabolism — Nitrogen-Containing
Nutrient Absorption and Digestion, and Pathologies of
Nitrogen Metabolism
Chapter 9: Human Genetics — An Introduction
,Chapter 1
Fuel Metabolism & Nutrition — Basic Principles
Q1
A 28-year-old marathon runner consumes a carbohydrate-rich meal immediately after
finishing a race. Which hormone profile in the first hour after the meal best explains
rapid glycogen synthesis in the liver?
A. ↑ Glucagon, ↑ Epinephrine
B. ↑ Insulin, ↓ Glucagon
C. ↓ Insulin, ↑ Cortisol
D. ↑ Glucagon, ↑ Cortisol
Answer: B
Rationale:
Postprandial carbohydrate intake raises blood glucose → pancreatic β-cells secrete
insulin. Insulin stimulates hepatic glycogen synthase and inhibits glycogen
phosphorylase (via dephosphorylation cascades), promoting glycogen synthesis. Insulin
also suppresses glucagon secretion from α-cells; low glucagon reduces cAMP–PKA
signaling that would otherwise activate glycogenolysis. Catecholamines and cortisol
favor catabolism and would oppose rapid glycogen deposition.
Key words: insulin, glucagon, hepatic glycogen synthase, postprandial, glycogen
synthesis
Q2
During an overnight fast (12–16 hours), which tissues are the principal consumers of
gluconeogenesis-derived glucose?
A. Skeletal muscle and heart
B. Red blood cells and brain
C. Liver and adipose tissue
D. Pancreas and spleen
,Answer: B
Rationale:
After overnight fasting hepatic gluconeogenesis supplies blood glucose primarily for
obligate glucose users: red blood cells (no mitochondria, anaerobic glycolysis only) and,
to a large extent, the brain (which prefers glucose though can use ketone bodies in
prolonged fast). Skeletal muscle primarily uses fatty acids and ketones during fasting;
liver performs gluconeogenesis but is a producer, not primary consumer.
Key words: overnight fast, gluconeogenesis, RBCs, brain, obligate glucose users
Q3
Which metabolic change occurs in adipose tissue in response to elevated insulin?
A. Increased hormone-sensitive lipase activity
B. Increased lipoprotein lipase expression and activity
C. Increased hepatic VLDL secretion
D. Increased release of free fatty acids into the circulation
Answer: B
Rationale:
Insulin promotes fat storage: it increases lipoprotein lipase (LPL) activity in adipose,
enabling uptake of circulating triglyceride-derived fatty acids for esterification into
triglycerides. Insulin inhibits hormone-sensitive lipase (HSL), decreasing lipolysis and
lowering plasma free fatty acids. Hepatic VLDL secretion is more related to hepatic lipid
metabolism and is not a direct adipose response to insulin.
Key words: adipose, insulin, lipoprotein lipase, HSL, fat storage
Q4
A patient with untreated type 1 diabetes has very high plasma glucagon and low insulin.
Which hepatic process best explains the formation of ketone bodies in this setting?
A. Upregulation of HMG-CoA synthase due to increased fatty acid β-oxidation and high
acetyl-CoA availability
B. Increased glycolysis leading to pyruvate accumulation and ketogenesis
,C. Increased activity of pyruvate carboxylase diverting acetyl-CoA into TCA cycle
D. Enhanced lipogenesis from excess dietary carbohydrate
Answer: A
Rationale:
In insulin deficiency with high glucagon, adipose lipolysis releases free fatty acids to liver
where increased β-oxidation produces excess acetyl-CoA. When TCA cycle capacity is
limited (due to low oxaloacetate or high NADH), acetyl-CoA is shunted into ketogenesis.
HMG-CoA synthase in mitochondria is the rate-limiting enzyme for ketone body
synthesis. Glycolysis and lipogenesis are not responsible for ketone overproduction in
this catabolic state.
Key words: type 1 diabetes, insulin deficiency, glucagon, β-oxidation, HMG-CoA
synthase, ketogenesis
Q5
Which statement best describes the hormonal regulation that distinguishes
gluconeogenesis from glycolysis in the liver?
A. Insulin activates fructose-1,6-bisphosphatase directly.
B. Glucagon increases PFK-2 kinase activity, raising F-2,6-BP and stimulating glycolysis.
C. Insulin increases fructose-2,6-bisphosphate (F-2,6-BP) levels, which stimulates PFK-1
and glycolysis.
D. Glucagon activates pyruvate kinase in the liver to enhance glycolysis.
Answer: C
Rationale:
Fructose-2,6-bisphosphate is a key allosteric regulator: high F-2,6-BP activates PFK-1
(glycolysis) and inhibits F-1,6-bisphosphatase (gluconeogenesis). Insulin stimulates PFK-
2 activity (increasing F-2,6-BP), promoting glycolysis. Glucagon triggers PKA-mediated
phosphorylation of bifunctional PFK-2/FBPase-2 decreasing F-2,6-BP and favoring
gluconeogenesis. Glucagon does not activate pyruvate kinase; it inhibits it via
phosphorylation.
Key words: F-2,6-BP, PFK-1, insulin, glucagon, gluconeogenesis vs glycolysis
, Q6
A patient is taking a drug that activates AMP-activated protein kinase (AMPK). Which
metabolic effect is expected in the liver?
A. Increased gluconeogenesis
B. Increased fatty acid synthesis via acetyl-CoA carboxylase activation
C. Increased fatty acid oxidation and decreased lipogenesis
D. Increased glycogen phosphorylase activation leading to glycogen breakdown
Answer: C
Rationale:
AMPK senses low cellular energy and switches metabolism toward ATP-producing
pathways: it inhibits anabolic processes (e.g., fatty acid synthesis by phosphorylating and
inhibiting acetyl-CoA carboxylase) and stimulates catabolic pathways (e.g., increases
fatty acid oxidation). AMPK activation decreases gluconeogenesis and lipogenesis.
Glycogen phosphorylase regulation is more hormonally controlled; AMPK has indirect
effects but the canonical answer is increased FA oxidation and decreased lipogenesis.
Key words: AMPK, liver, fatty acid oxidation, acetyl-CoA carboxylase inhibition, energy
sensor
Q7
During prolonged starvation (several days), which of the following is the major fuel
source for the brain?
A. Glucose exclusively
B. Free fatty acids exclusively
C. Ketone bodies (β-hydroxybutyrate and acetoacetate)
D. Amino acids only
Answer: C
Rationale:
In prolonged starvation, hepatic ketogenesis increases and ketone bodies become a
major fuel for the brain, reducing the brain’s glucose requirement and conserving
muscle protein. Free fatty acids cannot cross the blood-brain barrier efficiently. Amino
acids contribute via gluconeogenesis but are not the brain’s preferred direct fuel in
prolonged fasting.
Chapter 1: Fuel Metabolism and Nutrition — Basic Principles
Chapter 2: Basic Aspects of Biochemistry — Organic
Chemistry, Acid–Base Chemistry, Amino Acids, Protein
Structure and Function, and Enzyme Kinetics
Chapter 3: Genome Maintenance (Replication), Gene
Expression (Transcription), Protein Synthesis (Translation),
and Regulation of Gene Expression
Chapter 4: Cell Biology, Signal Transduction, and the
Molecular Biology of Cancer
Chapter 5: Generation of ATP From Metabolic Fuels and
Oxygen Toxicity
Chapter 6: Carbohydrate Metabolism
Chapter 7: Lipid and Ethanol Metabolism
Chapter 8: Tissue Metabolism — Nitrogen-Containing
Nutrient Absorption and Digestion, and Pathologies of
Nitrogen Metabolism
Chapter 9: Human Genetics — An Introduction
,Chapter 1
Fuel Metabolism & Nutrition — Basic Principles
Q1
A 28-year-old marathon runner consumes a carbohydrate-rich meal immediately after
finishing a race. Which hormone profile in the first hour after the meal best explains
rapid glycogen synthesis in the liver?
A. ↑ Glucagon, ↑ Epinephrine
B. ↑ Insulin, ↓ Glucagon
C. ↓ Insulin, ↑ Cortisol
D. ↑ Glucagon, ↑ Cortisol
Answer: B
Rationale:
Postprandial carbohydrate intake raises blood glucose → pancreatic β-cells secrete
insulin. Insulin stimulates hepatic glycogen synthase and inhibits glycogen
phosphorylase (via dephosphorylation cascades), promoting glycogen synthesis. Insulin
also suppresses glucagon secretion from α-cells; low glucagon reduces cAMP–PKA
signaling that would otherwise activate glycogenolysis. Catecholamines and cortisol
favor catabolism and would oppose rapid glycogen deposition.
Key words: insulin, glucagon, hepatic glycogen synthase, postprandial, glycogen
synthesis
Q2
During an overnight fast (12–16 hours), which tissues are the principal consumers of
gluconeogenesis-derived glucose?
A. Skeletal muscle and heart
B. Red blood cells and brain
C. Liver and adipose tissue
D. Pancreas and spleen
,Answer: B
Rationale:
After overnight fasting hepatic gluconeogenesis supplies blood glucose primarily for
obligate glucose users: red blood cells (no mitochondria, anaerobic glycolysis only) and,
to a large extent, the brain (which prefers glucose though can use ketone bodies in
prolonged fast). Skeletal muscle primarily uses fatty acids and ketones during fasting;
liver performs gluconeogenesis but is a producer, not primary consumer.
Key words: overnight fast, gluconeogenesis, RBCs, brain, obligate glucose users
Q3
Which metabolic change occurs in adipose tissue in response to elevated insulin?
A. Increased hormone-sensitive lipase activity
B. Increased lipoprotein lipase expression and activity
C. Increased hepatic VLDL secretion
D. Increased release of free fatty acids into the circulation
Answer: B
Rationale:
Insulin promotes fat storage: it increases lipoprotein lipase (LPL) activity in adipose,
enabling uptake of circulating triglyceride-derived fatty acids for esterification into
triglycerides. Insulin inhibits hormone-sensitive lipase (HSL), decreasing lipolysis and
lowering plasma free fatty acids. Hepatic VLDL secretion is more related to hepatic lipid
metabolism and is not a direct adipose response to insulin.
Key words: adipose, insulin, lipoprotein lipase, HSL, fat storage
Q4
A patient with untreated type 1 diabetes has very high plasma glucagon and low insulin.
Which hepatic process best explains the formation of ketone bodies in this setting?
A. Upregulation of HMG-CoA synthase due to increased fatty acid β-oxidation and high
acetyl-CoA availability
B. Increased glycolysis leading to pyruvate accumulation and ketogenesis
,C. Increased activity of pyruvate carboxylase diverting acetyl-CoA into TCA cycle
D. Enhanced lipogenesis from excess dietary carbohydrate
Answer: A
Rationale:
In insulin deficiency with high glucagon, adipose lipolysis releases free fatty acids to liver
where increased β-oxidation produces excess acetyl-CoA. When TCA cycle capacity is
limited (due to low oxaloacetate or high NADH), acetyl-CoA is shunted into ketogenesis.
HMG-CoA synthase in mitochondria is the rate-limiting enzyme for ketone body
synthesis. Glycolysis and lipogenesis are not responsible for ketone overproduction in
this catabolic state.
Key words: type 1 diabetes, insulin deficiency, glucagon, β-oxidation, HMG-CoA
synthase, ketogenesis
Q5
Which statement best describes the hormonal regulation that distinguishes
gluconeogenesis from glycolysis in the liver?
A. Insulin activates fructose-1,6-bisphosphatase directly.
B. Glucagon increases PFK-2 kinase activity, raising F-2,6-BP and stimulating glycolysis.
C. Insulin increases fructose-2,6-bisphosphate (F-2,6-BP) levels, which stimulates PFK-1
and glycolysis.
D. Glucagon activates pyruvate kinase in the liver to enhance glycolysis.
Answer: C
Rationale:
Fructose-2,6-bisphosphate is a key allosteric regulator: high F-2,6-BP activates PFK-1
(glycolysis) and inhibits F-1,6-bisphosphatase (gluconeogenesis). Insulin stimulates PFK-
2 activity (increasing F-2,6-BP), promoting glycolysis. Glucagon triggers PKA-mediated
phosphorylation of bifunctional PFK-2/FBPase-2 decreasing F-2,6-BP and favoring
gluconeogenesis. Glucagon does not activate pyruvate kinase; it inhibits it via
phosphorylation.
Key words: F-2,6-BP, PFK-1, insulin, glucagon, gluconeogenesis vs glycolysis
, Q6
A patient is taking a drug that activates AMP-activated protein kinase (AMPK). Which
metabolic effect is expected in the liver?
A. Increased gluconeogenesis
B. Increased fatty acid synthesis via acetyl-CoA carboxylase activation
C. Increased fatty acid oxidation and decreased lipogenesis
D. Increased glycogen phosphorylase activation leading to glycogen breakdown
Answer: C
Rationale:
AMPK senses low cellular energy and switches metabolism toward ATP-producing
pathways: it inhibits anabolic processes (e.g., fatty acid synthesis by phosphorylating and
inhibiting acetyl-CoA carboxylase) and stimulates catabolic pathways (e.g., increases
fatty acid oxidation). AMPK activation decreases gluconeogenesis and lipogenesis.
Glycogen phosphorylase regulation is more hormonally controlled; AMPK has indirect
effects but the canonical answer is increased FA oxidation and decreased lipogenesis.
Key words: AMPK, liver, fatty acid oxidation, acetyl-CoA carboxylase inhibition, energy
sensor
Q7
During prolonged starvation (several days), which of the following is the major fuel
source for the brain?
A. Glucose exclusively
B. Free fatty acids exclusively
C. Ketone bodies (β-hydroxybutyrate and acetoacetate)
D. Amino acids only
Answer: C
Rationale:
In prolonged starvation, hepatic ketogenesis increases and ketone bodies become a
major fuel for the brain, reducing the brain’s glucose requirement and conserving
muscle protein. Free fatty acids cannot cross the blood-brain barrier efficiently. Amino
acids contribute via gluconeogenesis but are not the brain’s preferred direct fuel in
prolonged fasting.
