BIOCHEM 210 MODULE 7 EXAM 2026/2027 | Glycolysis,
Gluconeogenesis & CAC | Portage Learning | Verified
Questions & Answers | Pass Guaranteed - A+ Graded
Q1: Which enzyme catalyzes the rate-limiting step in fatty acid synthesis?
A. Acetyl-CoA carboxylase [CORRECT]
B. Fatty acid synthase
C. Citrate lyase
D. Malic enzyme
Correct Answer: A
Rationale: Acetyl-CoA carboxylase (ACC) catalyzes the carboxylation of acetyl-CoA to
malonyl-CoA, the committed step in fatty acid synthesis. This reaction requires biotin
and ATP. ACC is regulated by citrate (allosteric activator) and palmitoyl-CoA (feedback
inhibitor), as well as by phosphorylation (inactivated by AMPK). Fatty acid synthase (B)
is the multifunctional enzyme that carries out the elongation steps but does not
catalyze the rate-limiting step. Citrate lyase (C) cleaves citrate to acetyl-CoA and
oxaloacetate in the cytoplasm, providing substrate but not regulating the pathway. Malic
enzyme (D) generates NADPH for fatty acid synthesis via the pentose phosphate
pathway but is not rate-limiting.
Q2: A 16-carbon saturated fatty acid (palmitate) undergoes complete beta-oxidation.
How many total ATP equivalents are net produced from one molecule of palmitate?
A. 96 ATP
B. 106 ATP [CORRECT]
C. 129 ATP
D. 146 ATP
Correct Answer: B
Rationale: Beta-oxidation of palmitate (16:0) yields: 8 acetyl-CoA (enter TCA cycle → 10
ATP each = 80 ATP), 7 FADH₂ (1.5 ATP each = 10.5 ATP), and 7 NADH (2.5 ATP each =
17.5 ATP). Total = 108 ATP. Subtract 2 ATP equivalents consumed in activation (fatty
acid → fatty acyl-CoA). Net yield = 106 ATP. Option A (96) incorrectly uses 2 ATP/FADH₂
, and 3 ATP/NADH with older P/O ratios. Option C (129) fails to subtract activation cost.
Option D (146) double-counts or uses incorrect stoichiometry.
Q3: Which of the following conditions would result in increased ketone body
production?
A. High carbohydrate diet with insulin elevation
B. Uncontrolled Type 1 diabetes mellitus [CORRECT]
C. Fed state with elevated malonyl-CoA
D. Liver glycogen stores full
Correct Answer: B
Rationale: Ketogenesis is stimulated when fatty acid oxidation exceeds the liver's
capacity for complete oxidation via the TCA cycle. In uncontrolled Type 1 diabetes (B),
absolute insulin deficiency and glucagon excess promote adipose lipolysis, delivering
excessive fatty acids to the liver. Oxaloacetate is diverted to gluconeogenesis, limiting
TCA cycle capacity and favoring ketogenesis. Option A is incorrect because insulin
inhibits hormone-sensitive lipase and ketogenesis. Option C is incorrect because
malonyl-CoA inhibits CPT-I, blocking fatty acid entry into mitochondria. Option D
describes a fed state that inhibits ketogenesis.
Q4: The primary regulatory mechanism that coordinates fatty acid synthesis and
beta-oxidation involves which molecule?
A. Carnitine
B. Malonyl-CoA [CORRECT]
C. Acetyl-CoA
D. HMG-CoA
Correct Answer: B
Rationale: Malonyl-CoA is the critical regulator that prevents simultaneous synthesis
and degradation of fatty acids. High malonyl-CoA (fed state) inhibits carnitine
palmitoyltransferase I (CPT-I), blocking fatty acid entry into mitochondria and
beta-oxidation, while serving as the substrate for fatty acid synthesis. When energy is
needed (fasting), malonyl-CoA levels drop, relieving CPT-I inhibition and allowing
beta-oxidation. Carnitine (A) is the shuttle molecule but not the primary regulator.
Acetyl-CoA (C) is a substrate for both pathways but does not coordinate them.
Gluconeogenesis & CAC | Portage Learning | Verified
Questions & Answers | Pass Guaranteed - A+ Graded
Q1: Which enzyme catalyzes the rate-limiting step in fatty acid synthesis?
A. Acetyl-CoA carboxylase [CORRECT]
B. Fatty acid synthase
C. Citrate lyase
D. Malic enzyme
Correct Answer: A
Rationale: Acetyl-CoA carboxylase (ACC) catalyzes the carboxylation of acetyl-CoA to
malonyl-CoA, the committed step in fatty acid synthesis. This reaction requires biotin
and ATP. ACC is regulated by citrate (allosteric activator) and palmitoyl-CoA (feedback
inhibitor), as well as by phosphorylation (inactivated by AMPK). Fatty acid synthase (B)
is the multifunctional enzyme that carries out the elongation steps but does not
catalyze the rate-limiting step. Citrate lyase (C) cleaves citrate to acetyl-CoA and
oxaloacetate in the cytoplasm, providing substrate but not regulating the pathway. Malic
enzyme (D) generates NADPH for fatty acid synthesis via the pentose phosphate
pathway but is not rate-limiting.
Q2: A 16-carbon saturated fatty acid (palmitate) undergoes complete beta-oxidation.
How many total ATP equivalents are net produced from one molecule of palmitate?
A. 96 ATP
B. 106 ATP [CORRECT]
C. 129 ATP
D. 146 ATP
Correct Answer: B
Rationale: Beta-oxidation of palmitate (16:0) yields: 8 acetyl-CoA (enter TCA cycle → 10
ATP each = 80 ATP), 7 FADH₂ (1.5 ATP each = 10.5 ATP), and 7 NADH (2.5 ATP each =
17.5 ATP). Total = 108 ATP. Subtract 2 ATP equivalents consumed in activation (fatty
acid → fatty acyl-CoA). Net yield = 106 ATP. Option A (96) incorrectly uses 2 ATP/FADH₂
, and 3 ATP/NADH with older P/O ratios. Option C (129) fails to subtract activation cost.
Option D (146) double-counts or uses incorrect stoichiometry.
Q3: Which of the following conditions would result in increased ketone body
production?
A. High carbohydrate diet with insulin elevation
B. Uncontrolled Type 1 diabetes mellitus [CORRECT]
C. Fed state with elevated malonyl-CoA
D. Liver glycogen stores full
Correct Answer: B
Rationale: Ketogenesis is stimulated when fatty acid oxidation exceeds the liver's
capacity for complete oxidation via the TCA cycle. In uncontrolled Type 1 diabetes (B),
absolute insulin deficiency and glucagon excess promote adipose lipolysis, delivering
excessive fatty acids to the liver. Oxaloacetate is diverted to gluconeogenesis, limiting
TCA cycle capacity and favoring ketogenesis. Option A is incorrect because insulin
inhibits hormone-sensitive lipase and ketogenesis. Option C is incorrect because
malonyl-CoA inhibits CPT-I, blocking fatty acid entry into mitochondria. Option D
describes a fed state that inhibits ketogenesis.
Q4: The primary regulatory mechanism that coordinates fatty acid synthesis and
beta-oxidation involves which molecule?
A. Carnitine
B. Malonyl-CoA [CORRECT]
C. Acetyl-CoA
D. HMG-CoA
Correct Answer: B
Rationale: Malonyl-CoA is the critical regulator that prevents simultaneous synthesis
and degradation of fatty acids. High malonyl-CoA (fed state) inhibits carnitine
palmitoyltransferase I (CPT-I), blocking fatty acid entry into mitochondria and
beta-oxidation, while serving as the substrate for fatty acid synthesis. When energy is
needed (fasting), malonyl-CoA levels drop, relieving CPT-I inhibition and allowing
beta-oxidation. Carnitine (A) is the shuttle molecule but not the primary regulator.
Acetyl-CoA (C) is a substrate for both pathways but does not coordinate them.
