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BIOCHEM 210 METABOLISM INTEGRATION & HORMONAL REGULATION MODULE 7 EXAM ACTUAL 2026/2027 | Portage Learning | Complete Questions & Verified Answers | Pass Guaranteed - A+ Graded

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Pass the BIOCHEM 210 Metabolism Integration & Hormonal Regulation Module 7 Exam on your first attempt with this complete 2026/2027 study guide for Portage Learning. This A+ Graded resource contains questions and verified answers covering all key topics for Module 7 including metabolic pathways integration (carbohydrate, lipid, protein metabolism), hormonal regulation (insulin, glucagon, epinephrine, cortisol, thyroid hormones), fed-state vs fasting-state metabolism, metabolic adaptations during starvation and exercise, diabetes mellitus, and metabolic disorders. Each answer includes clear rationales to reinforce understanding of how hormones coordinate metabolism across different tissues. Perfect for mastering module content and passing with confidence. With our Pass Guarantee, you can confidently prepare for your BIOCHEM 210 Module 7 exam. Download your complete BIOCHEM 210 Metabolism & Hormonal Regulation module 7 exam guide instantly!

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BIOCHEM 210 METABOLISM INTEGRATION & HORMONAL
REGULATION MODULE 7 EXAM ACTUAL 2026/2027 | Portage
Learning | Complete Questions & Verified Answers | Pass
Guaranteed - A+ Graded


Section 1: Metabolic Integration & Tissue Specialization (Questions 1–12)

Q1. During the absorptive (fed) state, a 25-year-old athlete consumes a
carbohydrate-rich meal. Which metabolic event occurs primarily in skeletal muscle
under the influence of elevated insulin?
A. Activation of hormone-sensitive lipase and release of free fatty acids into circulation
B. Stimulation of gluconeogenesis from alanine and lactate to maintain blood glucose
C. Translocation of GLUT4 vesicles to the sarcolemma, increasing glucose uptake by
facilitated diffusion [CORRECT]
D. Phosphorylation and inhibition of glycogen synthase by protein kinase A

Rationale: Insulin binding to its receptor tyrosine kinase activates the PI3K-Akt signaling
cascade, which triggers GLUT4 vesicle translocation to the plasma membrane in
muscle and adipose tissue, dramatically increasing glucose uptake. Option A describes
fasting-state adipose tissue; option B describes liver gluconeogenesis during fasting;
and option D describes glucagon/epinephrine signaling, not insulin action.

Correct Answer: C

Q2. A medical student is studying the hormonal profile of a patient who has fasted for
18 hours. Which statement best describes the insulin-to-glucagon ratio and its
metabolic consequences in the liver?
A. The ratio is high, promoting glycogen synthesis and lipogenesis while suppressing
gluconeogenesis
B. The ratio is low, leading to activation of glycogen phosphorylase and stimulation of
hepatic gluconeogenesis [CORRECT]

,C. The ratio is high, causing phosphorylation of the bifunctional enzyme and increased
fructose-2,6-bisphosphate levels
D. The ratio is low, resulting in GLUT4 translocation and increased peripheral glucose
disposal

Rationale: During fasting, declining blood glucose reduces insulin secretion and
increases glucagon secretion, producing a low insulin-to-glucagon ratio that activates
hepatic glycogenolysis and gluconeogenesis via cAMP/PKA signaling. Option A
describes the fed state; option C incorrectly associates low insulin with high
fructose-2,6-bisphosphate; and option D describes insulin-stimulated events in
muscle/adipose, not liver.

Correct Answer: B

Q3. During prolonged starvation (day 5), which tissue has undergone the most
significant metabolic adaptation by shifting its primary fuel source from glucose to
ketone bodies?
A. Erythrocytes, which lack mitochondria and rely exclusively on glycolysis
B. Skeletal muscle, which increases proteolysis to supply gluconeogenic amino acids
C. The brain, which upregulates monocarboxylate transporters to utilize
β-hydroxybutyrate and acetoacetate [CORRECT]
D. Adipose tissue, which ceases lipolysis and begins ketone body synthesis

Rationale: After approximately 3 days of starvation, the brain transitions from glucose
dependence to ketone body oxidation, reducing glucose demand from approximately
120 g/day to 40 g/day and sparing muscle protein. Erythrocytes cannot use ketones due
to absent mitochondria; skeletal muscle does not synthesize ketones; and adipose
tissue continues lipolysis during starvation.

Correct Answer: C

Q4. A marathon runner experiences severe leg cramping at mile 20. Anaerobic
glycolysis in working skeletal muscle generates lactate, which is released into the

,bloodstream. Which pathway describes the metabolic fate of this lactate and its return
to muscle as glucose?
A. The glucose-alanine cycle, where lactate is transaminated to alanine in muscle and
converted back to pyruvate in liver
B. The Cori cycle, where hepatic gluconeogenesis converts lactate to glucose, which is
then transported back to muscle for energy [CORRECT]
C. The pentose phosphate pathway, where lactate is oxidized to ribose-5-phosphate for
nucleotide synthesis
D. The urea cycle, where lactate nitrogen is incorporated into carbamoyl phosphate and
excreted

Rationale: The Cori cycle constitutes an inter-organ metabolic loop in which
muscle-derived lactate travels to the liver for gluconeogenesis (Cori cycle) and the
newly synthesized glucose returns via circulation to fuel muscle glycolysis. The
glucose-alanine cycle involves alanine, not lactate; the pentose phosphate pathway
does not metabolize lactate; and the urea cycle handles nitrogen disposal, not lactate
carbon.

Correct Answer: B

Q5. During extended fasting, skeletal muscle undergoes proteolysis to release alanine
into the bloodstream. In the liver, alanine is deaminated to pyruvate and converted to
glucose via gluconeogenesis. What is the name of this inter-organ nitrogen and carbon
shuttle?
A. The Cori cycle, which shuttles lactate between muscle and liver
B. The glucose-alanine cycle, which transports nitrogen from muscle to liver as alanine
and returns glucose to muscle [CORRECT]
C. The carnitine shuttle, which transports fatty acyl groups across the mitochondrial
inner membrane
D. The malate-aspartate shuttle, which transfers reducing equivalents across the
mitochondrial membrane

Rationale: The glucose-alanine cycle allows muscle to dispose of amino nitrogen (as
alanine) while providing the liver with a gluconeogenic substrate (pyruvate from alanine

, transamination), and the resulting glucose returns to muscle. The Cori cycle handles
lactate; the carnitine shuttle handles fatty acid oxidation; and the malate-aspartate
shuttle transfers electrons, not carbon skeletons.

Correct Answer: B

Q6. A first-year medical student is asked which tissue relies almost exclusively on
glucose under normal physiological conditions and cannot utilize fatty acids for ATP
production. Which tissue should the student identify?
A. Cardiac muscle, which preferentially oxidizes fatty acids and ketone bodies
B. The liver, which readily oxidizes free fatty acids and synthesizes ketone bodies during
fasting
C. Erythrocytes, which lack mitochondria and depend entirely on anaerobic glycolysis
for ATP [CORRECT]
D. Adipose tissue, which primarily performs lipolysis and fatty acid re-esterification

Rationale: Mature erythrocytes lack mitochondria and therefore cannot perform
β-oxidation, the TCA cycle, or oxidative phosphorylation, making them absolutely
dependent on glycolysis for ATP generation. Cardiac muscle, liver, and adipose tissue all
possess mitochondria and can oxidize fatty acids or perform other oxidative
metabolism.

Correct Answer: C

Q7. Which organ serves as the primary site of ketogenesis during prolonged fasting,
utilizing acetyl-CoA derived from β-oxidation of fatty acids to synthesize acetoacetate
and β-hydroxybutyrate?
A. Skeletal muscle, which exports ketone bodies to the brain during starvation
B. The liver, which lacks the enzyme succinyl-CoA:3-ketoacid CoA transferase
(thiophorase) and therefore cannot oxidize ketone bodies [CORRECT]
C. Adipose tissue, which synthesizes ketone bodies from glycerol released during
lipolysis
D. The kidney, which produces ketone bodies from glutamine during prolonged acidosis

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