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CHEM 210 Biochemistry Module 6 Exam 2025/2026 | Portage Learning Questions & Verified Answers | Comprehensive Study Guide - 240 Questions and Answers Already Graded A+ Premium Exam Tested And Verified

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Comprehensive examination on CHEM 210 Biochemistry Module 6 Exam 2025/2026 | Portage Learning Questions & Verified Answers | Comprehensive Study Guide.

Institution
CHEM 210
Course
CHEM 210

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CHEM 210 Biochemistry Module 6 Exam 2025/2026 | Portage
Learning Questions & Verified Answers | Comprehensive Study
Guide - 240 Questions and Answers Already Graded A+
Premium Exam Tested And Verified


Subject Area CHEM 210 Biochemistry Module 6 Exam 2025/2026 | Portage Learning
Questions & Verified Answers | Comprehensive Study Guide

Description Comprehensive examination on CHEM 210 Biochemistry Module 6 Exam
2025/2026 | Portage Learning Questions & Verified Answers | Comprehensive
Study Guide.

Expected Grade A+

Total Questions 240

Duration 3 hours

Learning Outcomes 1. Demonstrate mastery of core concepts

Accreditation Aligned with US university standards.




Page 1

,1. In the context of enzyme kinetics, a competitive inhibitor is found to increase the
apparent Km of an enzyme without affecting Vmax. Which of the following
experimental observations would best support the conclusion that the inhibitor binds
exclusively to the free enzyme and not to the enzyme-substrate complex?

A. Double-reciprocal plots show lines intersecting on the 1/V axis.
B. Double-reciprocal plots show lines intersecting on the 1/[S] axis.
C. Double-reciprocal plots show parallel lines.
D. Double-reciprocal plots show lines intersecting above the 1/[S] axis.
Answer: A. Double-reciprocal plots show lines intersecting on the 1/V axis.

Competitive inhibition yields double-reciprocal plots that intersect on the 1/V axis
(same Vmax) with increased slope (apparent Km). Intersection on the 1/[S] axis would
indicate uncompetitive inhibition, parallel lines indicate noncompetitive inhibition, and
intersection above the 1/[S] axis is not a standard pattern.

2. During gluconeogenesis, the conversion of oxaloacetate to phosphoenolpyruvate
(PEP) is catalyzed by PEP carboxykinase (PEPCK). This reaction requires GTP as
an energy source. In which cellular compartment does this reaction primarily occur
in humans?

A. Cytosol
B. Mitochondrial matrix
C. Both cytosol and mitochondrial matrix
D. Endoplasmic reticulum
Answer: C. Both cytosol and mitochondrial matrix

In humans, PEPCK exists in two isoforms: a cytosolic form (PEPCK-C) and a
mitochondrial form (PEPCK-M). The conversion of oxaloacetate to PEP occurs in both
compartments, depending on the precursor for gluconeogenesis. The mitochondrial
isoform is particularly important when lactate is the precursor.




Page 2

,3. Which of the following best explains why the oxidation of odd-chain fatty acids
yields net gluconeogenic precursors, whereas even-chain fatty acids do not?
A. Even-chain fatty acids produce exclusively acetyl-CoA, which cannot be converted to
glucose in animals.
B. Odd-chain fatty acids produce propionyl-CoA, which is converted to succinyl-CoA, a
TCA cycle intermediate that can feed into gluconeogenesis.
C. Odd-chain fatty acids produce malonyl-CoA, which directly enters gluconeogenesis.
D. Even-chain fatty acids produce ketone bodies that inhibit gluconeogenesis.
Answer: B. Odd-chain fatty acids produce propionyl-CoA, which is converted to
succinyl-CoA, a TCA cycle intermediate that can feed into gluconeogenesis.

Odd-chain fatty acids yield propionyl-CoA in the final round of -oxidation.
Propionyl-CoA is carboxylated to methylmalonyl-CoA and then isomerized to
succinyl-CoA, a TCA cycle intermediate that can be converted to oxaloacetate for
gluconeogenesis. Even-chain fatty acids yield only acetyl-CoA, which cannot be net
converted to glucose in animals because the pyruvate dehydrogenase reaction is
irreversible.

4. A researcher isolates a mutant form of glycogen phosphorylase that lacks the
serine residue normally phosphorylated by phosphorylase kinase. In a liver cell
extract with high glucagon signaling, what is the expected activity of this mutant
enzyme relative to wild-type?

A. Constitutively active, independent of allosteric regulation.
B. Inactive regardless of allosteric activators.
C. Active only in the presence of high AMP, but not responsive to phosphorylation.
D. Fully active under all conditions because the mutation mimics the phosphorylated state.
Answer: C. Active only in the presence of high AMP, but not responsive to
phosphorylation.

Phosphorylation of Ser14 (in humans) activates glycogen phosphorylase. Without this
serine, the enzyme cannot be activated by phosphorylation, but it retains allosteric
regulation. In the liver, the enzyme is primarily regulated by phosphorylation, but
allosteric activation by AMP can still partially activate the unphosphorylated form,
though less efficiently than in muscle.




Page 3

, 5. In the Cori cycle, lactate produced by anaerobic glycolysis in muscle is
transported to the liver and converted to glucose. Which of the following enzymes is
NOT directly involved in the conversion of lactate to glucose in the liver?
A. Pyruvate carboxylase
B. Phosphoenolpyruvate carboxykinase (PEPCK)
C. Fructose-1,6-bisphosphatase
D. Hexokinase
Answer: D. Hexokinase

Hexokinase is involved in glycolysis, not gluconeogenesis. In the liver, glucose is released
into the bloodstream, not phosphorylated. The conversion of lactate to glucose involves
pyruvate carboxylase (pyruvate to oxaloacetate), PEPCK (oxaloacetate to PEP), and
fructose-1,6-bisphosphatase (fructose-1,6-bisphosphate to fructose-6-phosphate).

6. A patient with a genetic deficiency in medium-chain acyl-CoA dehydrogenase
(MCAD) presents with hypoketotic hypoglycemia during fasting. Which metabolic
adaptation is most impaired in this condition?
A. Increased hepatic gluconeogenesis from amino acids.
B. Increased hepatic ketogenesis from fatty acids.
C. Increased muscle protein breakdown for gluconeogenesis.
D. Increased glycogenolysis in the liver.
Answer: B. Increased hepatic ketogenesis from fatty acids.

MCAD deficiency impairs -oxidation of medium-chain fatty acids, reducing acetyl-CoA
production. This limits ketogenesis, leading to hypoketosis. The lack of fatty acid
oxidation also reduces NADH and ATP, impairing gluconeogenesis and causing
hypoglycemia. Other pathways like glycogenolysis and proteolysis are not directly
affected by the enzyme defect.




Page 4

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