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BIOCHEM 210 MODULE 7 EXAM 2026/2027 | Portage Learning Complete Questions and Answers | Biochemistry Latest | Pass Guaranteed - A+ Graded

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Ace the BioChem 210 Module 7 Exam with this comprehensive 2026/2027 guide for Portage Learning featuring complete questions and answers. This A+ Graded resource covers all key biochemistry domains including metabolic pathways, carbohydrate metabolism, glycolysis, gluconeogenesis, citric acid cycle, oxidative phosphorylation, lipid metabolism, amino acid metabolism, and enzyme regulation. Each answer includes thorough rationales to reinforce understanding of complex biochemical processes and clinical correlations. Perfect for Portage Learning students seeking first-attempt success on their Biochemistry Module 7 exam. With our Pass Guarantee, you can confidently achieve top scores. Download your complete BioChem 210 Module 7 Exam guide instantly!

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BIOCHEM 210 MODULE 7 EXAM 2026/2027 | Portage
Learning Complete Questions and Answers |
Biochemistry Latest | Pass Guaranteed - A+ Graded



Section 1: Metabolic Pathways & Integration - Module 7 Core

Question 1

A 42-year-old patient presents with chronic alcoholism and elevated lactate levels. The
physician explains that excess NADH from ethanol metabolism inhibits pyruvate
dehydrogenase complex (PDC), causing pyruvate to be diverted toward lactate rather
than acetyl-CoA. Which metabolic consequence directly results from this PDC
inhibition?

A. Increased flux through the TCA cycle due to acetyl-CoA accumulation [INCORRECT]
B. Decreased gluconeogenesis from lactate due to pyruvate depletion [INCORRECT]
C. Accumulation of lactate and decreased acetyl-CoA production for the TCA cycle
[CORRECT]
D. Enhanced ketogenesis in the liver due to excess pyruvate availability [INCORRECT]

Rationale: When PDC is inhibited by high NADH/NAD+ ratio, pyruvate cannot be
converted to acetyl-CoA and instead accumulates, favoring lactate dehydrogenase
activity. This reduces acetyl-CoA entering the TCA cycle and impairs oxidative
metabolism. Option A is wrong because acetyl-CoA production decreases, not
increases. Option B reverses the problem—lactate accumulates rather than being
consumed. Option D is incorrect because ketogenesis requires acetyl-CoA from fatty
acid oxidation, not pyruvate.

,Correct Answer: C



Question 2

During a marathon, a runner's skeletal muscle switches from predominantly aerobic to
anaerobic metabolism. Which combination of metabolic changes occurs
simultaneously in the active muscle during this transition?

A. Decreased NADH, increased pyruvate carboxylase activity, and enhanced fatty acid
oxidation [INCORRECT]
B. Increased lactate dehydrogenase activity, decreased mitochondrial ATP production,
and elevated NADH/NAD+ ratio [CORRECT]
C. Enhanced pyruvate dehydrogenase complex activity, decreased lactate production,
and increased citrate synthase flux [INCORRECT]
D. Decreased phosphofructokinase-1 activity, increased gluconeogenic flux, and
reduced glycogenolysis [INCORRECT]

Rationale: Anaerobic conditions in exercising muscle generate NADH faster than the
electron transport chain can reoxidize it, raising the NADH/NAD+ ratio. This drives
lactate dehydrogenase to reduce pyruvate to lactate, regenerating NAD+ for continued
glycolysis. Mitochondrial ATP production decreases due to oxygen limitation. Option A
is incorrect because pyruvate carboxylase is gluconeogenic (liver/kidney only) and fatty
acid oxidation requires oxygen. Option C describes aerobic conditions. Option D
incorrectly suggests decreased PFK-1 activity when anaerobic glycolysis actually
increases flux through this rate-limiting step.

Correct Answer: B



Question 3

,A patient with type 2 diabetes exhibits fasting hyperglycemia despite normal glucagon
levels. Analysis reveals excessive hepatic glucose output. Which metabolic pathway
integration defect best explains this finding?

A. Excessive muscle glycogenolysis releasing glucose into circulation [INCORRECT]
B. Insulin resistance causing uninhibited hepatic gluconeogenesis and glycogenolysis
[CORRECT]
C. Impaired pancreatic beta-cell glucagon secretion [INCORRECT]
D. Decreased adipose tissue lipolysis reducing glycerol substrate for gluconeogenesis
[INCORRECT]

Rationale: In type 2 diabetes, insulin resistance prevents normal suppression of hepatic
glucose production. Without insulin signaling, the liver continues gluconeogenesis
(using amino acids, glycerol, lactate) and glycogenolysis despite fasting hyperglycemia.
Option A is incorrect because muscle lacks glucose-6-phosphatase and cannot release
free glucose. Option C contradicts the question (glucagon levels are normal). Option D
describes the opposite of what occurs—insulin resistance typically increases lipolysis,
providing more glycerol for gluconeogenesis.

Correct Answer: B



Question 4

In the fed state, which tissue-specific metabolic specialization allows the liver to
maintain blood glucose homeostasis while simultaneously storing excess carbohydrate
energy?

A. Exclusive expression of hexokinase IV (glucokinase) with high Km and lack of
glucose-6-phosphatase [INCORRECT]
B. Expression of both glucokinase (high Km) and glucose-6-phosphatase, enabling
glucose uptake and release [CORRECT]
C. Absence of pyruvate kinase and exclusive reliance on gluconeogenesis [INCORRECT]

, D. Expression of muscle-type phosphofructokinase-1 with allosteric regulation by AMP
[INCORRECT]

Rationale: The liver uniquely expresses both glucokinase (high Km allows
phosphorylation only when glucose is abundant) and glucose-6-phosphatase (enables
glucose release via gluconeogenesis/glycogenolysis). This dual capacity allows hepatic
glucose buffering—taking up glucose when blood levels are high and releasing it during
fasting. Option A is wrong because the liver DOES express glucose-6-phosphatase.
Option C is incorrect as the liver actively performs glycolysis in the fed state. Option D
describes muscle PFK-1 regulation, not liver.

Correct Answer: B



Question 5

A 28-year-old female presents with exercise intolerance, muscle cramps, and
myoglobinuria after intense exercise. A muscle biopsy reveals absence of
myophosphorylase activity. Which metabolic intermediate accumulates in her muscle
tissue during attempted glycogenolysis?

A. Free glucose [INCORRECT]
B. Glycogen with normal structure [INCORRECT]
C. Glucose-6-phosphate [INCORRECT]
D. Glycogen with short outer chains (limit dextrin accumulation) [CORRECT]

Rationale: McArdle disease (myophosphorylase deficiency) prevents glycogen
breakdown to glucose-1-phosphate. Glycogen phosphorylase cleaves α-1,4-glycosidic
bonds until reaching four glucose residues from branch points. Without this enzyme,
glycogen accumulates with abnormally short outer chains (limit dextrins). Option A is
incorrect because muscle cannot generate free glucose (lacks glucose-6-phosphatase).

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