Acids & Membranes | Geneva College / Portage Learning |
Verified Q&A | Pass Guaranteed - A+ Graded
Q1: Which enzyme catalyzes the first committed step of glycolysis and is the primary
site of allosteric regulation?
A. Hexokinase
B. Phosphofructokinase-1 (PFK-1)
C. Pyruvate kinase
D. Phosphoglucose isomerase
Correct Answer: B
Rationale: Phosphofructokinase-1 (PFK-1) catalyzes the phosphorylation of
fructose-6-phosphate to fructose-1,6-bisphosphate, the first irreversible step unique to
glycolysis. This is the major control point regulated by ATP/AMP ratios, citrate, and
hormonal signals. Hexokinase (A) catalyzes glucose → glucose-6-phosphate but is not
the committed step (G6P can enter multiple pathways). Pyruvate kinase (C) regulates
the final step but is not the first committed step. Phosphoglucose isomerase (D)
catalyzes a reversible isomerization with no regulatory significance.
Q2: A patient with Von Gierke's disease (Type I glycogen storage disease) presents with
hepatomegaly and severe fasting hypoglycemia. Which enzyme deficiency causes this
disorder?
A. Glycogen phosphorylase
,B. Glucose-6-phosphatase
C. α-1,4-Glucosidase (acid maltase)
D. Glycogen synthase
Correct Answer: B
Rationale: Von Gierke's disease results from glucose-6-phosphatase deficiency,
preventing liver export of glucose from either glycogenolysis or gluconeogenesis.
Glucose-6-phosphate cannot be dephosphorylated, trapping glucose in the liver.
Glycogen phosphorylase deficiency (A) causes McArdle's disease (Type V) with muscle
symptoms but no hypoglycemia. Acid maltase deficiency (C) causes Pompe's disease
(Type II) with cardiac and muscle involvement. Glycogen synthase deficiency (D) would
impair glycogen synthesis, not cause hepatomegaly.
Q3: In the fed state, insulin signaling leads to which of the following metabolic effects?
A. Activation of glycogen phosphorylase via dephosphorylation
B. Inhibition of acetyl-CoA carboxylase
C. Activation of phosphofructokinase-2 (PFK-2) leading to increased
fructose-2,6-bisphosphate
D. Stimulation of hormone-sensitive lipase
Correct Answer: C
Rationale: Insulin activates PFK-2 (via dephosphorylation), increasing
fructose-2,6-bisphosphate, the most potent allosteric activator of PFK-1 and inhibitor of
fructose-1,6-bisphosphatase, thereby stimulating glycolysis and inhibiting
, gluconeogenesis. Insulin inactivates glycogen phosphorylase (A) via
dephosphorylation. Insulin activates (not inhibits) acetyl-CoA carboxylase (B) for fatty
acid synthesis. Insulin inhibits hormone-sensitive lipase (D), preventing lipolysis.
Q4: Which of the following is a characteristic feature of the pentose phosphate pathway
(PPP)?
A. It generates ATP through substrate-level phosphorylation
B. It produces NADPH and ribose-5-phosphate for biosynthesis
C. It is active only in the fed state when glycolysis is high
D. It converts glucose directly to pyruvate without intermediates
Correct Answer: B
Rationale: The PPP generates NADPH for reductive biosynthesis (fatty acids,
cholesterol) and antioxidant defense (glutathione reduction), plus ribose-5-phosphate
for nucleotide synthesis. No ATP is produced (A). The PPP operates in all metabolic
states, especially in tissues with high biosynthetic needs (liver, adipose, adrenal cortex,
RBCs) regardless of fed/fasted status (C). Glucose is not converted directly to pyruvate
(D)—the PPP branches from glycolysis at glucose-6-phosphate.
Q5: Which reaction is unique to gluconeogenesis and represents a thermodynamic
bypass of an irreversible glycolytic step?
A. Glucose-6-phosphate → Fructose-6-phosphate
B. Oxaloacetate → Phosphoenolpyruvate (via PEP carboxykinase)
C. 1,3-Bisphosphoglycerate → 3-Phosphoglycerate