Q. ATP yield per acetyl-CoA in TCA cycle?
A. 10 ATP equivalents
Footnote: 3 NADH (7.5) + 1 FADH₂ (1.5) + 1 GTP (1)
Q. Committed step of gluconeogenesis?
The committed step is the conversion of fructose‑1,6‑bisphosphate to fructose‑6‑phosphate, catalyzed by fructose‑1,6‑bisphosphatase (FBPase‑1).
- Irreversible hydrolysis reaction.
- Unique to gluconeogenesis (cannot be diverted to other pathways).
Q. GLUT-4 is present in which tissues?
A. Skeletal muscle and adipose tissue
Footnote: Insulin-dependent transporter. Neurons use GLUT-3.
Q. Kinetics of allosteric enzymes?
A. Sigmoidal curve
Footnote: Cooperative substrate binding. Zero-order kinetics applies to saturated enzymes (e.g., ethanol).
Q. Enzyme deficient in classic homocystinuria?
A. Cystathionine β-synthase
Footnote: ↑ Homocysteine → thrombosis, downward lens dislocation, marfanoid habitus.
Q. Site of ketone body synthesis?
A. Liver mitochondria
Footnote: Only liver has HMG-CoA lyase. Liver exports but cannot use ketones.
Q. Major circulating ketone body?
A. β-hydroxybutyrate
Footnote: Predominates over acetoacetate during fasting and DKA.
Neurotoxic metabolite in PKU?
A. Phenylpyruvate
Footnote:
Phenylpyruvate is a ketoacid that accumulates in phenylketonuria (PKU) due to deficiency of phenylalanine hydroxylase (or BH₄ cofactor).
Causes intellectual disability and seizures.
- ↑ Homogentisic acid → alkaptonuria (black urine, ochronosis, arthritis). .
Q. Transketolase cofactor?
A. Thiamine (Vitamin B1)
Footnote: Key enzyme of HMP shunt → NADPH production.
Q. Cell most dependent on HMP shunt?
A. RBC
Footnote: No mitochondria; needs NADPH to maintain reduced glutathione.
Q. Amino acid deficiency causing fatty liver?
A. Methionine
Footnote: Required for apoprotein synthesis → triglyceride export.
Q. Effect of xanthine oxidase inhibition?
A. Decreased uric acid formation
Footnote: Basis of allopurinol therapy in gout
