Biochemistry - MCQ Practice Questions

Complete oxidation of glucose yields approximately 30-32 ATP molecules when accounting for the cost of transporting NADH across the mitochondrial membrane (P/O ratio of 2.5 for NADH and 1.5 for FADH2).

Sucrose (α-glucose + β-fructose) is a non-reducing sugar because both anomeric carbons are involved in the 1,2-glycosidic linkage, making it unable to reduce Benedict's reagent.

Fructokinase phosphorylates fructose to fructose-1-phosphate in the liver. This bypasses the rate-limiting phosphofructokinase step, making fructose metabolism less regulated.

The Cori cycle describes lactate produced in muscles during anaerobic glycolysis being transported to the liver where it is converted back to glucose via gluconeogenesis, which is then returned to muscles.

Ethanol metabolism consumes NAD+, reducing the NAD+/NADH ratio. This inhibits NAD+-dependent dehydrogenases including those in gluconeogenesis and lactate oxidation, leading to lactate accumulation.

Glucuronic acid, derived from glucose, is a key component of glycosaminoglycans like heparin, hyaluronic acid, and chondroitin sulfate, providing their acidic properties.

Through the non-oxidative phase of the pentose phosphate pathway, sugars are rearranged to produce fructose-6-phosphate and glyceraldehyde-3-phosphate, which directly enter glycolysis.

Essential fructosuria results from fructokinase deficiency. It is benign because fructose is simply excreted in urine without accumulating in tissues or causing metabolic harm.

G6Pase is the final enzyme in both gluconeogenesis and glycogenolysis. Its deficiency traps glucose-6-phosphate, forcing it through glycolysis and the pentose phosphate pathway, increasing pyruvate and lactate production.

Sedoheptulose is a seven-carbon ketose (heptose) that participates in the non-oxidative phase of the pentose phosphate pathway.

Glycogen synthase catalyzes the transfer of glucose from UDP-glucose to the C4-OH group of the terminal glucose in glycogen, forming α-1,4-glycosidic bonds.

Muscle phosphorylase deficiency prevents glycogen breakdown, depriving muscles of glucose-1-phosphate during exercise, causing severe energy crisis, fatigue, cramps, and myoglobinuria.

Phosphofructokinase-1 (PFK-1) is the rate-limiting enzyme of glycolysis. It is inhibited by ATP and citrate (signals of sufficient energy) and activated by AMP and ADP (signals of energy depletion).

GLUT4 is the insulin-responsive glucose transporter present in skeletal muscle and adipose tissue. Insulin signaling causes GLUT4 translocation to the cell membrane, increasing glucose uptake.

After liver glycogen is depleted (8-12 hours), gluconeogenesis becomes the primary source of glucose. The substrates are amino acids (from muscle proteolysis) and glycerol (from lipolysis).

While this is primarily a hemoglobin question, HbF (with γ-chains instead of β-chains) does not polymerize like HbS or aggregate like HbC, reducing hemolysis and RBC sickling/crystallization.

Mannose differs from glucose only at the C2 position (the configuration of the -OH group and -H). Therefore, mannose is the C2 epimer of glucose.

Transketolase requires thiamine pyrophosphate (TPP/vitamin B1) as a cofactor to transfer 2-carbon ketol groups between sugar phosphates in the non-oxidative phase of the pentose phosphate pathway.

In Pompe disease, acid α-glucosidase deficiency prevents lysosomal glycogen hydrolysis. Normally structured glycogen accumulates in lysosomes (unlike the abnormal structures seen in Type IV GSD), causing lysosomal dysfunction and cellular damage.

PFK-1 catalyzes the phosphorylation of fructose-6-phosphate to fructose-1,6-bisphosphate and is the rate-limiting enzyme of glycolysis. It is negatively regulated by ATP and citrate, making it a key control point.