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BI3.1-6 | Chemistry and Metabolism of Carbohydrates — Gate Quiz
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Glucose is an aldohexose. Which term correctly describes fructose?
Correct! Fructose has 6 carbons (hexose) and a ketone group at C-2 (keto), making it a ketohexose.
Monosaccharides are classified by number of carbons (triose=3, pentose=5, hexose=6) and carbonyl group type (aldose=aldehyde at C1, ketose=ketone at C2). Ribose = aldopentose. Fructose = ketohexose.
Incorrect. Fructose has 6 carbons and a ketone group — it is a ketohexose.
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Which enzyme catalyzes the rate-limiting (committed) step of glycolysis?
Correct! PFK-1 catalyzes the irreversible phosphorylation of fructose-6-phosphate to fructose-1,6-bisphosphate. This is the rate-limiting, committed step of glycolysis.
Three irreversible steps of glycolysis: Hexokinase, PFK-1 (rate-limiting), Pyruvate kinase. PFK-1 is regulated by ATP, AMP, citrate, and fructose-2,6-bisphosphate.
Incorrect. PFK-1 is the key regulatory enzyme and rate-limiting step of glycolysis.
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Starting from one molecule of glucose, how many net ATP molecules are produced by substrate-level phosphorylation during glycolysis?
Correct! Glycolysis produces 4 ATP but consumes 2 ATP in the investment phase. Net yield = 4 - 2 = 2 ATP per glucose.
Glycolysis energy accounting: Investment phase uses 2 ATP. Payoff phase generates 4 ATP + 2 NADH. Net: +2 ATP, +2 NADH, +2 pyruvate.
Incorrect. 4 ATP are produced but 2 are consumed (investment phase), giving a net of 2 ATP.
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Which step of the TCA cycle produces GTP directly by substrate-level phosphorylation?
Correct! The succinyl-CoA synthetase reaction (succinyl-CoA to succinate) produces GTP directly. This is the only substrate-level phosphorylation in the TCA cycle.
TCA cycle substrate-level phosphorylation: succinyl-CoA + Pi + GDP to succinate + GTP + CoA. GTP is interconverted with ATP by nucleoside diphosphate kinase.
Incorrect. Succinyl-CoA to succinate (succinyl-CoA synthetase) is the only substrate-level phosphorylation in the TCA cycle.
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A nutritionally deficient patient has thiamine (vitamin B1) deficiency. Which enzyme complex is most critically impaired, leading to accumulation of pyruvate and lactate?
Correct! Pyruvate dehydrogenase complex (PDC) requires thiamine pyrophosphate (TPP). In B1 deficiency, PDC is impaired, pyruvate accumulates, and is converted to lactate causing lactic acidosis.
PDC cofactors: TPP (B1), lipoate, FAD (B2), NAD+ (B3), CoA (pantothenate). B1 deficiency causes pyruvate accumulation and beriberi. Wernicke encephalopathy in alcoholics is also due to B1 deficiency.
Incorrect. Pyruvate dehydrogenase requires thiamine pyrophosphate (TPP).
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UDP-glucose is the activated glucose used in glycogen synthesis. Which enzyme transfers glucose from UDP-glucose to the growing glycogen chain?
Correct! Glycogen synthase adds glucose from UDP-glucose to the non-reducing end, forming alpha-1,4 glycosidic bonds.
Glycogen synthesis: Glycogenin (primer) then glycogen synthase (extends alpha-1,4 chains) then branching enzyme (creates alpha-1,6 branches). Stored in liver (blood glucose regulation) and muscle (local energy).
Incorrect. Glycogen synthase is the key enzyme that extends the glycogen chain using UDP-glucose.
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A 6-month-old infant presents with severe hypoglycaemia, hepatomegaly, and lactic acidosis. Blood glucose does not rise after glucagon injection. Which enzyme deficiency is most likely?
Correct! Von Gierke disease (Type I GSD) is due to glucose-6-phosphatase deficiency. Glycogenolysis and gluconeogenesis both produce glucose-6-phosphate, which cannot be converted to free glucose — hence no response to glucagon.
Von Gierke: G6Pase deficiency, Type I GSD; hypoglycaemia, hepatomegaly, lactic acidosis, hyperuricaemia, hyperlipidaemia. No response to glucagon or epinephrine. Treatment: frequent feeds, cornstarch.
Incorrect. Von Gierke disease (G6Pase deficiency) causes severe hypoglycaemia with no response to glucagon because the final step of glucose release is blocked.
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The hexose monophosphate (HMP) shunt pathway is the primary source of which essential molecules?
Correct! The HMP shunt produces NADPH (for reductive biosynthesis and antioxidant defence) and ribose-5-phosphate (for nucleotide synthesis).
HMP shunt functions: NADPH for fatty acid synthesis, steroid synthesis, glutathione reduction in RBCs; Ribose-5-phosphate for nucleotide synthesis. G6PD deficiency causes haemolytic anaemia with oxidative stress.
Incorrect. The HMP pathway specifically produces NADPH and ribose-5-phosphate.
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During prolonged fasting, which of the following substrates CANNOT be used for gluconeogenesis in humans?
Correct! Acetyl-CoA from fatty acid beta-oxidation cannot be converted to glucose in humans because the pyruvate dehydrogenase reaction is irreversible and there is no net synthesis of oxaloacetate from acetyl-CoA.
Gluconeogenic substrates: Lactate (Cori cycle), Glycerol (from triglyceride breakdown), Glucogenic amino acids. NOT acetyl-CoA. This explains why protein is broken down for glucose during starvation, not fat.
Incorrect. Acetyl-CoA from fatty acids cannot contribute net carbons to gluconeogenesis.
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During intense exercise, skeletal muscle produces large amounts of lactate. This lactate travels to the liver for gluconeogenesis, which then releases glucose back to muscle. This metabolic cooperation is called:
Correct! The Cori cycle describes the metabolic shuttle of lactate from muscle to liver and glucose from liver back to muscle.
Cori cycle: Muscle produces lactate (anaerobic glycolysis) which travels to liver for gluconeogenesis, and glucose returns to muscle. Net: 2 lactate + 6 ATP (liver) = 1 glucose. Regenerates NAD+ in muscle.
Incorrect. The Cori cycle describes lactate-glucose shuttling between muscle and liver.
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