I have quiz competition in vitro in our class only about the topic carbohydrate metabolism, MBBS first year biochemistry. So I want every possible quiz questions about carbohydrate metabolism now. Every possible.

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I now have enough comprehensive textbook material. Let me compile the complete quiz set now.

Here is your complete, exhaustive quiz on Carbohydrate Metabolism for MBBS First Year Biochemistry, organized by topic with answers and explanations.

🧪 COMPLETE QUIZ - CARBOHYDRATE METABOLISM

MBBS First Year Biochemistry

SECTION 1: GLUCOSE TRANSPORTERS (GLUTs)

Q1. Which GLUT transporter is found in most tissues and responsible for basal glucose uptake? A. GLUT-1 (Km ~1 mM; also found in brain, RBCs, blood-brain barrier)

Q2. GLUT-2 is found in which organs? A. Liver, kidneys, pancreatic β-cells. It has a HIGH Km (15-20 mM), so it only transports glucose when blood glucose is elevated.

Q3. Which GLUT transporter is insulin-sensitive? A. GLUT-4 - found in skeletal muscle and adipose tissue. Insulin increases the number of GLUT-4 transporters on cell surfaces.

Q4. Which GLUT primarily transports fructose (not glucose)? A. GLUT-5 - in small intestine and testes.

Q5. What type of transport do GLUT transporters use? A. Facilitated diffusion - passive, no energy required, down concentration gradient. They are uniporters (transport one molecule at a time).

Q6. The sodium-dependent glucose cotransporter (SGLT) is found where? A. Intestinal epithelial cells, renal tubules, and choroid plexus. It transports glucose AGAINST its concentration gradient using the Na+ electrochemical gradient (secondary active transport).

Q7. SGLT-2 inhibitors (e.g., dapagliflozin) work by blocking glucose reabsorption in which part of the kidney? A. Proximal convoluted tubule (PCT).

Q8. Why does glucokinase phosphorylate glucose only when blood glucose is high? A. Glucokinase has a HIGH Km for glucose (~10 mM) and shows a sigmoidal reaction curve. It is not subject to product inhibition by glucose 6-phosphate.

Q9. Hexokinase vs Glucokinase - key difference? A. Hexokinase: low Km (high affinity), product-inhibited by G-6-P, found in most tissues. Glucokinase: high Km, sigmoidal kinetics, not inhibited by G-6-P, found in liver and pancreatic β-cells. Glucokinase acts as a "glucose sensor" in the pancreas.

SECTION 2: GLYCOLYSIS - THE 10 STEPS

Q10. What is the overall equation for anaerobic glycolysis? A. Glucose + 2 ADP + 2 Pi → 2 Lactate + 2 ATP + 2 H2O

Q11. Name the 3 irreversible (regulated) steps of glycolysis with their enzymes: A.

Glucose → Glucose 6-phosphate (Glucokinase/Hexokinase)
Fructose 6-phosphate → Fructose 1,6-bisphosphate (Phosphofructokinase-1, PFK-1)
Phosphoenolpyruvate → Pyruvate (Pyruvate kinase)

Q12. What is the rate-limiting (pace-setting) enzyme of glycolysis? A. Phosphofructokinase-1 (PFK-1) - the most important regulatory enzyme.

Q13. What are the allosteric ACTIVATORS of PFK-1? A. AMP, ADP, Fructose 2,6-bisphosphate (most potent), Pi (inorganic phosphate)

Q14. What are the allosteric INHIBITORS of PFK-1? A. ATP (high energy charge), Citrate (signals TCA cycle is full), H+ (acidosis)

Q15. Which enzyme produces Fructose 2,6-bisphosphate (F-2,6-BP)? A. Phosphofructokinase-2 (PFK-2). It is a bifunctional enzyme with both kinase and phosphatase activity. Insulin activates PFK-2; glucagon inhibits it.

Q16. What is the net ATP yield from anaerobic glycolysis? A. 2 ATP per molecule of glucose. (2 ATPs consumed in the "investment phase"; 4 ATPs produced in "payoff phase" = net 2 ATP)

Q17. What is the net ATP yield from aerobic glycolysis (glycolysis alone, not including TCA)? A. 2 ATP + 2 NADH per glucose molecule. The NADH is later oxidized by the ETC for more ATP.

Q18. Which steps of glycolysis produce ATP by substrate-level phosphorylation? A. Step 7: 1,3-BPG → 3-phosphoglycerate (phosphoglycerate kinase) and Step 10: PEP → Pyruvate (pyruvate kinase). Each step occurs twice per glucose.

Q19. Which step of glycolysis produces NADH? A. Step 6: Glyceraldehyde 3-phosphate → 1,3-BPG by glyceraldehyde 3-phosphate dehydrogenase (GAPDH), using NAD+.

Q20. What enzyme catalyzes the aldol cleavage of Fructose 1,6-bisphosphate? A. Aldolase - produces Glyceraldehyde 3-phosphate (G3P) and Dihydroxyacetone phosphate (DHAP).

Q21. DHAP is converted to G3P by which enzyme? A. Triose phosphate isomerase (TPI). Deficiency causes hemolytic anemia.

Q22. What is the enzyme deficiency in Pyruvate Kinase (PK) deficiency? A. Pyruvate kinase - causes hemolytic anemia because RBCs rely solely on glycolysis for ATP. Low ATP → RBC membrane pump failure → hemolysis.

Q23. What is the Pasteur effect? A. Inhibition of glycolysis (and fermentation) by oxygen. When O2 is present, cells use oxidative phosphorylation, producing more ATP, which inhibits PFK-1.

Q24. What is the Warburg effect? A. Cancer cells preferentially use aerobic glycolysis (glucose → lactate even in the presence of O2). This produces lactate despite adequate oxygen - used for biosynthetic precursors.

Q25. In red blood cells (RBCs), what is the significance of the Rapoport-Luebering shunt? A. 1,3-BPG is converted to 2,3-BPG (2,3-bisphosphoglycerate) by BPG mutase, bypassing ATP production. 2,3-BPG decreases the oxygen affinity of hemoglobin (shifts O2 dissociation curve right).

Q26. Arsenic poisoning inhibits glycolysis at which step? A. Step 6 - GAPDH. Arsenate (AsO4³⁻) acts as an analog of inorganic phosphate, forming 1-arseno-3-phosphoglycerate which spontaneously hydrolyzes, uncoupling substrate-level phosphorylation. Net ATP from glycolysis becomes 0.

Q27. Fluoride inhibits which enzyme of glycolysis? A. Enolase (Step 9). Fluoride forms fluorophosphate which inhibits enolase. This is why fluoride is added to blood collection tubes to prevent glycolysis in blood samples.

Q28. Iodoacetate inhibits which enzyme of glycolysis? A. GAPDH (Glyceraldehyde-3-phosphate dehydrogenase) - it alkylates the active site cysteine residue.

SECTION 3: PYRUVATE DEHYDROGENASE COMPLEX (PDH Complex)

Q29. What is the overall reaction of the PDH complex? A. Pyruvate + CoA + NAD+ → Acetyl CoA + CO2 + NADH (oxidative decarboxylation)

Q30. Name the 5 cofactors (vitamins) required by the PDH complex: A.

TPP (Thiamine pyrophosphate) - Vitamin B1 (thiamine)
Lipoic acid (lipoamide)
CoA (Coenzyme A) - Pantothenic acid (Vitamin B5)
FAD - Riboflavin (Vitamin B2)
NAD+ - Niacin (Vitamin B3)

Mnemonic: "The Lovely Coenzyme For NAD" → TPP, Lipoate, CoA, FAD, NAD+

Q31. Name the 3 enzyme components of the PDH complex: A.

E1: Pyruvate dehydrogenase (uses TPP)
E2: Dihydrolipoyl transacetylase (uses lipoic acid and CoA)
E3: Dihydrolipoyl dehydrogenase (uses FAD and NAD+)

Q32. How is the PDH complex regulated? A.

Activated by: Ca²+, NAD+/CoA (substrates), AMP/ADP (low energy), pyruvate (via PDH phosphatase)
Inhibited by: NADH, Acetyl CoA, ATP (products), PDH kinase phosphorylates and INACTIVATES E1

Q33. PDH kinase is activated by which molecules? A. NADH, Acetyl CoA, ATP - i.e., when energy is abundant, PDH is turned OFF.

Q34. PDH phosphatase is activated by what? A. Ca²+ and Mg²+. This turns PDH ON (active dephosphorylated form).

Q35. Pyruvate dehydrogenase deficiency causes what condition? A. Lactic acidosis + neurological defects (because Acetyl CoA cannot be made from pyruvate; brain depends on acetyl CoA for energy). Treated with ketogenic diet (provides acetyl CoA from fat). Can occur due to thiamine (B1) deficiency.

Q36. Arsenic (specifically arsenite, As³+) inhibits which components of the PDH complex? A. E2 (Dihydrolipoyl transacetylase) - arsenite binds to the lipoic acid cofactor (dithiol groups).

SECTION 4: TCA CYCLE (KREBS CYCLE / CITRIC ACID CYCLE)

Q37. Where does the TCA cycle take place? A. Mitochondrial matrix (entirely within mitochondria).

Q38. What molecules enter the TCA cycle, and what are the products per turn? A. Per turn: 1 Acetyl CoA enters; 2 CO2, 3 NADH, 1 FADH2, 1 GTP produced; Oxaloacetate is regenerated.

Q39. Name all 8 intermediates of the TCA cycle in order: A.

Oxaloacetate (OAA, 4C)
Citrate (6C)
Isocitrate (6C)
α-Ketoglutarate (α-KG, 5C)
Succinyl CoA (4C)
Succinate (4C)
Fumarate (4C)
Malate (4C) → back to OAA

Mnemonic: "Can I Keep Selling Stuff For Money?" → Citrate, Isocitrate, α-Ketoglutarate, Succinyl CoA, Succinate, Fumarate, Malate

Q40. Which enzyme condenses Acetyl CoA with OAA to form Citrate? A. Citrate synthase (regulated by ATP, NADH, succinyl CoA - inhibited by these)

Q41. Which TCA enzyme catalyzes the rate-limiting step? A. Isocitrate dehydrogenase (isocitrate → α-ketoglutarate + CO2). Activated by ADP and Ca²+; inhibited by ATP and NADH.

Q42. Which two steps in the TCA cycle produce CO2? A.

Isocitrate → α-Ketoglutarate (by isocitrate dehydrogenase)
α-Ketoglutarate → Succinyl CoA (by α-ketoglutarate dehydrogenase complex)

Q43. α-Ketoglutarate dehydrogenase complex requires the same cofactors as which other complex? A. PDH complex - same 5 cofactors (TPP, Lipoic acid, CoA, FAD, NAD+).

Q44. Which TCA cycle step produces GTP (or ATP) directly by substrate-level phosphorylation? A. Succinyl CoA → Succinate, by succinyl CoA synthetase.

Q45. Which TCA enzyme uses FAD (produces FADH2)? A. Succinate dehydrogenase (succinate → fumarate). This is also Complex II of the ETC. It is embedded in the inner mitochondrial membrane.

Q46. What inhibits succinate dehydrogenase competitively? A. Malonate (a structural analog of succinate) - classic example of competitive inhibition.

Q47. What is the total ATP yield from one turn of the TCA cycle (per acetyl CoA)? A. 10 ATP: 3 NADH × 2.5 = 7.5 + 1 FADH2 × 1.5 = 1.5 + 1 GTP = 1 → total ~10 ATP

Q48. What is the total ATP yield from complete oxidation of ONE molecule of glucose? A. ~30-32 ATP (using P/O ratios of 2.5 for NADH and 1.5 for FADH2)

Glycolysis: 2 ATP + 2 NADH (cytoplasmic)
PDH: 2 NADH (mitochondrial)
TCA × 2: 6 NADH + 2 FADH2 + 2 GTP

Q49. What are anaplerotic reactions? Give examples. A. Reactions that replenish TCA cycle intermediates:

Pyruvate carboxylase: Pyruvate + CO2 → OAA (requires biotin, ATP) - major anaplerotic reaction
Transamination reactions: amino acids → TCA intermediates
Glutamate → α-ketoglutarate

Q50. Pyruvate carboxylase requires which vitamin as cofactor? A. Biotin (Vitamin B7). Activated by Acetyl CoA (allosteric). Occurs in mitochondria.

Q51. What is the role of the TCA cycle beyond energy production? A. Provides precursors for: gluconeogenesis (OAA), amino acid synthesis (α-KG, OAA), heme synthesis (succinyl CoA), fatty acid synthesis (citrate exported to cytoplasm), nucleotide synthesis (via NADH/NADPH).

Q52. Fluoroacetate (rat poison) inhibits which TCA enzyme? A. Aconitase. Fluoroacetate is converted to fluorocitrate which inhibits aconitase, blocking conversion of citrate to isocitrate. Citrate accumulates.

SECTION 5: GLUCONEOGENESIS

Q53. What is gluconeogenesis? A. Synthesis of glucose from non-carbohydrate precursors. Occurs mainly in the liver (~90% of overnight fasting) and kidneys (~10%). During prolonged fasting (>48 hrs), kidneys contribute ~40%.

Q54. What are the main gluconeogenic precursors? A.

Lactate (most important - from RBCs and exercising muscle)
Glycerol (from fat/TAG hydrolysis in adipose tissue)
Glucogenic amino acids (e.g., alanine - most important AA precursor)
Odd-chain fatty acid propionate (via succinyl CoA)

Q55. Which amino acids are purely KETOGENIC (cannot be used for gluconeogenesis)? A. Only Leucine and Lysine - purely ketogenic. (Mnemonic: "Lean Kids" = Leucine, Lysine)

Q56. What are the 4 unique (bypass) enzymes of gluconeogenesis (bypassing irreversible glycolytic steps)? A.

Pyruvate carboxylase (Pyruvate → OAA) - mitochondrial, requires Biotin
PEPCK (Phosphoenolpyruvate carboxykinase): OAA → PEP + CO2 - requires GTP
Fructose 1,6-bisphosphatase (F-1,6-BP → F-6-P) - cytosolic; inhibited by AMP and F-2,6-BP
Glucose 6-phosphatase (G-6-P → Glucose) - in ER of liver, kidneys, small intestine

Q57. Where is Glucose 6-phosphatase located? A. Endoplasmic reticulum (ER) of liver, kidney cortex, and small intestinal epithelium. Absent in muscle and brain (cannot release free glucose into blood).

Q58. What is the Cori cycle? A. Lactate produced by RBCs and exercising muscle is transported to the liver → converted to glucose by gluconeogenesis → glucose released back into blood → used by muscle/RBCs. It transfers metabolic burden from muscle to liver.

Q59. What is the glucose-alanine cycle? A. Alanine produced in muscle from pyruvate + amino acid nitrogen (transamination) is transported to liver → alanine converted back to pyruvate → gluconeogenesis → glucose returned to muscle. Transfers nitrogen from muscle to liver for urea synthesis.

Q60. What activates and inhibits Fructose 1,6-bisphosphatase? A.

Activated by: ATP, Citrate
Inhibited by: AMP, Fructose 2,6-bisphosphate (F-2,6-BP) - same signal that activates PFK-1

Q61. Glucagon promotes gluconeogenesis by what mechanism? A. Glucagon → cAMP → PKA → phosphorylates PFK-2/FBPase-2 → reduces F-2,6-BP → inhibits PFK-1 AND relieves inhibition of FBPase-1 → net shift toward gluconeogenesis.

Q62. Why can't muscle perform gluconeogenesis to release glucose into blood? A. Muscle lacks glucose 6-phosphatase, so it cannot convert G-6-P to free glucose for export.

SECTION 6: GLYCOGEN METABOLISM

Q63. What is glycogen? A. The storage form of glucose in animals. Stored mainly in the liver (up to ~100-120 g; lasts ~24 hrs) and skeletal muscle (~300-400 g; not released into blood). It is a highly branched polymer of glucose with α-1,4 glycosidic linkages in chains and α-1,6 linkages at branch points.

Q64. What enzyme adds glucose to the growing glycogen chain? A. Glycogen synthase - adds UDP-glucose to the non-reducing end via α-1,4 linkage.

Q65. What is the activated form of glucose used in glycogen synthesis? A. UDP-Glucose (uridine diphosphate glucose). Formed by: Glucose 1-phosphate + UTP → UDP-glucose + PPi (by UDP-glucose pyrophosphorylase).

Q66. What is the primer required for glycogen synthesis? A. Glycogenin - a self-glucosylating protein that acts as the primer. It adds the first ~8 glucose residues.

Q67. Which enzyme creates branch points in glycogen? A. Branching enzyme (α-1,4 → α-1,6 glucan transferase) - transfers a 6-7 residue segment from a chain end to form a new α-1,6 branch.

Q68. What is the first step in glycogen degradation? A. Glycogen phosphorylase cleaves α-1,4 glycosidic bonds from the non-reducing end, releasing Glucose 1-phosphate. Requires pyridoxal phosphate (PLP/Vitamin B6).

Q69. Glycogen phosphorylase stops cleaving when it reaches how many residues from a branch point? A. 4 residues (it cannot cleave closer than 4 residues from an α-1,6 branch point).

Q70. What enzyme removes glycogen branch points during degradation? A. Debranching enzyme - it has TWO activities:

Glucanotransferase activity - transfers 3 of the remaining 4 glucose residues to the main chain
α-1,6-Glucosidase activity - releases the single remaining glucose at the branch point as FREE glucose (not G-1-P)

Q71. After glycogen phosphorylase action, Glucose 1-phosphate is converted to what? A. Glucose 6-phosphate by phosphoglucomutase.

Q72. Glycogen phosphorylase is activated by what (two forms)? A.

Hormonal (covalent): Epinephrine/glucagon → cAMP → PKA → phosphorylates phosphorylase kinase → phosphorylates glycogen phosphorylase b → active phosphorylase a
Allosteric: AMP activates; ATP and G-6-P inhibit (in muscle: Ca²+ via calmodulin also activates)

Q73. How does insulin affect glycogen metabolism? A. Insulin activates protein phosphatase-1 (PP-1) → dephosphorylates glycogen synthase (activating it) AND dephosphorylates glycogen phosphorylase (inactivating it) → promotes glycogen SYNTHESIS.

Q74. What happens to blood glucose with liver glycogenolysis vs. muscle glycogenolysis? A. Liver glycogenolysis releases glucose into the blood (liver has glucose 6-phosphatase). Muscle glycogenolysis does NOT raise blood glucose (no glucose 6-phosphatase); glucose 6-phosphate enters glycolysis for muscle energy.

Q75. McArdle disease (Type V glycogen storage disease) - enzyme deficiency? A. Muscle glycogen phosphorylase deficiency. Features: exercise intolerance, painful cramps, myoglobinuria. Blood lactate does NOT rise with exercise (ischemic forearm test).

Q76. von Gierke disease (Type I GSD) - enzyme deficiency? A. Glucose 6-phosphatase deficiency (or its translocase). Features: severe fasting hypoglycemia, hepatomegaly, lactic acidosis, hyperlipidemia, hyperuricemia. "Doll-like facies."

Q77. Pompe disease (Type II GSD) - enzyme deficiency? A. Lysosomal α-1,4-glucosidase (acid maltase). Features: cardiomegaly, hypotonia, early death. Glycogen accumulates in lysosomes. Only GSD affecting the heart severely.

Q78. Cori disease (Type III GSD) - enzyme deficiency? A. Debranching enzyme (amylo-1,6-glucosidase). Features: mild hypoglycemia, hepatomegaly, accumulation of limit dextrin.

Q79. Andersen disease (Type IV GSD) - enzyme deficiency? A. Branching enzyme. Features: hepatosplenomegaly, cirrhosis.

Q80. Hers disease (Type VI GSD) - enzyme deficiency? A. Hepatic glycogen phosphorylase. Mild hypoglycemia, hepatomegaly.

SECTION 7: PENTOSE PHOSPHATE PATHWAY (HMP Shunt)

Q81. What is the main purpose of the HMP shunt? A.

Generate NADPH (for reductive biosynthesis - fatty acid synthesis, cholesterol synthesis, steroid synthesis - and for glutathione reduction)
Generate Ribose 5-phosphate (for nucleotide and nucleic acid synthesis)

Q82. Where does the pentose phosphate pathway occur? A. Cytoplasm (cytosol). Active in liver, adipose tissue, adrenal cortex, RBCs, lactating mammary gland, gonads.

Q83. What is the rate-limiting enzyme of the pentose phosphate pathway? A. Glucose 6-phosphate dehydrogenase (G6PD). NADP+ is its allosteric activator; NADPH is its inhibitor.

Q84. What are the two phases of the HMP shunt? A.

Oxidative phase (irreversible): G-6-P → Ribulose 5-P; produces 2 NADPH and 1 CO2. Enzymes: G6PD, Lactonase, 6-Phosphogluconate dehydrogenase.
Non-oxidative phase (reversible): Interconversion of 3C, 4C, 5C, 6C, 7C sugars via transketolase and transaldolase. Produces F-6-P and G-3-P (glycolytic intermediates).

Q85. G6PD deficiency causes what clinical picture? A. X-linked disorder. Episodic hemolytic anemia triggered by oxidative stress (primaquine, dapsone, fava beans, infections, naphthalene). RBCs cannot regenerate NADPH → cannot reduce glutathione → oxidative damage → Heinz body formation (denatured Hb) → bite cells on smear.

Q86. What is the role of NADPH in RBCs? A. NADPH reduces oxidized glutathione (GSSG → GSH) via glutathione reductase. GSH reduces H2O2 via glutathione peroxidase, protecting cell membranes and Hb from oxidative damage.

Q87. Transketolase requires which vitamin? A. Thiamine (Vitamin B1) - as TPP. Transketolase activity is used as a laboratory marker of thiamine status.

Q88. In which tissues does the HMP shunt operate most actively? A. Liver, adrenal cortex (steroid synthesis), lactating mammary gland, adipose tissue, RBCs.

Q89. What happens to the products (F-6-P and G-3-P) of the non-oxidative phase? A. They re-enter glycolysis, allowing the carbon from glucose to be fully oxidized to CO2 even when only NADPH is needed (not ribose 5-P).

SECTION 8: FRUCTOSE AND GALACTOSE METABOLISM

Q90. Where is fructose primarily metabolized? A. Liver (mainly), and also kidney and small intestine.

Q91. What enzyme metabolizes fructose in the liver? A. Fructokinase (not hexokinase) phosphorylates fructose to fructose 1-phosphate. Then aldolase B cleaves it to DHAP + glyceraldehyde.

Q92. What enzyme metabolizes fructose in muscle and adipose tissue? A. Hexokinase (low affinity for fructose; produces F-6-P directly).

Q93. Essential fructosuria - enzyme deficiency? A. Fructokinase deficiency. Benign condition - fructose accumulates in blood and urine. No symptoms.

Q94. Hereditary fructose intolerance (HFI) - enzyme deficiency? A. Aldolase B deficiency. Fructose 1-phosphate accumulates → severe hypoglycemia (inhibits PK and phosphorylase), vomiting, liver damage. Liver failure if untreated. Aversion to sweets develops.

Q95. Why does Aldolase B deficiency cause hypoglycemia? A. Accumulated fructose 1-phosphate inhibits:

Glycogen phosphorylase (blocks glycogenolysis)
Fructose 1,6-bisphosphatase and aldolase A (blocks gluconeogenesis)

Q96. What is the Leloir pathway (galactose metabolism)? A. Galactose → Galactose 1-P (galactokinase) → UDP-Galactose (GALT enzyme; uses UDP-glucose as donor) → UDP-Glucose (UDP-galactose 4-epimerase) → enters mainstream metabolism.

Q97. Classic galactosemia - enzyme deficiency? A. Galactose-1-phosphate uridylyltransferase (GALT) deficiency. Features: jaundice, liver cirrhosis, cataracts, E. coli sepsis in neonates, intellectual disability, ovarian failure. Gal-1-P accumulates.

Q98. Galactokinase deficiency causes what? A. Milder galactosemia - only cataracts (galactose is converted to galactitol by aldose reductase; galactitol accumulates in the lens).

Q99. What is galactitol and how does it form? A. Galactitol is the alcohol reduction product of galactose, formed by aldose reductase (alternative pathway when normal metabolism is blocked). Accumulates in lens → osmotic damage → cataracts.

Q100. What is sorbitol (glucitol) and why is it clinically relevant? A. Sorbitol is formed from glucose by aldose reductase using NADPH. In hyperglycemia (diabetes), excess sorbitol accumulates in tissues lacking sorbitol dehydrogenase (lens, peripheral nerves, retina, kidneys) → osmotic damage → diabetic cataracts, neuropathy, retinopathy, nephropathy.

SECTION 9: REGULATION OF BLOOD GLUCOSE

Q101. What is normal fasting blood glucose? A. 70-110 mg/dL (3.9-6.1 mmol/L)

Q102. What is the renal threshold for glucose? A. ~180 mg/dL (10 mmol/L). Above this, glucose appears in urine (glycosuria).

Q103. Which hormones RAISE blood glucose (counter-regulatory)? A. Glucagon, Epinephrine, Cortisol, Growth hormone, Thyroid hormone (the 4 "stress hormones" + glucagon)

Q104. What is the primary action of insulin on carbohydrate metabolism? A.

Promotes glucose uptake (via GLUT-4 in muscle/fat)
Activates glycogen synthase (promotes glycogen storage)
Activates PFK-2 → increases F-2,6-BP → activates PFK-1 (stimulates glycolysis)
Inhibits gluconeogenesis and glycogenolysis
Activates pyruvate kinase

Q105. Glucagon is secreted by which pancreatic cells? A. Alpha (α) cells of the islets of Langerhans. Acts mainly on the liver.

Q106. What is the mechanism of glucagon action on the liver? A. Glucagon → Gs → adenylyl cyclase → ↑cAMP → PKA activation → phosphorylates and activates phosphorylase kinase (activates glycogenolysis) AND inactivates glycogen synthase AND inactivates PFK-2/activates FBP-2 (reduces F-2,6-BP, inhibits glycolysis, stimulates gluconeogenesis).

Q107. What is the role of AMP/ATP ratio in regulating carbohydrate metabolism? A. Low energy (high AMP:ATP ratio) → activates AMPK (AMP-activated protein kinase) → activates PFK-1 (via F-2,6-BP), inhibits glycogen synthase, inhibits fatty acid synthesis → net effect: catabolism increases.

SECTION 10: PYRUVATE METABOLISM - FATES OF PYRUVATE

Q108. Name the 5 fates of pyruvate: A.

→ Acetyl CoA (by PDH; aerobic)
→ Lactate (by LDH; anaerobic)
→ OAA (by pyruvate carboxylase; anaplerosis/gluconeogenesis)
→ Alanine (by transamination/ALT)
→ Ethanol (in yeast only, via pyruvate decarboxylase)

Q109. Lactate dehydrogenase (LDH) reaction: A. Pyruvate + NADH + H+ ⇌ Lactate + NAD+. In anaerobic conditions, this regenerates NAD+ for continued glycolysis.

Q110. What is lactic acidosis? Causes? A. Plasma lactate >5 mmol/L + pH <7.35.

Type A: Tissue hypoxia (shock, severe anemia, CO poisoning)
Type B: No hypoxia (metformin toxicity, liver failure, malignancy, thiamine deficiency)

Q111. Metformin causes lactic acidosis by what mechanism? A. Inhibits Complex I of the ETC → impaired oxidative phosphorylation → compensatory increase in anaerobic glycolysis → lactic acid accumulation.

SECTION 11: INTEGRATION AND CLINICAL CONCEPTS

Q112. What happens metabolically during the absorptive state (after a meal)? A. Insulin dominant: glycolysis ↑, glycogen synthesis ↑, glycogenolysis ↓, gluconeogenesis ↓, fatty acid synthesis ↑, protein synthesis ↑. Liver becomes net consumer of glucose.

Q113. What happens metabolically during the post-absorptive/fasting state? A. Glucagon/epinephrine dominant: glycogenolysis ↑ (liver), gluconeogenesis ↑, glycolysis ↓, fatty acid oxidation ↑, ketone body formation ↑. Blood glucose is maintained.

Q114. Which tissues REQUIRE glucose as obligate fuel (cannot use fatty acids)? A. Brain (mainly), RBCs, renal medulla, lens and cornea of eye, testes, retina. (RBCs have no mitochondria; brain normally uses glucose but can adapt to ketones in prolonged starvation.)

Q115. Thiamine (B1) deficiency affects which enzymes? A. PDH complex, α-Ketoglutarate dehydrogenase, Transketolase (HMP shunt). Clinically: Beriberi (cardiovascular/neurological), Wernicke-Korsakoff syndrome, lactic acidosis.

Q116. What is substrate-level phosphorylation? Give examples from carbohydrate metabolism. A. Direct synthesis of ATP/GTP from a high-energy substrate (no ETC needed):

1,3-BPG → 3-PG (glycolysis; phosphoglycerate kinase)
PEP → Pyruvate (glycolysis; pyruvate kinase)
Succinyl CoA → Succinate (TCA cycle; succinyl CoA synthetase)

Q117. What is the significance of the MALATE-ASPARTATE SHUTTLE? A. Transfers reducing equivalents (NADH) from the cytoplasm into the mitochondrial matrix. Yields 2.5 ATP per cytoplasmic NADH. Used in heart, liver, kidney.

Q118. What is the GLYCEROL 3-PHOSPHATE SHUTTLE? A. Transfers cytoplasmic NADH reducing equivalents to FADH2 in the inner mitochondrial membrane. Yields only 1.5 ATP per cytoplasmic NADH. Used in brain and skeletal muscle.

Q119. Fructose 2,6-bisphosphate (F-2,6-BP) is the most important regulator of which pathways? A. It is the most potent activator of PFK-1 (glycolysis) and inhibitor of FBPase-1 (gluconeogenesis). It coordinately regulates the reciprocal relationship between glycolysis and gluconeogenesis in the liver.

Q120. In uncontrolled diabetes mellitus, why does hyperglycemia occur? A. Lack of insulin → reduced GLUT-4 mediated glucose uptake in muscle/fat → glucagon unopposed → glycogenolysis and gluconeogenesis increase → blood glucose rises. Also: decreased glycolysis, decreased glycogen synthesis.

SECTION 12: RAPID-FIRE / ONE-LINERS (HIGH YIELD FOR MCQs)

Q121. Which sugar is used as a carrier/activating nucleotide in glycogen synthesis? UDP-glucose

Q122. The enzyme that catalyzes the committed step of glycolysis? PFK-1 (phosphofructokinase-1)

Q123. Which glycolytic enzyme is inhibited by citrate? PFK-1

Q124. Which TCA intermediate inhibits PFK-1? Citrate (exported from mitochondria when energy is high)

Q125. The only purely irreversible reaction in gluconeogenesis unique to that pathway at the pyruvate level? Pyruvate carboxylase and PEPCK (two reactions needed to bypass pyruvate kinase)

Q126. PEPCK requires which cofactor? GTP (or ITP)

Q127. Pyruvate carboxylase is allosterically activated by? Acetyl CoA (signals excess acetyl CoA available)

Q128. The enzyme that phosphorylates glucose in most tissues? Hexokinase (low Km, inhibited by G-6-P)

Q129. Brain primarily uses which GLUT? GLUT-1 (blood-brain barrier) and GLUT-3 (neurons)

Q130. Which enzyme links glycolysis to the TCA cycle? Pyruvate dehydrogenase (PDH)

Q131. Which coenzyme carries acetyl groups in the TCA cycle? Coenzyme A (CoA-SH)

Q132. What is the product when citrate is exported to the cytoplasm? Citrate is cleaved by ATP citrate lyase to Acetyl CoA + OAA (for fatty acid synthesis)

Q133. Ribose 5-phosphate (for DNA/RNA synthesis) comes from which pathway? Pentose phosphate pathway (HMP shunt)

Q134. What is the first irreversible step unique to gluconeogenesis? Pyruvate carboxylase (pyruvate → OAA)

Q135. Which enzyme is deficient in Galactosemia (classic)? GALT (galactose-1-phosphate uridylyltransferase)

Q136. Which GSD is the only one affecting lysosomes? Pompe disease (Type II) - acid maltase deficiency

Q137. Which condition features "Rice water stools" and how does cholera toxin affect carbohydrate-related transporters? Cholera toxin activates SGLT in gut - causing water to follow Na+/glucose into the lumen. Oral rehydration therapy (ORS) exploits SGLT to reabsorb Na+ and water along with glucose.

Q138. Glycolysis is inhibited by high levels of? ATP and Citrate (via inhibition of PFK-1)

Q139. Glucagon:insulin ratio determines which pathway predominates? High ratio → gluconeogenesis/glycogenolysis. Low ratio → glycolysis/glycogenesis.

Q140. The only two purely ketogenic amino acids? Leucine and Lysine

Q141. "Ischemic forearm exercise test" - no lactate rise indicates? Deficiency of muscle glycogen phosphorylase (McArdle disease) or other enzymes of glycogen breakdown/glycolysis.

Q142. What is a "limit dextrin"? Glycogen with branch points intact - formed when phosphorylase degrades glycogen up to 4 residues from each branch. Debranching enzyme is required to continue.

Q143. In which GSD does glycogen accumulate in lysosomes? Type II (Pompe) - acid maltase deficiency

Q144. Which GSD is associated with fasting hypoglycemia + enlarged liver + lactic acidosis? Type I (von Gierke) - G6Pase deficiency

Q145. Oral glucose tolerance test (OGTT) - diagnosis of diabetes? Plasma glucose ≥200 mg/dL at 2 hours after 75g glucose load.

Q146. G6PD is X-linked - who is more commonly affected? Males (hemizygous); females need two defective alleles for full expression.

Q147. What does the "O2 debt" refer to? Extra O2 needed after exercise/hypoxia to oxidize accumulated lactate and replenish ATP/phosphocreatine stores.

Q148. Oxaloacetate (OAA) is the junction molecule between which pathways? TCA cycle, gluconeogenesis, aspartate synthesis, malate-aspartate shuttle.

Q149. Which enzyme converts Glucose 1-phosphate ↔ Glucose 6-phosphate? Phosphoglucomutase

Q150. Which metabolic pathway is unique to the liver/kidney for glucose production from G6P? Glucose 6-phosphatase reaction - releases free glucose into blood.

BONUS - CLINICAL VIGNETTE-STYLE MCQs

Q151. A 3-month-old presents with hypotonia, massive cardiomegaly, and respiratory failure. Muscle biopsy shows lysosomal glycogen accumulation. Enzyme deficiency? A. Acid α-1,4-glucosidase (acid maltase) - Pompe disease (Type II GSD)

Q152. A 1-year-old child develops severe hypoglycemia and vomits after eating fruit. Urine reduces copper but tests negative with glucose oxidase. What is the diagnosis? A. Hereditary fructose intolerance (Aldolase B deficiency). Fructose in urine gives positive Benedict's test (reduces copper) but is not glucose.

Q153. A patient with malaria is treated with primaquine and develops hemolytic anemia with Heinz bodies. What enzyme is deficient? A. G6PD (Glucose 6-phosphate dehydrogenase)

Q154. A newborn develops jaundice, cataracts, and E. coli sepsis after breastfeeding. What disorder? A. Classic galactosemia (GALT deficiency). Breastmilk contains lactose → galactose → accumulation of Gal-1-P.

Q155. A 30-year-old alcoholic presents with confusion, ophthalmoplegia, ataxia. Labs: elevated lactate, low transketolase activity. Diagnosis? A. Wernicke encephalopathy due to thiamine (Vitamin B1) deficiency. Thiamine is required for PDH and α-KGDH (both produce NADH for energy) and transketolase.

Q156. A long-distance runner has elevated blood lactate but normal pH. Muscle biopsies show no PAS stain improvement after exercise. Probable diagnosis? A. This is normal lactate elevation from exercise (if pH normal). If no glycogen depletion with normal staining - consider McArdle (Type V GSD): muscle phosphorylase deficiency; blood lactate paradoxically DOES NOT rise with ischemic exercise.

Q157. A diabetic patient on metformin develops lactic acidosis. Mechanism? A. Metformin inhibits Complex I (NADH dehydrogenase) of the ETC → reduced NADH oxidation → cells switch to anaerobic glycolysis → lactate accumulation.

QUICK REFERENCE TABLE: Glycogen Storage Diseases

Type	Disease	Enzyme Deficient	Key Features
I	von Gierke	Glucose 6-phosphatase	Severe hypoglycemia, hepatomegaly, lactic acidosis
II	Pompe	Acid maltase (α-1,4-glucosidase)	Cardiomegaly, hypotonia, lysosomal storage
III	Cori (Forbes)	Debranching enzyme	Mild hypoglycemia, limit dextrin accumulation
IV	Andersen	Branching enzyme	Cirrhosis, amylopectin-like glycogen
V	McArdle	Muscle phosphorylase	Exercise intolerance, no lactate rise with exercise
VI	Hers	Liver phosphorylase	Mild hypoglycemia, hepatomegaly

QUICK REFERENCE TABLE: Key Glycolytic Enzymes and Their Regulation

Enzyme	Activators	Inhibitors
Hexokinase	-	Glucose 6-phosphate
Glucokinase	Glucose (high)	-
PFK-1	AMP, F-2,6-BP, ADP, Pi	ATP, Citrate, H+
Pyruvate kinase	F-1,6-BP	ATP, Alanine, Glucagon (via phosphorylation)
PDH complex	Ca²+, AMP, NAD+, CoA	NADH, Acetyl CoA, ATP
Isocitrate dehydrogenase	ADP, Ca²+	ATP, NADH
Citrate synthase	-	ATP, NADH, Succinyl CoA

Sources: Lippincott Illustrated Reviews: Biochemistry, 8th ed; Basic Medical Biochemistry - A Clinical Approach, 6th ed; Harper's Illustrated Biochemistry, 32nd ed; Guyton and Hall Textbook of Medical Physiology.

That's 157 questions covering every testable angle on carbohydrate metabolism for MBBS First Year. Good luck in your quiz competition!

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