Biochemistry
MBBS Biochemistry question bank: biomolecules, enzymes, metabolism, molecular biology, vitamins, nutrition and clinical biochemistry.
12chapters144questions75High-Yield
Definition
Glycolysis is the cytoplasmic pathway that breaks down one glucose into two pyruvate molecules with net ATP gain — the central pathway of carbohydrate metabolism.
Key Features
- Occurs in the cytoplasm (all cells)
- Glucose (6C) → 2 pyruvate (3C)
- Aerobic → pyruvate; anaerobic → lactate
- Rate-limiting enzyme: PFK-1
Key Regulatory Enzymes
- Hexokinase / glucokinase
- Phosphofructokinase-1 (main)
- Pyruvate kinase
Energetics
- Net gain: 2 ATP (anaerobic)
- + 2 NADH → aerobic yields more via the ETC
One glucose is split into two pyruvate with a net gain of 2 ATP. Condition Product ATP Aerobic Pyruvate 2 (+ NADH) Anaerobic Lactate 2 Applied
- Only ATP source in RBCs
- Cancer (Warburg effect)
🔑KEY POINTS TO REMEMBER- Glycolysis: glucose → 2 pyruvate in cytoplasm.
- Rate-limiting = PFK-1; net 2 ATP + 2 NADH.
- Only ATP source in RBCs.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
The citric acid cycle (Krebs / TCA cycle) is the final common oxidative pathway in mitochondria that oxidises acetyl-CoA to CO₂, generating reduced coenzymes.
Key Features
- Occurs in the mitochondrial matrix
- Acetyl-CoA + oxaloacetate → citrate
- 8 steps, regenerates oxaloacetate
- Amphibolic (catabolic + anabolic)
Products (per acetyl-CoA)
- 3 NADH, 1 FADH₂
- 1 GTP (≈ ATP)
- 2 CO₂
Energetics
- Reduced coenzymes → ETC → ~10 ATP per acetyl-CoA
Acetyl-CoA is fully oxidised, yielding reduced coenzymes for the ETC. Product Per acetyl-CoA NADH 3 FADH₂ 1 GTP 1 CO₂ 2 Applied
- Central hub of metabolism
- Fluoroacetate poisoning (aconitase)
🔑KEY POINTS TO REMEMBER- TCA in mitochondrial matrix; acetyl-CoA → 2 CO₂.
- Per acetyl-CoA: 3 NADH, 1 FADH₂, 1 GTP.
- Amphibolic; ~10 ATP via the ETC.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Gluconeogenesis is the synthesis of glucose from non-carbohydrate precursors, mainly in the liver, to maintain blood glucose during fasting.
Precursors
- Lactate (via the Cori cycle)
- Glucogenic amino acids
- Glycerol (from fat)
Key Bypass Enzymes
- Pyruvate carboxylase
- PEP carboxykinase
- Fructose-1,6-bisphosphatase
- Glucose-6-phosphatase
Sites
- Mainly the liver (also the kidney)
Non-carbohydrate precursors are converted to glucose using bypass enzymes. Precursor Source Lactate Muscle (Cori) Amino acids Protein Glycerol Fat Applied
- Maintains glucose during fasting
- Impaired in liver disease
🔑KEY POINTS TO REMEMBER- Gluconeogenesis: glucose from lactate, amino acids, glycerol.
- Four bypass enzymes circumvent glycolysis.
- Mainly hepatic; maintains fasting glucose.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
The oxidative decarboxylation of pyruvate converts pyruvate to acetyl-CoA, linking glycolysis to the citric acid cycle.
Reaction
- Pyruvate → acetyl-CoA + CO₂ + NADH
- By the pyruvate dehydrogenase complex (PDH)
- Irreversible
- Needs 5 coenzymes (TPP, lipoate, FAD, NAD, CoA)
Fate of Pyruvate
- Aerobic → acetyl-CoA (TCA)
- Anaerobic → lactate
- → oxaloacetate (gluconeogenesis)
- → alanine
Pyruvate’s fate depends on oxygen and the cell’s needs. Fate Enzyme Acetyl-CoA PDH Lactate LDH Oxaloacetate Pyruvate carboxylase Applied
- PDH deficiency → lactic acidosis
- Thiamine (TPP) deficiency
🔑KEY POINTS TO REMEMBER- PDH: pyruvate → acetyl-CoA + CO₂ + NADH (irreversible).
- Needs 5 coenzymes (incl. TPP/thiamine).
- Pyruvate → acetyl-CoA / lactate / OAA / alanine.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Blood glucose is maintained within a narrow range (70–110 mg/dL) by hormones balancing intake, storage and production.
Hormone Lowering Glucose
- Insulin — ↑ uptake, glycogenesis
Hormones Raising Glucose
- Glucagon — glycogenolysis, gluconeogenesis
- Adrenaline, cortisol, growth hormone
Pathways
- Fed state — glycolysis, glycogenesis
- Fasting — glycogenolysis, gluconeogenesis
Insulin and counter-regulatory hormones hold glucose in a tight range. Hormone Effect on glucose Insulin ↓ (lowers) Glucagon ↑ (raises) Cortisol ↑ Applied
- Diabetes mellitus
- Hypoglycaemia
🔑KEY POINTS TO REMEMBER- Glucose 70–110 mg/dL; insulin lowers, glucagon raises.
- Fed → storage; fasting → release.
- Dysregulation → diabetes / hypoglycaemia.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
The Cori cycle is the cycling of lactate (from muscle) to the liver, where it is reconverted to glucose.
Steps
- Muscle: glucose → lactate (anaerobic)
- Lactate → blood → liver
- Liver: lactate → glucose (gluconeogenesis)
- Glucose → back to muscle
Lactate from muscle is recycled to glucose in the liver. Organ Reaction Muscle Glucose → lactate Liver Lactate → glucose Applied
- Prevents lactic acidosis
- Important during exercise
🔑KEY POINTS TO REMEMBER- Cori cycle: muscle lactate → liver glucose → muscle.
- Prevents lactic acidosis.
- Active in exercise.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
The Rapoport–Luebering shunt is a side pathway of glycolysis in red cells that produces 2,3-bisphosphoglycerate (2,3-BPG).
Features
- Bypasses one ATP-generating step
- Forms 2,3-BPG
- 2,3-BPG binds haemoglobin → ↓ O₂ affinity
The shunt makes 2,3-BPG, which helps haemoglobin unload oxygen. Feature Effect 2,3-BPG ↓ O₂ affinity ↑ in hypoxia More O₂ delivery Applied
- ↑ 2,3-BPG at high altitude, in anaemia
- Right shift of the O₂ curve
🔑KEY POINTS TO REMEMBER- Shunt produces 2,3-BPG in RBCs (no ATP gain).
- 2,3-BPG ↓ haemoglobin O₂ affinity.
- ↑ in hypoxia → right shift.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Anaerobic glycolysis is the breakdown of glucose to lactate in the absence of oxygen, producing ATP without the electron transport chain.
Features
- Glucose → 2 lactate
- Net 2 ATP (no oxygen needed)
- NADH reoxidised by lactate formation (LDH)
Without oxygen, pyruvate becomes lactate to regenerate NAD⁺ for ATP. Feature Detail Product Lactate ATP 2 net Site Cytoplasm Applied
- RBCs, exercising muscle
- Lactic acidosis
🔑KEY POINTS TO REMEMBER- Anaerobic glycolysis: glucose → lactate, net 2 ATP.
- LDH regenerates NAD⁺.
- In RBCs and exercising muscle.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Substrate-level phosphorylation is the direct formation of ATP (or GTP) by transfer of phosphate from a high-energy substrate, not requiring the ETC.
Examples
- Glycolysis — 1,3-BPG → 3-PG (phosphoglycerate kinase)
- Glycolysis — PEP → pyruvate (pyruvate kinase)
- TCA — succinyl-CoA → succinate (GTP)
A phosphate is handed directly from substrate to ADP, making ATP. Pathway Step Glycolysis 1,3-BPG, PEP TCA Succinyl-CoA Applied
- Only ATP source in anaerobic conditions
🔑KEY POINTS TO REMEMBER- Direct phosphate transfer → ATP/GTP (no ETC).
- Glycolysis (1,3-BPG, PEP) & TCA (succinyl-CoA).
- Vital anaerobically.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
The Pasteur effect is the inhibition of glycolysis (and lactate production) by the presence of oxygen.
Mechanism
- Oxygen present → aerobic respiration is efficient
- ↓ Rate of glycolysis, ↓ glucose use
- ↓ Lactate formation
- (ATP inhibits PFK-1)
Ample oxygen makes oxidative ATP efficient, so glycolysis slows. Condition Glycolysis Oxygen present Inhibited Oxygen absent Increased Applied
- Explains efficient aerobic metabolism
- Opposite of the Warburg effect (tumours)
🔑KEY POINTS TO REMEMBER- Pasteur effect: O₂ inhibits glycolysis.
- ↑ ATP inhibits PFK-1.
- Opposite = Warburg effect.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
The citric acid cycle is amphibolic — it functions in both catabolism (energy) and anabolism (biosynthesis).
Catabolic Role
- Oxidises acetyl-CoA → energy (NADH, FADH₂)
Anabolic Role (intermediates used)
- Citrate → fatty acid synthesis
- α-ketoglutarate → amino acids
- Oxaloacetate → gluconeogenesis, aspartate
- Succinyl-CoA → haem
The cycle both releases energy and supplies biosynthetic intermediates. Intermediate Used for Citrate Fatty acids α-KG Amino acids Succinyl-CoA Haem Applied
- Anaplerotic reactions replenish intermediates
🔑KEY POINTS TO REMEMBER- TCA is amphibolic: catabolic + anabolic.
- Intermediates → fatty acids, amino acids, haem.
- Anaplerotic reactions refill it.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Fluoride is added to blood-collection tubes as an antiglycolytic agent to preserve glucose for accurate estimation.
Mechanism
- Inhibits enolase (a glycolytic enzyme)
- Stops glycolysis in the sample
- Prevents glucose consumption by cells
Fluoride blocks enolase, halting glycolysis so glucose is not lost. Feature Detail Agent Sodium fluoride Target Enolase Applied
- Grey-top tube for glucose
- Accurate glucose estimation
🔑KEY POINTS TO REMEMBER- Fluoride inhibits enolase → stops glycolysis.
- Preserves glucose in the sample.
- Grey-top collection tube.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).