Biochemistry
MBBS Biochemistry question bank: biomolecules, enzymes, metabolism, molecular biology, vitamins, nutrition and clinical biochemistry.
12chapters144questions75High-Yield
Definition
β-oxidation is the mitochondrial breakdown of fatty acids into acetyl-CoA, generating energy.
Steps
- Fatty acid activated → acyl-CoA (cytoplasm)
- Carnitine shuttle → mitochondria
- Four repeated steps: oxidation, hydration, oxidation, thiolysis
- Each cycle removes 2 carbons (as acetyl-CoA)
Energy Yield
- Each cycle: 1 FADH₂ + 1 NADH + 1 acetyl-CoA
- Palmitate (16C) → ~106 ATP net
Fatty acids are chopped two carbons at a time into acetyl-CoA. Per cycle Yield Acetyl-CoA 1 FADH₂ 1 NADH 1 Applied
- Carnitine deficiency
- MCAD deficiency
🔑KEY POINTS TO REMEMBER- β-oxidation: mitochondrial, removes 2C per cycle.
- Each cycle → acetyl-CoA + FADH₂ + NADH.
- Palmitate → ~106 ATP.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Ketone bodies (acetoacetate, β-hydroxybutyrate, acetone) are produced from acetyl-CoA in the liver during fasting and used as fuel by extrahepatic tissues.
Ketogenesis
- From acetyl-CoA (excess β-oxidation)
- In liver mitochondria (via HMG-CoA)
- During fasting, starvation, diabetes
Utilisation
- By brain, muscle, heart (not the liver)
- Reconverted to acetyl-CoA
- Brain fuel in prolonged starvation
Ketosis
- Overproduction → ketonaemia, ketonuria
- Metabolic acidosis (diabetic ketoacidosis)
The liver exports ketones for other tissues to burn when glucose is scarce. Ketone body Note Acetoacetate Primary β-hydroxybutyrate Major in blood Acetone Breath (fruity) Applied
- Diabetic ketoacidosis
- Starvation ketosis
🔑KEY POINTS TO REMEMBER- Ketone bodies from liver acetyl-CoA in fasting.
- Used by brain/muscle/heart, not liver.
- Excess → ketoacidosis.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Cholesterol metabolism involves its synthesis, transport and conversion into bile acids and hormones; it is tightly regulated.
Synthesis
- From acetyl-CoA (cytoplasm, liver)
- Rate-limiting enzyme: HMG-CoA reductase
- Inhibited by statins
Fate
- Membrane component
- Bile acids
- Steroid hormones, vitamin D
Regulation
- Feedback by cholesterol on HMG-CoA reductase
- Dietary cholesterol
Cholesterol is built from acetyl-CoA and feeds bile acids and hormones. Feature Detail Rate enzyme HMG-CoA reductase Inhibitor Statins Applied
- Hypercholesterolaemia, atherosclerosis
- Statin therapy
🔑KEY POINTS TO REMEMBER- Cholesterol from acetyl-CoA; HMG-CoA reductase rate-limiting.
- Statins inhibit it.
- Precursor of bile acids, hormones, vitamin D.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Lipoproteins are complexes of lipid and protein that transport water-insoluble lipids in the blood.
Classes (by density)
- Chylomicrons — dietary triglycerides
- VLDL — endogenous triglycerides
- LDL — cholesterol to tissues (‘bad’)
- HDL — reverse transport (‘good’)
Function
- Transport triglycerides & cholesterol
- Apolipoproteins for recognition
Lipoproteins ferry fat from gut and liver to tissues and back. Lipoprotein Carries Chylomicron Dietary TG LDL Cholesterol (bad) HDL Cholesterol (good) Applied
- ↑ LDL → atherosclerosis
- Lipid profile
🔑KEY POINTS TO REMEMBER- Chylomicron (dietary TG), VLDL (endogenous TG), LDL (bad), HDL (good).
- Apolipoproteins direct them.
- ↑ LDL → atherosclerosis.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Lipogenesis (fatty acid synthesis) is the cytoplasmic synthesis of fatty acids from acetyl-CoA, mainly in liver and adipose tissue.
Features
- Occurs in the cytoplasm
- Acetyl-CoA → malonyl-CoA (acetyl-CoA carboxylase, rate-limiting)
- Fatty acid synthase complex
- Uses NADPH (from the HMP shunt)
Product
- Palmitate (16C)
- Stimulated by insulin (fed state)
Acetyl-CoA is built up to palmitate using NADPH in the cytoplasm. Feature Detail Rate enzyme Acetyl-CoA carboxylase Reductant NADPH Product Palmitate Applied
- Insulin promotes lipogenesis
- Contrast with β-oxidation
🔑KEY POINTS TO REMEMBER- Lipogenesis: cytoplasmic, from acetyl-CoA.
- ACC rate-limiting; uses NADPH; product palmitate.
- Stimulated by insulin.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
The carnitine shuttle transports long-chain fatty acids (as acyl-CoA) from the cytoplasm into the mitochondria for β-oxidation.
Mechanism
- Acyl-CoA + carnitine → acylcarnitine (CPT-I)
- Crosses the inner mitochondrial membrane
- Acylcarnitine → acyl-CoA (CPT-II)
- CPT-I is rate-limiting for β-oxidation
Carnitine ferries fatty acids across the inner membrane for oxidation. Enzyme Location CPT-I Outer membrane CPT-II Inner membrane Applied
- Carnitine deficiency → impaired fat oxidation
- Muscle weakness, hypoglycaemia
🔑KEY POINTS TO REMEMBER- Carnitine shuttle moves long-chain acyl-CoA into mitochondria.
- CPT-I (rate-limiting) → CPT-II.
- Deficiency → impaired fat oxidation.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Bile acids are cholesterol derivatives that, as bile salts, emulsify dietary fat for digestion and absorption.
Types
- Primary — cholic, chenodeoxycholic (from liver)
- Secondary — deoxycholic, lithocholic (gut bacteria)
- Conjugated with glycine / taurine → bile salts
Functions
- Emulsify fat (↓ surface tension)
- Aid absorption of fat & fat-soluble vitamins
- Enterohepatic circulation
Cholesterol becomes bile salts that emulsify fat and are recycled. Type Example Primary Cholic acid Secondary Deoxycholic acid Applied
- Cholesterol gallstones
- Fat malabsorption
🔑KEY POINTS TO REMEMBER- Bile acids from cholesterol; conjugated → bile salts.
- Emulsify fat; enterohepatic circulation.
- Primary vs secondary bile acids.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Fatty liver (hepatic steatosis) is abnormal accumulation of triglycerides in liver cells due to imbalance between fat synthesis and export.
Causes
- Alcohol (commonest)
- Obesity, diabetes (NAFLD)
- Protein / lipotropic-factor deficiency
- ↓ lipoprotein (VLDL) synthesis
Fat builds up when the liver makes more triglyceride than it can export. Cause Mechanism Alcohol ↑ TG, ↓ oxidation Obesity NAFLD Applied
- NAFLD, alcoholic liver disease
- Reversible if treated early
🔑KEY POINTS TO REMEMBER- Fatty liver = TG accumulation (synthesis > export).
- Alcohol, obesity/diabetes, lipotropic deficiency.
- NAFLD; reversible early.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Lipotropic factors are substances that prevent fat accumulation in the liver by promoting fat mobilisation or phospholipid synthesis.
Examples
- Choline
- Methionine
- Inositol
- Vitamin B12, folate (methyl donors)
Mechanism
- Promote synthesis of phospholipids (lecithin)
- Aid export of fat as lipoprotein
- Prevent fatty liver
These factors help package and export liver fat, preventing steatosis. Factor Role Choline Lecithin synthesis Methionine Methyl donor Applied
- Deficiency → fatty liver
🔑KEY POINTS TO REMEMBER- Lipotropic factors: choline, methionine, inositol, B12/folate.
- Promote phospholipid synthesis & VLDL export.
- Deficiency → fatty liver.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Eicosanoids are local hormones (prostaglandins, thromboxanes, leukotrienes) derived from arachidonic acid.
Types & Pathways
- Prostaglandins / thromboxanes — cyclooxygenase (COX)
- Leukotrienes — lipoxygenase (LOX)
Functions
- Inflammation, pain, fever
- Platelet aggregation (thromboxane)
- Vasodilation / constriction, bronchoconstriction
Arachidonic acid is converted by COX and LOX into local mediators. Pathway Product COX Prostaglandins, thromboxane LOX Leukotrienes Applied
- NSAIDs inhibit COX
- Aspirin → ↓ thromboxane
🔑KEY POINTS TO REMEMBER- Eicosanoids from arachidonic acid.
- COX → prostaglandins/thromboxane; LOX → leukotrienes.
- NSAIDs inhibit COX.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Hormone-sensitive lipase (HSL) catalyses lipolysis — the breakdown of stored triglycerides in adipose tissue to release fatty acids.
Regulation
- Activated by glucagon, adrenaline, cortisol (fasting)
- Inhibited by insulin (fed state)
- Releases free fatty acids + glycerol
Fasting hormones switch on HSL to mobilise stored fat. Hormone Effect on HSL Glucagon/adrenaline Activate Insulin Inhibit Applied
- Fasting fuel mobilisation
- ↑ FFA in diabetes
🔑KEY POINTS TO REMEMBER- HSL breaks down adipose triglyceride (lipolysis).
- Activated by glucagon/adrenaline; inhibited by insulin.
- Releases FFA + glycerol.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Lipoprotein lipase (LPL) is an enzyme on capillary endothelium that hydrolyses triglycerides in chylomicrons and VLDL, releasing fatty acids to tissues.
Features
- On capillary walls (adipose, muscle)
- Activated by apo C-II
- Hydrolyses TG → free fatty acids + glycerol
- Insulin ↑ LPL activity
LPL unloads triglyceride from lipoproteins to feed the tissues. Feature Detail Location Capillary endothelium Activator Apo C-II Applied
- LPL deficiency → hypertriglyceridaemia
- Type I hyperlipoproteinaemia
🔑KEY POINTS TO REMEMBER- LPL on capillaries hydrolyses chylomicron/VLDL triglyceride.
- Activated by apo C-II; ↑ by insulin.
- Deficiency → hypertriglyceridaemia.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).