NEET PG Rapid Revision
Biochemistry One-Liners for NEET PG: Rapid Revision
High-yield biochemistry one-liners for NEET PG covering enzymology, metabolism, molecular biology and clinical biochemistry.
MedNext Academy | 5 min read
Biochemistry One-Liners for NEET PG: Rapid Revision
High-yield biochemistry one-liners for NEET PG covering enzymology, metabolism, molecular biology and clinical biochemistry.
Biochemistry: rapid revision one-liners for NEET PG
Biochemistry in NEET PG focuses heavily on enzymes, metabolic pathways, vitamins, molecular biology and inborn errors of metabolism. These one-liners capture the most testable associations and facts from the subject.
Rather than trying to memorise entire pathways, use these statements to reinforce rate-limiting enzymes, key substrates, vitamin cofactors and the classic biochemical basis of inherited metabolic diseases.
Must-know one-liners
- The rate-limiting enzyme of glycolysis is phosphofructokinase-1 (PFK-1)
- The rate-limiting enzyme of gluconeogenesis is fructose-1,6-bisphosphatase
- The rate-limiting enzyme of the TCA cycle is isocitrate dehydrogenase
- The rate-limiting enzyme of the HMP shunt (pentose phosphate pathway) is glucose-6-phosphate dehydrogenase (G6PD)
- The rate-limiting enzyme of fatty acid synthesis is acetyl-CoA carboxylase
- The rate-limiting enzyme of cholesterol synthesis is HMG-CoA reductase (target of statins)
- The rate-limiting enzyme of the urea cycle is carbamoyl phosphate synthetase I (CPS-I)
- The rate-limiting enzyme of de novo purine synthesis is PRPP amidotransferase
- The rate-limiting enzyme of de novo pyrimidine synthesis is carbamoyl phosphate synthetase II (CPS-II)
- The rate-limiting enzyme of haem synthesis is ALA synthase (delta-aminolevulinic acid synthase)
- The rate-limiting enzyme of glycogenesis is glycogen synthase
- The rate-limiting enzyme of glycogenolysis is glycogen phosphorylase
- Pyruvate dehydrogenase complex requires 5 cofactors: TPP (B1), lipoic acid, CoA (B5), FAD (B2) and NAD+ (B3)
- Biotin (vitamin B7) is a cofactor for carboxylase enzymes (pyruvate carboxylase, acetyl-CoA carboxylase, propionyl-CoA carboxylase)
- Thiamine (vitamin B1) deficiency causes beriberi (wet = cardiac, dry = neurological) and Wernicke encephalopathy
- Niacin (vitamin B3) deficiency causes pellagra (dermatitis, diarrhoea, dementia, death -- the 4 Ds)
- Pyridoxine (vitamin B6) is the cofactor for transaminases (ALT, AST) and ALA synthase
- Vitamin B12 (cobalamin) deficiency causes megaloblastic anaemia and subacute combined degeneration of the spinal cord
- Folate deficiency causes megaloblastic anaemia WITHOUT neurological features
- Scurvy (vitamin C deficiency) causes defective collagen synthesis due to impaired hydroxylation of proline and lysine
- Vitamin A deficiency causes night blindness (nyctalopia) and Bitot spots
- Vitamin D is hydroxylated at position 25 in the liver and at position 1 in the kidney (1,25-dihydroxycholecalciferol is the active form)
- Vitamin K is required for gamma-carboxylation of clotting factors II, VII, IX and X (and proteins C and S)
- Vitamin E is an antioxidant that protects cell membranes from lipid peroxidation
- Phenylketonuria (PKU) is caused by deficiency of phenylalanine hydroxylase; musty odour of urine
- Maple syrup urine disease is caused by deficiency of branched-chain alpha-keto acid dehydrogenase
- Alkaptonuria is caused by deficiency of homogentisic acid oxidase; causes ochronosis
- Homocystinuria is caused by deficiency of cystathionine beta-synthase; causes lens subluxation (downward), marfanoid habitus and thromboembolism
- In Marfan syndrome lens subluxation is upward; in homocystinuria it is downward
- Gaucher disease is the most common lysosomal storage disorder; caused by deficiency of glucocerebrosidase
- Tay-Sachs disease is caused by deficiency of hexosaminidase A; causes cherry-red spot on macula
- Niemann-Pick disease is caused by deficiency of sphingomyelinase; also causes cherry-red spot
- Fabry disease is caused by deficiency of alpha-galactosidase A; X-linked, causes angiokeratomas and renal failure
- Hunter syndrome (MPS II) is the only X-linked mucopolysaccharidosis; no corneal clouding (unlike Hurler)
- Hurler syndrome (MPS IH) is caused by deficiency of alpha-L-iduronidase; autosomal recessive with corneal clouding
- Von Gierke disease (GSD type I) is caused by deficiency of glucose-6-phosphatase; causes severe fasting hypoglycaemia and hepatomegaly
- McArdle disease (GSD type V) is caused by deficiency of muscle glycogen phosphorylase; causes exercise intolerance and myoglobinuria
- Pompe disease (GSD type II) is caused by deficiency of acid maltase (acid alpha-glucosidase); causes cardiomegaly
- Lesch-Nyhan syndrome is caused by deficiency of HGPRT (hypoxanthine-guanine phosphoribosyltransferase); causes self-mutilation, hyperuricaemia and gout
- Cori cycle involves the transfer of lactate from muscle to liver for gluconeogenesis
- Glucose-alanine cycle transfers amino groups from muscle to liver for gluconeogenesis and urea synthesis
- Beta-oxidation of fatty acids occurs in the mitochondrial matrix; carnitine shuttle (CPT-I and CPT-II) is required for long-chain fatty acid entry
- Ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are synthesised in the liver but utilised by extrahepatic tissues
- The liver cannot utilise ketone bodies because it lacks thiophorase (succinyl-CoA:acetoacetate CoA transferase)
- Collagen synthesis requires vitamin C for hydroxylation of proline and lysine residues
- Type I collagen is found in bone, skin, tendon and cornea (most abundant collagen)
- Type II collagen is found in cartilage and vitreous humour
- Type IV collagen is found in basement membranes
- Osteogenesis imperfecta is caused by defective type I collagen synthesis
- Ehlers-Danlos syndrome (classical type) involves defective type V collagen or lysyl hydroxylase
- PCR (polymerase chain reaction) uses Taq polymerase and requires primers, template DNA, dNTPs and thermal cycling
- Southern blot detects DNA; Northern blot detects RNA; Western blot detects proteins
- ELISA (enzyme-linked immunosorbent assay) is used for quantitative detection of antigens or antibodies
- Restriction enzymes cut DNA at specific palindromic sequences
- Proto-oncogenes promote cell growth; when mutated they become oncogenes (gain of function)
- Tumour suppressor genes inhibit cell growth; both alleles must be lost for tumour development (Knudson two-hit hypothesis)
- p53 is the guardian of the genome; most commonly mutated gene in human cancers
- Rb gene product controls the G1-S checkpoint of the cell cycle
- Fluoride inhibits enolase in the glycolytic pathway; sodium fluoride tubes are used for blood glucose estimation
How to use these one-liners
Focus first on rate-limiting enzymes and inborn errors of metabolism -- these two categories alone can yield 4-6 questions in NEET PG. Read the enzyme-disease-deficiency triplets as flashcards.
For vitamins, learn them as cofactor-enzyme pairs rather than in isolation. When you encounter a clinical scenario in the exam, the vitamin cofactor association will often lead you to the correct answer.
Key mnemonics
Tender Loving Care For Nancy (cofactors of the pyruvate dehydrogenase complex): Thiamine (B1), Lipoic acid, CoA (B5/pantothenate), FAD (B2/riboflavin), NAD+ (B3/niacin).
The 4 Ds of Pellagra: Dermatitis, Diarrhoea, Dementia, Death (niacin/B3 deficiency).
Southern = DNA, Northern = RNA, Western = Protein -- alphabetical order: D before R before P (SNW = DRP).
Revision schedule
Biochemistry rewards frequent short revision sessions rather than long marathons. Go through these one-liners every 2-3 days, grouping them by topic (enzymes one day, vitamins the next, storage disorders the next). In the last week, revise the entire set daily -- biochemistry facts fade fast without reinforcement.
Frequently Asked Questions
How many biochemistry questions appear in NEET PG?
Typically 10-15 questions, with a heavy focus on enzymology, metabolic pathways and inborn errors of metabolism. Molecular biology and vitamins are also regularly tested.
Which storage disorders should I focus on?
Gaucher, Tay-Sachs, Niemann-Pick, Fabry, Hunter and Hurler are the most commonly tested. Know the enzyme deficiency, accumulated substrate and key clinical features for each.
Are metabolic pathways asked in detail?
Usually not step-by-step. The exam focuses on rate-limiting enzymes, key regulatory steps, energy yield and clinical correlations rather than memorisation of every intermediate.
How important is molecular biology for NEET PG?
Increasingly important. PCR, blotting techniques, CRISPR basics, gene regulation and oncogenes/tumour suppressor genes are all fair game. Expect 2-3 questions from this area.
Inside MedNext for this topic
- 411 MedNext-authored chapters
- 80,000+ MCQ bank
- 15 study modes
- Growing visual cheat sheets
Study modes
- Notes
- MCQ
- Audio
- Video
- Visual
- 3D Anatomy
- Trace
- Flashcards
- Mnemonics
- Image Bank
- Clinical
- Microscopy
- Audio QBank
- Cadaver
- Book Match
Continue reading
NEET PG StrategyHow to Prepare Biochemistry
Study strategy, time allocation and high-yield topics.
NEET PG PYQBiochemistry PYQ Analysis
Previous year question trends and patterns.
Subject HubBiochemistry Hub
All Biochemistry resources in one place.
Test your Biochemistry revision
You have read the one-liners. Now test whether they stuck -- a quick recall quiz on this subject takes five minutes and shows what needs another pass.
Test this revision