Biochemistry
MBBS Biochemistry question bank: biomolecules, enzymes, metabolism, molecular biology, vitamins, nutrition and clinical biochemistry.
12chapters144questions75High-Yield
Definition
Glycogen metabolism comprises glycogenesis (synthesis) and glycogenolysis (breakdown), storing and releasing glucose.
Glycogenesis (synthesis)
- Glucose → glucose-6-P → glucose-1-P → UDP-glucose
- Key enzyme: glycogen synthase
- Stimulated by insulin
- Occurs in liver & muscle
Glycogenolysis (breakdown)
- Glycogen → glucose-1-P → glucose-6-P
- Key enzyme: glycogen phosphorylase
- Stimulated by glucagon / adrenaline
- Liver → free glucose; muscle → energy
Glycogen is built by synthase and broken down by phosphorylase. Process Enzyme Hormone Glycogenesis Glycogen synthase Insulin Glycogenolysis Phosphorylase Glucagon Applied
- Glycogen storage diseases
- Liver stores maintain blood glucose
🔑KEY POINTS TO REMEMBER- Glycogenesis (synthase, insulin) vs glycogenolysis (phosphorylase, glucagon).
- Liver glycogen → free glucose; muscle → energy.
- Enzyme defects → storage diseases.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
The HMP shunt (pentose phosphate pathway) is an alternative glucose pathway producing NADPH and ribose-5-phosphate, without generating ATP.
Two Phases
- Oxidative — produces NADPH + CO₂ (irreversible)
- Non-oxidative — produces ribose-5-phosphate
Products & Uses
- NADPH — fatty-acid/steroid synthesis, glutathione
- Ribose-5-P — nucleotide synthesis
Sites
- Cytoplasm; liver, RBC, adrenal cortex, mammary gland
The shunt yields NADPH for synthesis and ribose for nucleotides. Product Function NADPH Reductive synthesis Ribose-5-P Nucleotides Applied
- G6PD deficiency (haemolysis)
- No ATP produced
🔑KEY POINTS TO REMEMBER- HMP shunt: NADPH + ribose-5-P; no ATP.
- NADPH for synthesis & glutathione; ribose for nucleotides.
- G6PD deficiency → haemolysis.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Diabetes mellitus is a metabolic disorder of chronic hyperglycaemia due to insulin deficiency (Type 1) or resistance (Type 2).
Types
- Type 1 — autoimmune β-cell loss (insulin deficiency)
- Type 2 — insulin resistance (commonest)
- Gestational diabetes
Metabolic Effects
- Hyperglycaemia, glycosuria
- ↑ Lipolysis → ketosis (Type 1)
- ↑ Protein breakdown
Clinical Features
- Polyuria, polydipsia, polyphagia, weight loss
Lack of insulin action raises glucose and drives the classic symptoms. Feature Type 1 Type 2 Insulin Deficient Resistance Onset Young Adult Ketosis Common Rare Applied
- Complications: retino-, nephro-, neuropathy
- DKA, hyperosmolar state
🔑KEY POINTS TO REMEMBER- Diabetes = chronic hyperglycaemia (T1 deficiency, T2 resistance).
- 3 P’s + weight loss; ketosis in T1.
- Micro- & macrovascular complications.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Diabetes is diagnosed by blood glucose criteria; the glucose tolerance test (GTT) assesses the body’s ability to handle a glucose load.
Diagnostic Criteria
- Fasting glucose ≥ 126 mg/dL
- 2-h post-glucose (OGTT) ≥ 200 mg/dL
- Random ≥ 200 + symptoms
- HbA1c ≥ 6.5%
Oral Glucose Tolerance Test
- 75 g oral glucose load
- Measure glucose at 0 & 2 h
- Normal <140; diabetes ≥200 (2 h)
Any of the standard thresholds confirms the diagnosis. Test Diabetes cutoff Fasting ≥126 mg/dL OGTT 2-h ≥200 mg/dL HbA1c ≥6.5% Applied
- Screening; gestational diabetes
- Impaired glucose tolerance (prediabetes)
🔑KEY POINTS TO REMEMBER- Diagnosis: fasting ≥126, OGTT 2-h ≥200, or HbA1c ≥6.5%.
- OGTT uses 75 g glucose.
- Prediabetes = impaired glucose tolerance.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Glycogen storage diseases (GSDs) and inborn errors of carbohydrate metabolism are genetic enzyme deficiencies affecting glycogen or sugar metabolism.
Glycogen Storage Diseases
- von Gierke (I) — glucose-6-phosphatase
- Pompe (II) — lysosomal α-glucosidase
- McArdle (V) — muscle phosphorylase
Other Inborn Errors
- Galactosaemia (galactose-1-P uridyltransferase)
- Fructose intolerance (aldolase B)
- Essential fructosuria (benign)
A missing enzyme lets its substrate build up and damage organs. Disease Enzyme von Gierke Glucose-6-phosphatase Pompe α-glucosidase Galactosaemia GALT Applied
- Newborn screening
- Dietary management
🔑KEY POINTS TO REMEMBER- GSDs: von Gierke (I), Pompe (II), McArdle (V).
- Galactosaemia (GALT), fructose intolerance (aldolase B).
- Managed by diet / screening.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked disorder impairing NADPH production, causing oxidative haemolysis.
Mechanism
- G6PD = first enzyme of the HMP shunt
- ↓ NADPH → ↓ reduced glutathione
- RBCs vulnerable to oxidative stress → haemolysis
Triggers
- Oxidant drugs (primaquine, sulfonamides)
- Fava beans (favism)
- Infection
Low NADPH leaves RBCs defenceless against oxidant stress. Feature Detail Inheritance X-linked Trigger Oxidant drugs Result Haemolysis Applied
- Avoid oxidant drugs
- Heinz bodies, bite cells
🔑KEY POINTS TO REMEMBER- G6PD deficiency: X-linked, ↓ NADPH → haemolysis.
- Triggered by oxidant drugs, fava beans, infection.
- Heinz bodies on smear.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Glycated haemoglobin (HbA1c) reflects the average blood glucose over the preceding 2–3 months, used to monitor diabetes.
Principle
- Glucose binds non-enzymatically to haemoglobin
- Proportional to blood glucose
- Reflects ~120 days (RBC lifespan)
Values
- Normal <5.7%
- Prediabetes 5.7–6.4%
- Diabetes ≥6.5%
Glucose sticks to haemoglobin in proportion to its long-term level. HbA1c Interpretation <5.7% Normal 5.7–6.4% Prediabetes ≥6.5% Diabetes Applied
- Long-term glycaemic control
- Target <7% in most diabetics
🔑KEY POINTS TO REMEMBER- HbA1c = average glucose over 2–3 months.
- Diabetes ≥6.5%; target <7%.
- Non-enzymatic glycation.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Diabetic ketoacidosis (DKA) is an acute complication of (mainly Type 1) diabetes with hyperglycaemia, ketosis and metabolic acidosis.
Mechanism
- Insulin deficiency → ↑ lipolysis
- ↑ Free fatty acids → ketone bodies
- Ketoacids → metabolic acidosis
Features
- Hyperglycaemia, ketonuria
- Kussmaul breathing (acidosis)
- Fruity breath, dehydration
Without insulin, fat breakdown floods the blood with acidic ketones. Feature Finding Glucose ↑↑ Ketones ↑ pH ↓ (acidosis) Applied
- Emergency: insulin + fluids
- Often precipitated by infection
🔑KEY POINTS TO REMEMBER- DKA: hyperglycaemia + ketosis + acidosis (mainly T1).
- Kussmaul breathing, fruity breath.
- Treat with insulin + fluids.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
NADPH is the reduced coenzyme (from the HMP shunt) providing reducing power for biosynthesis and antioxidant defence.
Functions
- Reductive biosynthesis — fatty acids, cholesterol, steroids
- Maintains reduced glutathione (antioxidant)
- Respiratory burst (phagocytes)
- Detoxification (cytochrome P450)
NADPH powers synthesis, antioxidant defence and the respiratory burst. Use Example Synthesis Fatty acids Antioxidant Glutathione Defence Respiratory burst Applied
- G6PD deficiency → ↓ NADPH
- Chronic granulomatous disease
🔑KEY POINTS TO REMEMBER- NADPH: reductive synthesis + antioxidant defence.
- Maintains glutathione; drives respiratory burst.
- From the HMP shunt.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
The uronic acid pathway is a minor pathway of glucose metabolism producing glucuronic acid and (in some species) vitamin C.
Functions
- Produces glucuronic acid → conjugation / detoxification
- Synthesis of glycosaminoglycans
- Vitamin C synthesis (not in humans — lack gulonolactone oxidase)
The pathway makes glucuronic acid for detoxification and GAGs. Product Use Glucuronic acid Detoxification Vitamin C (not in humans) Applied
- Bilirubin conjugation
- Drug glucuronidation
🔑KEY POINTS TO REMEMBER- Uronic acid pathway → glucuronic acid.
- Used for conjugation/detoxification & GAGs.
- Humans cannot make vitamin C (no gulonolactone oxidase).
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
Insulin is the anabolic hormone from pancreatic β-cells that lowers blood glucose and promotes storage.
Carbohydrate Effects
- ↑ Glucose uptake (GLUT4)
- ↑ Glycogenesis and glycolysis
- ↓ Gluconeogenesis
Lipid & Protein Effects
- ↑ Lipogenesis, ↓ lipolysis
- ↑ Protein synthesis
Insulin drives uptake and storage of glucose, fat and protein. Nutrient Effect Glucose ↑ uptake / storage Fat ↑ synthesis Protein ↑ synthesis Applied
- Deficiency → diabetes
- Insulin therapy
🔑KEY POINTS TO REMEMBER- Insulin = anabolic; lowers glucose.
- ↑ uptake (GLUT4), glycogen, fat, protein.
- Deficiency → diabetes.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).Definition
The sorbitol (polyol) pathway converts glucose to sorbitol and then fructose; it becomes significant in hyperglycaemia.
Pathway
- Glucose → sorbitol (aldose reductase)
- Sorbitol → fructose (sorbitol dehydrogenase)
- Insulin-independent
In Diabetes
- Sorbitol accumulates in tissues (lens, nerve, kidney)
- Causes osmotic damage
In diabetes, trapped sorbitol draws in water and damages tissues. Tissue Complication Lens Cataract Nerve Neuropathy Retina Retinopathy Applied
- Diabetic cataract, neuropathy
- Aldose reductase inhibitors
🔑KEY POINTS TO REMEMBER- Glucose → sorbitol → fructose (insulin-independent).
- Sorbitol accumulation → osmotic damage.
- Diabetic cataract, neuropathy.
📚SOURCES: Textbook of Biochemistry (U. Satyanarayana); Harper’s Illustrated Biochemistry; Textbook of Medical Biochemistry (M.N. Chatterjea).