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BI7.1-2 | Integration of Metabolism and Biological Oxidation — Gate Quiz
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The majority of ATP produced from glucose oxidation is generated by which process in the mitochondria?
Correct! Oxidative phosphorylation via the electron transport chain generates approximately 32-34 ATP out of the total approximately 36-38 ATP from complete glucose oxidation.
ATP yield from glucose: Glycolysis = 2 ATP (substrate-level) + 2 NADH. PDC = 2 NADH. TCA cycle = 2 GTP + 6 NADH + 2 FADH2. NADH = 2.5 ATP each; FADH2 = 1.5 ATP each via ETC. Total approximately 30-32 ATP (modern estimates). ETC provides the vast majority.
Incorrect. Oxidative phosphorylation via ETC generates the majority of ATP from glucose.
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Complex IV (cytochrome c oxidase) is the terminal oxidase of the electron transport chain. It transfers electrons to the final acceptor, which is:
Correct! Complex IV (cytochrome c oxidase) is the terminal electron acceptor of the ETC, transferring electrons to molecular oxygen (O2) to form water. This is the step inhibited by cyanide.
ETC inhibitors: Complex I (rotenone, amytal), Complex II (malonate), Complex III (antimycin A), Complex IV (cyanide, CO, azide). Uncouplers (dinitrophenol, FCCP) dissipate the proton gradient, producing heat instead of ATP. Brown adipose tissue uses uncoupling protein (thermogenin) for thermogenesis.
Incorrect. Complex IV transfers electrons to molecular oxygen, reducing it to water.
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A victim of cyanide poisoning shows cherry-red skin (venous blood appearing arterial) due to elevated venous O2. This occurs because:
Correct! Cyanide binds to cytochrome a3 in Complex IV (cytochrome c oxidase), blocking electron transfer to O2. Cells cannot use O2, so venous blood retains its oxygen content, appearing bright red like arterial blood.
Cyanide antidotes: Hydroxocobalamin (binds cyanide to form cyanocobalamin), Sodium thiosulfate (provides sulfur for rhodanese enzyme, converting cyanide to thiocyanate), Dicobalt edetate. Nitrites generate methaemoglobin which has high affinity for cyanide, diverting it from Complex IV.
Incorrect. Cyanide inhibits Complex IV, preventing O2 utilization, so venous blood remains oxygenated.
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According to Mitchell chemiosmotic theory, ATP synthesis by ATP synthase (Complex V) is driven by:
Correct! Mitchell chemiosmotic theory: the ETC pumps H+ from the matrix to the intermembrane space, creating an electrochemical proton gradient. H+ flows back through ATP synthase (F0F1-ATPase), driving ATP synthesis.
Chemiosmotic coupling: ETC complexes I, III, IV pump H+ outward. Proton motive force = membrane potential + pH gradient. ATP synthase (Complex V) = F0 (membrane channel for H+) + F1 (catalytic ATP synthesis). P:O ratio: NADH = 2.5 ATP; FADH2 = 1.5 ATP (modern estimates).
Incorrect. The proton gradient (proton motive force) drives ATP synthase per the chemiosmotic hypothesis.
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Dinitrophenol (DNP) is a metabolic uncoupler used historically as a weight-loss agent. It causes weight loss by:
Correct! DNP is a lipophilic proton carrier that shuttles H+ across the inner mitochondrial membrane, bypassing ATP synthase. The proton gradient is dissipated as heat, requiring more substrate oxidation for the same ATP output.
Physiological uncoupling: thermogenin (UCP1) in brown adipose tissue is the natural uncoupler for non-shivering thermogenesis in neonates. DNP was used as a diet pill in the 1930s but caused hyperthermia and deaths. The heat generated = calories released without ATP production.
Incorrect. Uncouplers like DNP dissipate the proton gradient as heat, uncoupling substrate oxidation from ATP synthesis.
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In the well-fed (postprandial) state, which hormone primarily drives the shift toward anabolic metabolism (glycogen synthesis, fatty acid synthesis, protein synthesis)?
Correct! Insulin (released after a meal) promotes glucose uptake, glycogen synthesis (activates glycogen synthase), fatty acid synthesis (activates ACC), and protein synthesis. It inhibits lipolysis and gluconeogenesis.
Hormonal integration: Fed state = high insulin, low glucagon. Fasting = low insulin, high glucagon. Glucagon activates cAMP-PKA, promoting glycogenolysis, gluconeogenesis, and lipolysis. Insulin activates phosphodiesterase (degrades cAMP) and protein phosphatases (reverse PKA effects).
Incorrect. Insulin is the anabolic hormone of the fed state.
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After 24 hours of fasting, which metabolic change is expected in skeletal muscle?
Correct! During fasting, low insulin and high glucagon/cortisol promote glycogen breakdown in muscle and increased fatty acid oxidation to spare glucose for the brain.
Fasting metabolic changes: Liver: glycogenolysis (first 12h), then gluconeogenesis from lactate/alanine/glycerol. Muscle: glycogenolysis, then fatty acid oxidation, releases alanine (nitrogen carrier). Adipose: lipolysis releases FFA + glycerol. Brain: initially glucose, then switches to ketones (prolonged starvation).
Incorrect. During fasting, muscle breaks down glycogen and oxidizes fatty acids.
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Superoxide radical (O2-) generated as a byproduct of the electron transport chain is primarily neutralized by:
Correct! Superoxide dismutase (SOD) catalyzes the dismutation of superoxide (O2-) to hydrogen peroxide (H2O2) and O2. H2O2 is then further degraded by catalase or glutathione peroxidase.
Antioxidant defence: O2- (superoxide) is neutralized by SOD to H2O2. H2O2 is neutralized by catalase (to H2O + O2) or glutathione peroxidase (using GSH). NADPH (from HMP shunt) regenerates GSH via glutathione reductase. G6PD deficiency impairs this system, causing oxidative haemolysis.
Incorrect. Superoxide dismutase is the first line of defence against superoxide radicals.
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Insulin stimulates glucose uptake in muscle and adipose tissue by causing translocation of which glucose transporter to the plasma membrane?
Correct! Insulin causes GLUT4 vesicles to translocate from intracellular stores to the plasma membrane in muscle and adipose tissue, increasing glucose uptake.
GLUT transporters: GLUT1 (ubiquitous, basal glucose uptake, RBCs), GLUT2 (liver, pancreatic beta cells — low affinity, high capacity, glucose sensor), GLUT3 (neurons — high affinity), GLUT4 (muscle, adipose — insulin-responsive). In Type 2 diabetes, GLUT4 translocation is impaired (insulin resistance).
Incorrect. GLUT4 is the insulin-responsive transporter in muscle and adipose tissue.
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A 48-year-old patient with central obesity, hypertriglyceridaemia (TG 350 mg/dL), low HDL (28 mg/dL), hypertension, and fasting glucose 108 mg/dL has metabolic syndrome. The central metabolic defect is:
Correct! Metabolic syndrome is centred on insulin resistance. Adipose and muscle cells are resistant to insulin, leading to compensatory hyperinsulinaemia, which over time cannot maintain normoglycaemia.
Metabolic syndrome (IDF criteria): central obesity (waist >90 cm men/80 cm women in South Asians) plus any two of: TG >150, HDL <40 men/<50 women, BP >130/85, FG >100 mg/dL. Insulin resistance links all features: impaired glucose uptake, increased VLDL secretion (hypertriglyceridaemia), low HDL, hypertension. Treatment: weight loss, exercise, metformin.
Incorrect. Insulin resistance with compensatory hyperinsulinaemia is the central defect in metabolic syndrome.
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