Biochemistry
Metabolism and Homeostasis
Metabolism and homeostasis for MBBS: fed and fasting states, oxidative phosphorylation, nucleotide metabolism and gout, vitamins, minerals and haem, mapped to NMC codes BI6.1 to BI6.15.
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Metabolism and Homeostasis
Metabolism and homeostasis for MBBS: fed and fasting states, oxidative phosphorylation, nucleotide metabolism and gout, vitamins, minerals and haem, mapped to NMC codes BI6.1 to BI6.15.
This chapter integrates metabolism across the fed and fasting states and the organs that coordinate it. It covers bioenergetics and oxidative phosphorylation, nucleotide metabolism and gout, the vitamins and minerals, haem synthesis and its disorders, and the interpretation of acid-base and organ function tests.
High-yield: Metabolism and Homeostasis
- In the fed state insulin drives glycogen, fat and protein synthesis; in fasting glucagon drives glycogenolysis, gluconeogenesis and lipolysis.
- The brain relies on glucose, but after prolonged fasting it adapts to use ketone bodies to spare protein.
- The electron transport chain pumps protons across the inner mitochondrial membrane; ATP synthase uses that gradient to make ATP.
- Complex IV, cytochrome c oxidase, is inhibited by cyanide and carbon monoxide, blocking oxidative phosphorylation.
- Uncouplers such as 2,4-dinitrophenol dissipate the proton gradient as heat, so oxygen use continues but ATP falls.
- Purines are degraded to uric acid; xanthine oxidase catalyses the final steps and is inhibited by allopurinol.
- Gout results from hyperuricaemia with urate crystal deposition, showing negatively birefringent needle-shaped crystals.
- Lesch-Nyhan syndrome is HGPRT deficiency causing purine overproduction, self-mutilation and hyperuricaemia.
- Water-soluble vitamins, the B group and vitamin C, are not stored and their deficiencies appear relatively quickly.
- Thiamine deficiency causes beriberi and Wernicke-Korsakoff syndrome; niacin deficiency causes pellagra with dermatitis, diarrhoea and dementia.
- Fat-soluble vitamins A, D, E and K are stored in the liver and fat and can accumulate to toxic levels.
- Vitamin K is needed to gamma-carboxylate clotting factors II, VII, IX and X; warfarin blocks its recycling.
- Haem synthesis begins with ALA synthase, the rate-limiting enzyme; lead inhibits ALA dehydratase and ferrochelatase.
- Arterial blood gas interpretation starts with pH, then carbon dioxide for respiratory and bicarbonate for metabolic components.
- Iron deficiency gives microcytic hypochromic anaemia with low ferritin and raised total iron binding capacity.
Metabolic fuel switching
- **Fed state (insulin):** Glycogen, triglyceride and protein synthesis. Glucose uptake and storage.
- **Fasting (glucagon):** Glycogenolysis, then gluconeogenesis and lipolysis.
- **Prolonged starvation:** Ketone bodies fuel the brain, sparing muscle protein.
- **Poisons of oxidative phosphorylation:** Cyanide and carbon monoxide block complex IV; dinitrophenol uncouples.
NMC competencies in this chapter
- **BI6.1:** Metabolic processes in specific organs in the fed and fasting states
- **BI6.3:** Common disorders of nucleotide metabolism
- **BI6.5:** Biochemical role of vitamins and manifestations of their deficiency
- **BI6.6:** Generation of energy in cells and oxidative phosphorylation
- **BI6.8:** Interpretation of arterial blood gas analysis in various disorders
- **BI6.9:** Functions, metabolism and homeostasis of minerals
- **BI6.11:** Functions of haem and porphyrin metabolism
- **BI6.15:** Abnormalities of kidney, liver, thyroid and adrenal function
Frequently Asked Questions
How does the body switch fuels between eating and fasting?
Insulin dominates after a meal and promotes storage of glucose, fat and protein. During fasting glucagon takes over, mobilising glycogen, then gluconeogenesis and fat breakdown, and finally ketone bodies to fuel the brain.
Why does cyanide stop ATP production?
Cyanide inhibits cytochrome c oxidase, complex IV of the electron transport chain, so electrons can no longer pass to oxygen and the proton gradient that drives ATP synthase collapses.
What is the biochemical basis of gout?
Gout arises from hyperuricaemia, the end product of purine breakdown. Urate crystals deposit in joints, and drugs such as allopurinol lower uric acid by inhibiting xanthine oxidase.
Which clotting factors depend on vitamin K?
Factors II, VII, IX and X, plus proteins C and S. Vitamin K is needed for their gamma-carboxylation, which is why warfarin, a vitamin K antagonist, prolongs clotting.
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