Metabolism of Ketone Bodies
Start with the big picture
Ketogenesis occurs in liver mitochondria when fatty acid oxidation supplies acetyl-CoA, commonly in low-insulin, high-glucagon states. Reduced oxaloacetate availability, as it is diverted toward gluconeogenesis, slows TCA-cycle entry and favors acetyl-CoA conversion to ketone bodies. Mitochondrial HMG-CoA synthase is the rate-limiting enzyme; subsequent reactions produce acetoacetate, which can interconvert with β-hydroxybutyrate or form acetone. The liver produces ketones but cannot use them because it lacks thiophorase. Peripheral tissues can convert ketones to acetyl-CoA for energy, while red blood cells cannot use them. Excess ketogenesis contributes to ketoacidosis; laboratory interpretation also depends on which ketone bodies a test detects.
What you'll learn
- Identify the three ketone bodies and the circumstances that promote their production.
- Outline the key enzymatic steps in hepatic ketogenesis.
- Explain why the liver produces ketones but cannot consume them.
- Describe ketone use by peripheral tissues and the limitations of laboratory testing.
- Relate excess ketogenesis to ketoacidosis and its clinical features.
Continue your study
Work through the complete notes and reinforce the topic with the study tools available in the full lesson.
