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Not all energy is meant to be spent quickly. In this episode, Medlock Holmes follows fatty acids — dense, efficient stores of energy — as they are released, transported, and broken down with deliberate precision.
Fatty acid catabolism is revealed as a process designed for endurance rather than urgency. We explore how fatty acids are mobilised from storage, activated, and transported into mitochondria, where β-oxidation systematically shortens them, releasing acetyl-CoA and reducing equivalents step by step. There is no haste here — only efficiency and inevitability.
Drawing on Lehninger’s mechanistic clarity and Harper’s clinically grounded discussion of fatty acid oxidation and ketogenesis, this episode shows how fat becomes the dominant fuel during fasting, prolonged exercise, and carbohydrate scarcity. Ketone bodies emerge not as pathological curiosities, but as adaptive solutions for energy delivery when glucose is limited.
Medlock learns that fatty acid catabolism reflects a different metabolic philosophy. Where glycolysis is responsive and rapid, fat oxidation is patient and sustaining. Disease arises when this system is inaccessible, incomplete, or misregulated — particularly in tissues that depend on long-term energy continuity.
This is metabolism built for distance, not speed.
Key Topics Explored
* Mobilisation and activation of fatty acids
* Transport into mitochondria
* β-oxidation and acetyl-CoA production
* Ketogenesis and metabolic adaptation
* Hormonal regulation during fasting
* Clinical relevance of fatty acid oxidation defects
By From the Medlock Holmes desk — where clinical questions are taken seriously.Not all energy is meant to be spent quickly. In this episode, Medlock Holmes follows fatty acids — dense, efficient stores of energy — as they are released, transported, and broken down with deliberate precision.
Fatty acid catabolism is revealed as a process designed for endurance rather than urgency. We explore how fatty acids are mobilised from storage, activated, and transported into mitochondria, where β-oxidation systematically shortens them, releasing acetyl-CoA and reducing equivalents step by step. There is no haste here — only efficiency and inevitability.
Drawing on Lehninger’s mechanistic clarity and Harper’s clinically grounded discussion of fatty acid oxidation and ketogenesis, this episode shows how fat becomes the dominant fuel during fasting, prolonged exercise, and carbohydrate scarcity. Ketone bodies emerge not as pathological curiosities, but as adaptive solutions for energy delivery when glucose is limited.
Medlock learns that fatty acid catabolism reflects a different metabolic philosophy. Where glycolysis is responsive and rapid, fat oxidation is patient and sustaining. Disease arises when this system is inaccessible, incomplete, or misregulated — particularly in tissues that depend on long-term energy continuity.
This is metabolism built for distance, not speed.
Key Topics Explored
* Mobilisation and activation of fatty acids
* Transport into mitochondria
* β-oxidation and acetyl-CoA production
* Ketogenesis and metabolic adaptation
* Hormonal regulation during fasting
* Clinical relevance of fatty acid oxidation defects