During prolonged starvation (>5 days), the brain reduces its dependence on glucose and uses an alternative fuel. Which metabolic adaptation enables this shift?
- A Increased brain uptake of fatty acids from VLDL particles due to upregulation of lipoprotein lipase in cerebral capillaries
- B Gluconeogenesis from leucine and lysine in brain astrocytes, providing sufficient glucose autonomously
- C Upregulation of MCT1 transporters in the blood-brain barrier enabling ketone body (beta-hydroxybutyrate and acetoacetate) uptake, which provide up to 70% of brain energy ✓
- D Glycogen mobilisation from astrocytes providing glucose equivalent to hepatic glycogenolysis for up to 14 days
Correct answer: C. Upregulation of MCT1 transporters in the blood-brain barrier enabling ketone body (beta-hydroxybutyrate and acetoacetate) uptake, which provide up to 70% of brain energy
Explanation
During prolonged starvation, hepatic ketogenesis produces beta-hydroxybutyrate and acetoacetate from fatty acid-derived acetyl-CoA. These ketone bodies cross the blood-brain barrier via monocarboxylate transporters (MCT1/MCT2), and can supply up to 60–70% of the brain's energy needs, sparing glucose and reducing the need for muscle protein catabolism for gluconeogenesis. The brain cannot oxidise fatty acids directly (long-chain FAs do not cross the BBB efficiently). Astrocyte glycogen stores are minimal and not a prolonged fuel source.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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