A malnourished child develops refeeding syndrome after aggressive intravenous glucose administration. The biochemical mechanism underlying hypophosphataemia in refeeding syndrome is:

• A Glucose infusion suppresses PTH, reducing tubular phosphate reabsorption
• B Glucose metabolism generates organic acids that bind phosphate
• C Refeeding activates alkaline phosphatase which hydrolyses serum phosphate esters
• D Insulin-stimulated cellular uptake of phosphate for ATP synthesis and phosphorylation of glycolytic intermediates depletes serum phosphate ✓

Explanation

Refeeding syndrome occurs when glucose is reintroduced to chronically starved individuals. Glucose infusion stimulates insulin secretion, which drives anabolic processes including cellular uptake of phosphate for ATP regeneration, phosphorylation of glycolytic intermediates (G-6-P, F-1,6-BP, 3-PG), and phosphocreatine synthesis. Since chronically malnourished patients have depleted total body phosphate stores, serum phosphate drops precipitously (hypophosphataemia <0.5 mmol/L). This impairs ATP-dependent membrane pumps, causing cardiac arrhythmias, respiratory failure and haemolytic anaemia. PTH changes are not the mechanism. Organic acid binding to phosphate does not occur. Alkaline phosphatase does not deplete serum phosphate in this context.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

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Written and medically reviewed by the StethoPrep medical team.