In kwashiorkor, hypoalbuminaemia is the central biochemical defect causing oedema. What is the primary mechanism by which isolated protein deficiency leads to hypoalbuminaemia despite adequate caloric intake?

• A Increased renal albumin loss due to protein-deficiency-induced nephrotic syndrome
• B Decreased albumin half-life due to autoimmune destruction
• C Decreased hepatic albumin synthesis due to insufficient amino acid substrate, particularly essential amino acids ✓
• D Increased albumin catabolism by muscle proteases to provide gluconeogenic substrates

Explanation

In kwashiorkor, adequate caloric intake (carbohydrates) spares gluconeogenesis but the specific deficiency of dietary protein — particularly essential amino acids — starves the liver of precursors for albumin synthesis. Albumin is constitutively synthesised by hepatocytes at ~12–25 g/day, with a half-life of ~20 days. Without essential amino acids, hepatic protein synthesis is profoundly impaired. Low plasma albumin reduces oncotic pressure → oedema. Simultaneously, aflatoxin exposure may contribute hepatocellular damage. In marasmus (combined calorie-protein deficiency), the body catabolizes muscle and fat without oedema because amino acids from muscle maintain some albumin synthesis.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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