A patient recovering from major surgery receives total parenteral nutrition (TPN). After 2 weeks, the patient develops liver steatosis. The MOST likely biochemical reason for TPN-associated steatosis is:

• A TPN-induced hyperinsulinaemia activates adipose lipolysis, flooding the liver with free fatty acids
• B Excess glucose in TPN is converted to fatty acids via de novo lipogenesis, overwhelming hepatic VLDL secretion capacity ✓
• C Absence of dietary fat in TPN prevents essential fatty acid synthesis needed for phospholipid-VLDL assembly
• D Intravenous amino acids in TPN directly inhibit mitochondrial beta-oxidation

Explanation

High glucose load in TPN chronically elevates insulin, driving hepatic de novo lipogenesis (glucose → pyruvate → acetyl-CoA → malonyl-CoA → fatty acids) at rates exceeding the liver's capacity to assemble and export VLDL (limited by apoB-100 synthesis rate). Concurrent carbohydrate excess also suppresses fatty acid oxidation via elevated malonyl-CoA inhibiting CPT-I. The net result is hepatic triglyceride accumulation (steatosis). Essential fatty acid deficiency is also a concern in TPN but causes different manifestations (dermatitis, not primarily steatosis).

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.