Lipoprotein lipase (LPL) deficiency causes hyperchylomicronemia. A patient presents with pancreatitis, eruptive xanthomas, lipemia retinalis, and triglycerides >2000 mg/dL. The role of LPL in normal triglyceride clearance is:
- A LPL on hepatocyte surfaces cleaves VLDL-TG, releasing fatty acids for hepatic re-esterification
- B LPL is a hepatic enzyme that phosphorylates apoB-48 to facilitate chylomicron internalization via the LDL receptor
- C LPL on capillary endothelium (especially muscle and adipose) hydrolyzes TG in chylomicrons and VLDL, releasing fatty acids for tissue uptake, activated by apolipoprotein C-II ✓
- D LPL cleaves phospholipids in the chylomicron surface, releasing lyso-PC that activates LCAT for cholesterol esterification
Correct answer: C. LPL on capillary endothelium (especially muscle and adipose) hydrolyzes TG in chylomicrons and VLDL, releasing fatty acids for tissue uptake, activated by apolipoprotein C-II
Explanation
LPL is anchored to endothelial cell surfaces (especially in adipose tissue and skeletal muscle) via heparan sulfate proteoglycans. It hydrolyzes triglycerides in circulating chylomicrons and VLDL particles, releasing free fatty acids for uptake by adjacent tissues (oxidation in muscle; re-esterification to TG in adipose). ApoC-II on chylomicron/VLDL surface is essential for LPL activation; ApoC-III inhibits LPL. LPL deficiency (or ApoC-II deficiency) causes massive hypertriglyceridemia with pancreatitis risk. Hepatic lipase (HL) acts on IDL and HDL, not LPL.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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