Lipoprotein lipase (LPL)
Cofactors used
Clinical / pharmacological. LPL or apoC-II deficiency: familial chylomicronaemia (type I), pancreatitis
What it does, reaction by reaction
Lipoprotein Metabolism (Exogenous and Endogenous Pathways: chylomicrons, VLDL, LDL, HDL) Lipid Metabolism · Intestine, liver, plasma, capillary endothelium
Chylomicron TAG + H2O → fatty acids + glycerol
Converts Chylomicron TAG H2O into Fatty acid Glycerol
› Notes
Endothelial LPL, activated by apoC-II and anchored by GPIHBP1, hydrolyzes core TAG. Insulin increases LPL activity in adipose tissue in the fed state, whereas cardiac/skeletal muscle LPL favors fatty-acid uptake according to local energy demand. Released fatty acids enter adipocytes for storage or muscle for oxidation; glycerol returns to liver.
VLDL TAG + H2O → fatty acids + glycerol; VLDL → IDL
Converts VLDL TAG H2O into Fatty acid Glycerol VLDL
› Notes
LPL, activated by apoC-II, removes much of the VLDL TAG in capillary beds. ApoC-II is returned to HDL, and the particle becomes an intermediate-density lipoprotein (IDL; VLDL remnant) enriched in cholesteryl esters and retaining apoB-100 and apoE.
Showing all 2 reactions.
What accelerates and inhibits it
Regulation is pathway-specific, so each context is listed separately
Lipoprotein Metabolism (Exogenous and Endogenous Pathways: chylomicrons, VLDL, LDL, HDL)
ApoC-II; GPIHBP1-mediated endothelial presentation; ANGPTL8 in the fed state favors adipose LPL
ApoC-III; ANGPTL3/ANGPTL4 (tissue/context dependent)
Insulin increases adipose LPL after feeding; fasting shifts relative LPL activity toward oxidative tissues
Recent literature
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