LPL pathway is the primary mechanism by which plasma triglycerides (TGs) are hydrolysed leading to subsequent efficient removal. Apolipoprotein C-III (ApoC-III) modulates triglyceride levels primarily by inhibiting the LPL-dependent pathway but also the LPL-independent pathway.1
Triglycerides enter the blood plasma from dietary fat absorption in the intestine, in the form of chylomicrons, and from the liver, in the form of very low-density lipoprotein (VLDL) particles.1
Loss-of-function mutations in LPL make the LPL-pathway inefficient and lead to accumulation of chylomicrons in the blood.1
Limited functionality.
ApoC-III: apolipoprotein C-III, FCS: familial chylomicronemia syndrome, LPL: lipoprotein lipase, TG: triglycerides, TRL: triglyceride-rich lipoprotein, VLDL: very low-density lipoprotein
Adapted from Gaudet D et al. N Engl J Med 2014;371(23):2200–6 and Crooke RM. Expert Opin Biol Ther 2005;5(7):907–17.
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