Apolipoprotein C-III (apo C-III) (molecular weight 9 kDa) is actinic mainly in the alarmist and, to a bottom extent, the intestine. It forms a above structural basic of VLDL but is aswell present in chylomicrons and HDL. It acts as an inhibitor of LPL, and has added afresh been apparent to advance hepatic accumulation and beard of VLDL. Apo C-III aswell inhibits hepatic uptake of chylomicron and VLDL balance particles, possibly by preventing alternation of apo E on these balance particles with the hepatic receptor. Top claret apo C-III concentrations are associated with top claret triglyceride concentrations.
Null mutations accept been appear which are associated with low claret triglyceride and LDL, and top HDL concentrations. However, the APOC3 gene is abutting to the APOA1 gene, and both are amiss in some forms of apo A1 deficiency, which could cause low claret HDL and triglyceride concentrations.
APOC3 inhibits lipoprotein lipase and hepatic lipase; it is anticipation to arrest hepatic uptake of triglyceride-rich particles. The APOA1, APOC3 and APOA4 genes are carefully affiliated in both rat and animal genomes. The A-I and A-IV genes are transcribed from the aforementioned strand, while the A-1 and C-III genes are convergently transcribed. An access in apoC-III levels induces the development of hypertriglyceridemia. Recent evidences advance an intracellular role for Apo-CIII in announcement the accumulation and beard of triglyceride-rich VLDL particles from hepatic beef beneath lipid-rich conditions. However, two by itself occurring point mutations in animal apoC3 coding sequence, namely Ala23Thr and Lys58Glu accept been apparent to abate the intracellular accumulation and beard of triglyceride-rich VLDL particles from hepatic cells.