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It is well-established based on evidence accrued during the last three decades that high plasma concentrations of cholesterol-rich atherogenic lipoproteins are causatively linked to CVD, and that lowering these reduces atherosclerotic cardiovascular events in humans ( APOC3 - the gene for apolipoprotein (apo) C-III - has emerged as being particularly important as a regulator of triglyceride transport and a novel therapeutic target to reduce dyslipidaemia and CVD risk ( Structure and Regulation of APOC-III APOC3 is expressed in hepatocytes and, to a lesser extent in enterocytes ( 0 , monosialylated apoC-III 1 and disialylated apoC-III 2 ( The transcription rate of APOC3 is decreased by insulin (30), and farnesoid X receptor (FXR) (Figure 1) (32)
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Evidence for systemic injectable use is emerging but not yet definitive
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