Newly formed very low-density lipoprotein (VLDL) released from the liver can acquire lipoproteins in the circulation. Apolipoprotein C-I (APOC1) is a 6.6 kDa apolipoprotein that is synthesised mainly in the liver but also in other tissues. It is a constituent of triglyceride-rich lipoproteins (around 10% of the protein of VLDLs and 2% of HDLs) that slow the circulatory clearance of triglyceride-rich lipoproteins by a variety of mechanisms. As well as binding and inhibiting triglyceride-rich lipoprotein uptake by the very low-density lipoprotein receptor (VLDLR), it can also binds free fatty acids (FAs) in the circulation, reducing their uptake by cells (Shachter 2001, Hansen et al. 2011). A minor constituent of VLDL is apolipoprotein IV (APO4) (Kotite et al. 2003).
Shachter, NS
Kotite, L, Zhang, LH, Yu, Z, Burlingame, AL, Havel, RJ
Hansen, JB, Fernández, JA, Notø, AT, Deguchi, H, Björkegren, J, Mathiesen, EB
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