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).