NEFAs may also promote a complex dyslipidemia characterized by increased VLDL-triglyceride rich particles, reduced levels of HDL-cholesterol, and an increased number of small dense LDL-cholesterol particles. Potential mechanisms by which NEFAs may contribute to these complex disturbance of lipid metabolism include increasing hepatic apoprotein B production and VLDL synthesis, with an increase in the number of VLDL-triglyceride rich particles (4). HDL-cholesterol concentrations fall in part as cholesterol is transferred from HDL to VLDL by the activity of cholesterol-ester transfer protein (CETP). As triglycerides are hydrolyzed from the greater number of VLDL-particles by endothelial lipoprotein lipase, large numbers of small, dense LDL particles are produced (18).
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