Fig. 1

The proposed pro-inflammatory pathway following ingestion of a HFM. Triglycerides (TRG), Triglyceride Rich Lipoproteins (TRL), Postprandial lipemia (PPL), High-density lipoprotein cholesterol (HDL), Low Density Lipoprotein cholesterol (LDL), Nuclear Factor Kappa B (NF-κB), Interleukin 1β (IL-1β), Interleukin-6 (IL-6), Tumor Necrosis Factor-α (TNF-α). Increased TRG in circulation leads to increase HDL clearance from circulation and an increase in small dense LDL particles. This process increases subendothelial retention of lipoproteins, leads to oxidized LDL, and activation of the vascular endothelium. The activated endothelium increases the recruitment of immune cells, mainly monocytes, to the vascular surface to scavenge oxidized LDL molecules. Accumulation of lipid inside monocytes leads to formation of macrophages and secretion of several pro-inflammatory cytokines. Macrophages accumulate enough lipid to form foam cells that result in fatty streaks within the vascular endothelium