Following a fat-rich meal, endotoxins are transported into the bloodstream with the products of lipid digestion, thus potentially contributing to the initiation and continuation of postprandial inflammation.32,61–63 Higher blood concentrations of LBP and sCD14, markers of blood endotoxin exposure involved in the further inflammatory response,31,64 may be a link between postprandial lipemia and endothelial dysfunction.65,66 We found no significant postprandial increases in endotoxemia markers following spreads, but there was an elevation in sCD14 at 8 h following RO. This evidence concerns the gene LBP and endothelial dysfunction.