Postprandial hypertriglyceridemia is an emerging risk factor for cardiovascular diseases and is associated with metabolic syndrome, obesity and insulin resistance. The small intestine participates in the postprandial triglyceridemia since both the size and number of secreted chylomicrons modulate lipoprotein lipase activity (LPL). Chylomicron synthesis is a complex mechanism in which the lipidation of Apolipoprotein B48 (ApoB48) by the Microsomal Triglyceride Transfer Protein (MTP) and the transfer between reticulum and Golgi in which the Liver Fatty Acid Binding Protein (L -FABP) is involved are limiting steps. An intestinal fat-mediated adaptation in postprandial period has been demonstrated by in vivo (transgenic and wild type mice) and ex vivo (intestinal segments) approches. This postprandial adaptation is triggered by the glycoprotein CD36 in the presence of Long chain Fatty Acids (LCFA) that regulates the ERK1/2 pathway and leads to the induction of ApoB48, MTP and L-FABP. The rapid degradation of CD36 by the ubiquitin-proteasome pathway in the presence of LCFA, which leads to ERK1/2 deactivation, has a feature of a receptor. Since firstly, Peroxisome Proliferator Activated Receptor (PPAR) knockout mice display an alteration of postprandial adaptation associated with a hypertriglyceridemia and secondly, dietary fat-mediated PPAR up-regulation is CD36 dependent, CD36 and PPAR might participate to a common regulation mechanism. In conclusion, CD36 and PPAR contribute to the enterocyte LCFA sensing responsible for postprandial adaptation that promotes the formation of large chylomicrons efficiently cleared into the blood.
