Intestinally derived lipids: Metabolic regulation and consequences - An overview

Various dietary factors affect postprandial metabolism yet precise mechanisms have not necessarily been pinpointed. The effects of various meal components on postprandial lipemia lead to the following question: do we need a standardized oral lipid tolerance test? A number of transporters, enzymes, receptors and hormones directly influence and act as "gatekeepers" of these processes. Each protein appears to have specific and individual functional roles in the overall process and selected developments in these areas will be reviewed Within the intestinal cells. FABP2 (fatty acid-binding protein 2) and MTP (microsomal triglyceride transfer protein) are required for the formation of chylomicrons. Niemann-Pick Cl-like L (NPCl-Ll) plays an important role in echolesterol absorption and provides a pharmacological target. Hormones such as GLP1 and GLP2 influence this absorption process. Within the periphery, lipoprotein lipase (LPL) is a key gatekeeper of clearance. Of the massive amouints of fatty acids released by LPL, 36% escape peripheral adipose and muscle uptake and fatty acid overload can result in LPL product inhibition. Acylation stimulating protein (ASP) and insulin are two key hormones in maintaining efficient tissue uptake and re-esterification of fatty acids while TNF alpha negatively influences this process. In both ASP deficient (C3 KO) and C5L2KO mice. Postprandial lipemia increased with reduced adipose tissue storage. This is componsated by increased enegy expenditure and muscle lipid oxidation. Clearance of hepatic remnants iscontrolled through many factors, including SR-BI and ABCAI. Intestinal, peripheral and hepatic gatekeepers serve important and individual roles in regulating postprandial lipemia and provide potential targets for regulation. (C) 2008 Elsevier Ireland Ltd. All rights reserved.