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 C1-like 1 (NPC1-L1) plays an important role in
cholesterol 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 amounts 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
TNFalpha negatively influences this process. In both ASP deficient (C3 KO) and C5L2 KO mice, postprandial
lipemia increased with reduced adipose tissue storage. This is compensated by increased energy expenditure and muscle
lipid oxidation. Clearance of hepatic remnants is controlled through many factors, including SR-B1 and ABCA1. Intestinal, peripheral and hepatic gatekeepers serve important and individual roles in regulating postprandial
lipemia and provide potential targets for regulation.