The digestion and absorption of lipids has been extensively reviewed in the literature (Nutting et al., 1999; Ros, 2000; Nordskog et al., 2001; Phan and Tso, 2001). Briefly, lipid digestion involves three main sequential steps: (i) dispersion of fat globules into a coarse emulsion (ii) enzymatic hydrolysis of triglyceride (TG) at the oil/water interface and (iii) dispersion of the digestion products into a fine emulsion of high surface area from which absorption can readily occur (Carey et al., 1983). Digestion of dietary lipids, which are predominantly in the form of poorly water soluble neutral TG, begins in the stomach where lingual and gastric lipases secreted by the salivary gland and gastric mucosa, respectively, initiate the hydrolysis of TG to its component diglyceride (DG) and free fatty acid (FA) components. Liberation of these more water soluble lipid digestion products, in combination with the shear force encountered during antral contraction and gastric emptying, facilitates the formation of a coarse emulsion which upon entry into the duodenum, stimulates the secretion of bile salts and biliary lipids from the gall bladder and the release of lipase enzymes from the pancreas (Borgstrom and Hildebrand, 1975; Ladas et al., 1984; Hernell et al., 1990). Biliary-derived phospholipid and cholesterol adsorb to the surface of the oil droplets comprising the crude emulsion, resulting in improved colloidal stability and a reduction in the oil droplet size with an attendant increase in surface area. These changes facilitate lipid hydrolysis, which occurs at the oil/water interface through the combined actions of colipase and pancreatic lipase enzymes, and results in the production of one molecule of 2-monoglyceride (MG) and two molecules of FA for each TG molecule hydrolysed. As lipolysis proceeds, these digestion products collect at the surface of the lipid droplets, typically forming liquid crystalline structures which slough off from the droplet surface and, in conjunction with bile salts and phospholipids, form multilamellar and unilamellar vesicles and ultimately, bile salt-lipid mixed micelles (Hernell et al., 1990; Staggers et al., 1990). While the specific mechanisms controlling the gastrointestinal absorption of lipids have not been fully elucidated, it is known that bile salt mixed micelles are not absorbed intact but must dissociate and release the emulsified lipid digestion products prior to absorption into the enterocyte (Hoffman, 1970; Simmonds, 1972). Dissociation of mixed micelles may be triggered by a microclimate of lower pH associated with the intestinal brush border membrane (Shiau, 1990; Thomson et al., 1993).
In addition to passive diffusion, there is now evidence to suggest that specific membrane bound carrier proteins may facilitate the transport of lipid digestion products across the apical membrane of the enterocyte (Stremmel et al., 1985; Stremmel, 1988; Poirier et al., 1996). Once within the enterocyte, the cytosolic fatty acid binding proteins L-FABP and I-FABP bind to FA and facilitate FA solubili-sation and distribution to the cell nucleus and endoplasmic reticulum (Ockner and Manning, 1974; McArthur et al., 1999; Besnard et al., 2002; Huang et al., 2002).
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