secreted by the salivary glands (salivary
lipase) as well as by the fundic region of
the stomach (Gargouri et al., 1989).
Salivary lipase possesses significant
hydrolytic activity at pH 3.5, near that of
the stomach. Gastric lipase is present at
higher activities in neonatal animals and
has higher hydrolytic activity toward milk
triacylglycerols than does pancreatic lipase
(Jensen et al., 1997). Gastric lipase attacks
primarily short- and medium-chain fatty
acid linkages on the sn-3 position of
triacylglycerol, such as those prevalent in
milk of ruminants and swine.
Bile is essential for further lipid diges-
tion and absorption in the small intestine
(Brindley, 1984). The primary components
of bile necessary for lipid digestion are the
bile salts and phospholipids. Bile salts,
which are responsible for emulsification of
lipid droplets, are synthesized from
cholesterol in hepatocytes of the liver. The
bile salts are conjugated by the liver with
the amino acids taurine or glycine, which
increases the water solubility and
decreases the cellular toxicity of the bile
salts. Pigs conjugate bile salts to both
taurine and glycine, whereas poultry only
produce taurine conjugates (Freeman,
1984). The structure of the bile salts is such
that it provides a flat molecule, with one
side being polar and hydrophilic and the
other non-polar and hydrophobic. Thus,
the bile salts lie at the water–lipid interface
and do not penetrate deeply into either
surface. Bile salts in bile are present in
cylindrical structures termed bile micelles
(Brindley, 1984). The presence of bile
imparts detergent-like effects on dietary
lipids, causing lipid droplets to be sub-
divided into smaller and smaller droplets.
Pancreatic secretions into the small
intestine are also critical for lipid digestion
and absorption. Dispersion of lipid by bile
salts enables attachment of the pancreatic
polypeptide colipase, which attracts
pancreatic lipase and enables it to interact
at the surface of the lipid droplet (Brindley,
1984). Although the pancreatic lipase itself
has no specific requirement for bile salts,
the increased surface area created by the
action of bile salts greatly increases the rate
of pancreatic lipase-catalysed triacyl-
glycerol hydrolysis. Pancreatic lipase
specifically attacks the sn-1 and sn-3 link-
ages of triacylglycerols, resulting in forma-
tion of 2-monoacylglycerols and free fatty
acids. Phospholipases, particularly of the
A 1 and A 2 types, are secreted in pancreatic
juice and convert the phospholipid lecithin
(phosphatidylcholine) to lysolecithin
(lysophosphatidylcholine).
Absorption of lipids is dependent on
the formation of mixed micelles and on
continued movement of lipids from oil
droplets in the intestinal lumen into the
mixed micelles. In the presence of bile
salts, the fatty acids and monoacylglycerols
produced by pancreatic lipase action spon-
taneously aggregate into mixed micelles.
Lysolecithin produced from biliary and
dietary phospholipids plays a key role in
formation and stabilization of micelles. In
particular, lysolecithin is highly efficient at
solubilizing highly non-polar lipids such
as stearic acid (18:0) into mixed micelles
(Brindley, 1984). Formation of mixed
micelles is necessary to move the non-
polar lipids across the unstirred water
layer present at the surface of the intestinal
microvillus membranes; this unstirred
water layer is thought to be the main
barrier to lipid absorption (Brindley, 1984).
Fatty acids and monoacylglycerols can
enter the intestinal cells by simple diffu-
sion into the lipid membrane, although the
presence of transmembrane carrier proteins
has been postulated (Glatz et al., 1997).
Absorption of fatty lipids into intestinal
epithelial cells is an energy-independent
process that is facilitated by maintenance
of a concentration gradient into the cells.
Several putative fatty acid translocase
proteins have been identified in tissues,
but their role and mechanism of action
have not been resolved (Glatz et al., 1997).
After fatty acids are absorbed into cells,
they become bound to low-molecular
weight (12–15 kDa) binding proteins (Glatz
et al., 1997). These binding proteins aid in
fatty acid absorption, prevent accumula-
tion of potentially toxic free fatty acids and
may direct fatty acids to the appropriate
intracellular sites for metabolism.98 J.K. Drackley