Most absorption of fatty acids and
monoacylglycerols takes place in the
jejunum in mammals. In fowl, some fatty
acid absorption has been demonstrated in
both the duodenum and the ileum. The
extensive degree of antiperistaltic or reflux
activity in the avian intestinal tract may
contribute to this more diffuse location of
lipid absorption (Freeman, 1984). Bile salts
are not absorbed until they reach the
terminal ileum, but instead cycle back to
the intestinal lumen to participate in
further micelle formation. The bile salts are
absorbed efficiently in the ileum by an
active transport process and are returned to
the liver (enterohepatic circulation) to be
reincorporated into bile. In both pigs and
fowl, this active recycling means that the
quantity of bile salts that must be synthe-
sized by the liver is quite low (Freeman,
1984). Small quantities of bile salts are not
reabsorbed but enter the large intestine,
where they are converted into products
known as ‘secondary bile salts’ by
anaerobic gut bacteria. Loss of this quantity
of bile salts in the faeces is the only route
for cholesterol excretion from the body.
Fatty acids are activated for further
metabolism within intestinal epithelial
cells by esterification to coenzyme A
(CoA), a process that consumes two high-
energy phosphate bonds from ATP. In non-
ruminants, the acyl-CoA molecules largely
are re-esterified to triacylglycerols by the
monoacylglycerol pathway, in which acyl-
CoA molecules are added sequentially to
2-monoacylglycerols absorbed from the
intestinal lumen. A smaller quantity of
triacylglycerol is formed by the -glycerol-
phosphate pathway. Absorbed lysolecithin
is re-acylated in intestinal cells to form
lecithin. Cholesterol is actively synthesized
from acetyl-CoA in intestinal cells of most
farm animal species. Some of the
cholesterol is esterified with a long-chain
fatty acyl-CoA by acyl-CoA–cholesterol
acyltransferase (ACAT) to form cholesterol
esters.
Delivery of triacylglycerol from the
intestine to other organs of the body
requires that these highly non-polar lipids
are packaged into a form that is stable in
aqueous environments. To do so, the non-
polar lipids (triacylglycerol, cholesterol
esters, fat-soluble vitamins) are surrounded
by amphipathic compounds such as free
cholesterol, phospholipids and specific
proteins called apoproteins (Hussain et al.,
1996). The major apoproteins synthesized
by intestinal cells of most species are apo-
B48, apo-AI and apo-AIV. The resulting
particles, called chylomicrons, are quite
large in mammalian species (50–500 nm)
and contain by weight 85–95% triacyl-
glycerol, 4–9% phospholipids, ~1% free
cholesterol, ~0.5% esterified cholesterol
and ~0.6% protein (Brindley, 1984). The
size, but not number, of the chylomicrons
increases in proportion to larger dietary
intakes of lipid. Chylomicrons are secreted
from the intestinal cells and enter the
lacteals of the lymphatic system, which
then drains into the venous blood at the
thoracic duct. Fatty acids of less than 14
carbons are not actively esterified by
intestinal enzymes, and instead are
absorbed directly into the portal vein as
free fatty acids.
In fowl, the intestinally synthesized
lipoprotein particles are classified as very
low-density lipoproteins (VLDLs), and are
much lower in triacylglycerol content than
mammalian chylomicrons or even VLDLs
from pigs or humans (Freeman, 1984). The
lymphatic system is poorly developed in
fowl, and consequently the VLDL are
absorbed directly into the portal vein.
Fatty acid digestibility is high in non-
ruminants, with values often >80% in pigs
and poultry and >90% in pre-ruminant
calves (Doreau and Chilliard, 1997).
Intestinal fatty acid digestibility decreases
with increasing chain length and increases
with increasing unsaturation. Absorption
of saturated fatty acids is greater when they
are in the sn-2 position of triacylglycerols,
because they are absorbed as the 2-mono-
acylglycerol after pancreatic lipase action.
Fatty acid digestibility increases somewhat
with age in both pigs and poultry; fat
digestibility in young chicks in particular
is quite poor because of the limited pro-
duction of bile salts (Doreau and Chilliard,
1997).Lipid Metabolism 99