dietary intake. Such a simulation of Zn
metabolism was constructed for this
chapter from the results of numerous Zn
metabolism studies. The objective of the
simulation is to compile results of studies
which have addressed different aspects of
Zn metabolism or different ranges of condi-
tions. It is hoped that the whole-body
simulation of Zn metabolism will help to
identify productive areas of investigation
for other elements as well as Zn.
Simulation of whole body metabolism pro-
vides a method of reviewing Zn dynamics
as well as providing unique insight into
trace element dynamics in general.
Zinc
MetabolismZinc metabolism in animals and man has
been the subject of extensive reviews (e.g.
Chesters, 1997). Zinc is absorbed mainly by
the small intestine, although the major
section(s) from which absorption takes
place have not been identified. During
absorption, the rate of intramucosal Zn
transport may be controlled by an inter-
action between cysteine-rich intestinal
protein (CRIP), serving as an intracellular
carrier, and metallothionein, which
appears to inhibit intracellular transport
(Chesters, 1997). As a result of desquama-
tion of mucosal cells, more Zn enters the
mucosa than is transported to plasma. This
mechanism appears to be important in the
regulation of Zn absorption. Zinc absorp-
tion determined by the isotope dilution
technique (Weigand and Kirchgessner, 1976)
does not include the fraction of Zn which
enters, but does not cross, the mucosal
lining to the bloodstream. Once in the
plasma, Zn is transported predominantly
in association with albumin and to a lesser
extent with a high-molecular weight
protein fraction. Transfer of Zn to liver
from plasma is 5–6 times faster than
transfer to other major tissues (House and
Wastney, 1997). Although the liver is very
active in Zn metabolism, it represents <5%
of whole-body Zn, while bone and muscle
are normally the largest Zn pools. In small
animals, however, the integument becomes
quantitatively significant. In the rat, the Zn
pool in the pelt (skin plus hair) may exceed
that in the bone or muscle. Sources of
endogenous Zn entering the gastrointestinal
tract include saliva, gastric secretions, pan-
creatic secretions, bile and intestinal secre-
tions. Of these, pancreatic secretions may
be the most quantitatively significant. In
normal pigs, more Zn was secreted in pan-
creatic fluid than in bile, but this order was
reversed in Zn-deficient pigs since pan-
creatic secretion was reduced to a greater
extent than biliary secretion, indicating that
regulation of both pancreatic and biliary
secretion of Zn is important in Zn homeo-
stasis (Sullivan et al., 1981). The quantity of
Zn secreted into the intestine from all
sources may be as much as dietary Zn
intake. Although biliary Cu is known to be
absorbed with much lower efficiency than
dietary Cu, there has been insufficient work
to determine if Zn responds in a similar
manner. A lower rate of resorption of
biliary and/or pancreatic Zn compared with
dietary Zn could be a factor in maintaining
homeostasis.
Growth depression is characteristic of
Zn deficiency in the young of all species
studied. Zinc deficiency normally results
in the loss of Zn from bone and liver, but
not from skeletal muscle. Integument
losses also are a significant fraction of
whole-body loss during Zn deficiency in
rats and presumably other small animals.
Loss of bone Zn has been found as a result
of Zn deficiency in rats, calves, chickens
and quail, but not in monkeys or cows.
Loss of liver Zn has been reported for rats,
calves, chickens, quail and monkeys, but
not cows. Except for the stability of Zn in
skeletal muscle, variable responses to Zn
deficiency have been found in other
tissues.
Above the nutritional requirement,
whole-body Zn and Zn content of tissues
appear to be regulated over a range of Zn
intakes, although homeostatic control
varies with species and physiological state.
A small increase in digestive tract tissue
Zn was observed in rats fed 104 comparedTrace Element Dynamics 163