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Department of Bioscience and Chemistry, Faculty of Agriculture, Hokkaido University, Sapporo 060-8589, Japan
1To whom correspondence should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • zinc absorption • large intestine • coprophagy prevention • cecocolonectomy • rats
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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) and impairment of many functions, including
those of the immune system and antioxidative systems (Bray and Bettger 1990
). Moderate zinc deficiency results in a reduction
of immune capacity (Fraker et al. 1987
, Keen and Gershwin 1990
). Recently, the mechanism of intestinal
absorption of zinc was partially elucidated (Hempe and Cousins 1992
), yet it is not fully understood. It is evident that zinc
is absorbed by a carrier-mediated process; however, there are
several controversial results concerning the major intestinal site
involved (Antonson et al. 1979
, Davies 1980
, Meneely and Ghishan 1982
, Wapnir et al. 1985
). We demonstrated previously that large intestinal
absorption of calcium compensates for lowered absorption in the small
intestine in rats (Hara et al. 1996
, Shiga et al. 1998
). The large intestine has a high capacity for zinc
absorption (Meneely and Ghishan 1982
, Seal and Mathers 1989
); however, the contribution of the large intestine
to zinc absorption in vivo remains to be clarified.
The aim of this study was to clarify the role of the large intestine in
zinc absorption. We determined whether the large intestine absorbs zinc
administered into the cecum as an insoluble salt, under conditions that
prevented coprophagy. Also, we examined the contribution of the large
intestine to zinc absorption when zinc absorption was reduced in the
small intestine by determining the effects of resection of the large
intestine (cecocolonectomy) in rats. It has been reported that
inhibition of gastric acid secretion reduces zinc absorption
(Sturniolo et al. 1991
). We used a proton pump inhibitor
to suppress gastric acid secretion. We also measured apparent zinc
absorption and tissue zinc concentrations in an effort to determine the
zinc status of rats when they were fed diets containing graded levels
of zinc.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Male Sprague-Dawley rats (Japan SLC, Hamamatsu, Japan), weighing
~100 g (Experiment 1) or 150 g (Experiments 2 and 3), were given
free access to deionized water and a semipurified stock diet, shown in
Table 1
, for 3–7 d. The stock diet and all test diets were sucrose-based
semipurified diets containing 150 g powdered egg white/kg diet
(Taiyo Kagaku, Yokkaichi, Japan). D-Biotin was added up to
8.19 µmol/kg diet to prevent its deficiency. The rats
were divided into several groups by randomized block design based on
body weight for three separate experiments after acclimation
(Experiment 1) or recovery from surgery (Experiments 2 and 3). The rats
used in all experiments were housed individually in stainless steel
cages with mesh bottoms. The cages were placed in a room with
controlled temperature (22–24°C), relative humidity (40–60%) and
lighting (lights on 0800–2000h).
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so that zinc excreted into feces would not
pass through the upper intestine as a result of reingestion.
The cecum and colon were removed after ligation of several vessels that
supplied blood to those organs, and a surgical procedure was performed
to obtain end-to-end anastomosis between the cut edge of the ileum (end
of the ileum) and the rectum (cecocolonectomy, Lambert 1965
). In rats of the other group, the end of the ileum was
transected and anastomosed (sham operation). The rats were deprived of
food and water for 24 h before and after surgery. Both operations
were performed in rats under pentobarbital anesthesia (Nembutal: sodium
pentobarbital, 40 mg/kg body weight, Abbott Laboratories, North
Chicago, IL, Experiment 3).
Guar gum hydrolysate (GGH, Guar fiber, Meiji Seika Kaisha, Tokyo, Japan) is a partial hydrolysate of guar gum, prepared by ß-1,4-mannanase treatment, with an average molecular weight of 15,000; this fiber source was added to the test diet at the expense of the whole diet (50 g/kg diet) in Experiment 2. In all experiments, rats were allowed free access to the assigned test diet and deionized water during the test period. Body weight and food intake were measured daily. Spilled portions of the diet were carefully collected and weighed, and food intake values for all periods were corrected accordingly.
Feces were collected during the last 3 d (Experiment1) or 4 d (Experiment 2) to evaluate apparent absorption of zinc. The feces were sampled via stainless wire mesh set under the cages (Experiment 1) or were collected from the anal cup (Experiment 2). The collected feces were freeze-dried. In Experiment 3, feces could not be collected because of severe diarrhea.
At the end of all experiments, the rats were killed by withdrawal of aortic blood while under anesthesia with Nembutal (pentobarbital sodium, 50 mg/kg body weight; Abbott); some organs were removed in Experiment 1. The right femur was removed and carefully cleaned of adherent tissue in all experiments. The cecum and colon were removed without loss of their contents; contents were collected, frozen immediately with liquid nitrogen and stored at -40°C until subsequent analyses (Experiment 2).
The study was approved by the Hokkaido University Animal Committee, and animals were maintained in accordance with the guidelines for the care and use of laboratory animals of Hokkaido University.
Experimental protocols.
In Experiment 1 (effects of zinc levels in diets), acclimated rats divided into five groups (n = 6) were fed diets containing five levels of zinc carbonate [0.015 (1), 0.076 (5), 0.153 (10), 0.229 (15) and 0.535 (35) mmol (mg) Zn/kg diet] for 3 wk. To create graded levels of zinc in the diets, zinc carbonate was added at the expense of sucrose.
In Experiment 2 (instillation of zinc into the cecum), with the use of a 2 x 2 factorial design, acclimated rats (n = 32) were implanted with a cecal catheter as described above and were divided into four groups (n = 8) after a 3-d recovery period. Rats of two groups were fed a test diet containing GGH (50 g/kg diet); the rats of the other two groups were fed a test diet without GGH. Two subgroups of each diet group received a suspension of zinc carbonate in water administered into the stomach via an orogastric tube and water administered into the cecum via the implanted catheter daily for 7 d (Stomach). Another two subgroups of each diet group received zinc carbonate suspension administered via the catheter implanted in the cecum and water administered into the stomach daily for 7 d (Cecum). The suspension and the water were administered once a day at 0900–1000 h. Coprophagy was prevented from 1 d before zinc instillation into the cecum or the stomach. We prepared a control group of six rats fed a diet without GGH, containing 0.229 mmol Zn/kg diet as zinc carbonate, by the same protocol as that described above for the test groups (Stomach and Cecum), without the operation. The average amount of zinc carbonate ingested by the rats of this control group was instilled daily into the stomach or the cecum of the test groups.
In Experiment 3 (effects of cecocolonectomy and omeprazole treatment) again with a 2 x 2 factorial design, acclimated rats (n = 36) were divided into two groups of 20 and 16 rats. In the case of the first group, cecocolonectomy was performed; the second group underwent a sham operation as described above. All of these rats were fed the stock diet for a 12- to 13-d recovery period postsurgery. Two cecocolonectomized rats and one sham-operated rat were killed because of surgical damage. The rats of each surgically treated group were divided into two subgroups. Two of the subgroups, i.e., one subgroup each of the cecocolonectomized and sham-operated groups, were administered omeprazole (15 mg/kg body weight, kindly provided by Astra Japan, Osaka, Japan) subcutaneously; the other two subgroups were administered its vehicle (polyethylene glycol 400/10 mmol/L NaHCO3, 1:1). Omeprazole or vehicle was injected once a day at 1600–1700 h for 7 d.
Analyses.
Freeze-dried feces and organs were milled. Powdered feces and organs (~70 mg) and freeze-dried whole femur specimens were wet-ashed with a nitric acid (10 mol/L) and perchloric acid (2.3 mol/L) mixture; zinc concentrations in these solutions were measured by atomic absorption spectrometry (AA-6400F, Shimadzu, Kyoto, Japan) after adequate dilution with water.
The cecal and colonic contents, diluted with 9 vol of deionized water, were homogenized by means of a teflon homogenizer. The total zinc in each of the homogenates was measured after the samples had been wet-ashed in the same way as for feces. Soluble zinc was assayed in the supernatant obtained upon centrifugation (30,000 x g for 20 min) of the homogenate.
Serum zinc concentration was measured by means of a commercially available kit (Zn test-Wako, Wako Pure Chemical Industries, Osaka, Japan).
Calculations and statistics.
Calculations were performed as follows: apparent zinc absorption (%) = 100 x [total zinc intake - fecal zinc excretion]/total zinc intake.
The results of Experiment 1 (effects of zinc levels) were
analyzed by one-way ANOVA. The effects of GGH feeding and
administration site (Experiment 2) and the effects of cecocolonectomy
and omeprazole treatment (Experiment 3) were analyzed by two-way
ANOVA. Duncan’s multiple range test was used to determine whether mean
values were significantly different (Duncan 1995
,
P < 0.05). These statistical analyses were done by
the General Linear Models procedure of SAS (SAS version 6.07, SAS
Institute, Cary, NC).
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Body weight and food intake were not different among groups fed diets
with graded levels of zinc, except for rats fed the lowest level of
zinc (0.015 mmol Zn/kg diet, a deficient level, Table 2
). In this zinc-deficient group, both body weight and food intake
were lower than in the other groups. Apparent zinc absorption
(µmol/d) reached a maximum at a zinc concentration of
0.153 mmol/kg diet. Apparent absorption rates (%) were very high in
rats fed 0.076 and 0.153 mmol Zn/kg diet, then gradually decreased as
the zinc concentration of the diet was increased towards the highest
level.
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). The value in rats fed this zinc level was not different from that in
rats fed 0.229 mmol/kg diet, whereas the value in rats fed 0.535
mmol/kg diet, the highest level, was slightly but significantly higher
than that of rats fed 0.153 or 0.229 mmol/kg diet. The kidney zinc
concentrations differed in a manner similar to that seen in serum
concentrations. Femoral and pancreatic zinc concentrations increased
linearly as the dietary zinc concentration increased to 0.229 mmol/kg
diet from the zinc-deficient level (0.015 mmol Zn/kg diet). In
contrast, the liver zinc concentration was highest in rats fed the diet
with the lowest zinc content, and the values in the case of rats fed
diets with other levels of zinc did not differ.
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Body weight gain and food intake in the groups that received zinc
instilled into the cecum were lower than those in the groups that
received zinc instilled into the stomach, with or without feeding GGH
(Table 3
). Body weight gains in rats fed a zinc-containing diet and in rats
administered zinc into the stomach in this experiment were lower than
those in rats fed the diet (zinc levels > 0.229 mmol/kg diet) of
Experiment 1 (Tables 2
and 3)
. The lower body weight gain in Experiment
2 may have resulted from the prevention of coprophagy. The amount and
rates of zinc absorption in the cecally instilled rats were each half
of those observed in the case of stomach-instilled rats, and
feeding GGH did not influence these values. The amount of zinc absorbed
when administered into the stomach (µmol/d) was similar to
that observed in rats fed a diet containing 0.229 mmol Zn/kg diet
(shown on the bottom line in Table 3
).
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, upper panel). Femur zinc concentrations were significantly
lower in the cecally instilled groups than in the stomach-instilled
groups, with or without feeding GGH (Fig. 2
, lower panel).
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); however, there was no difference in the amount of soluble zinc in the
cecal contents among all of the groups. The amount of soluble zinc in
the colonic contents was influenced by the site of instillation.
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Body weight gain was not influenced by cecocolonectomy or omeprazole
treatment; however, food intake and stomach wall weight were higher in
the omeprazole-treated group than in the vehicle group in the case
of cecocolonectomized rats (Table 5
).
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).
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). Cecocolonectomy also influenced bone dry weight. The values of both
variables were lower in the omeprazole group of cecocolonectomized rats
than in the vehicle group of sham-operated rats. Zinc
concentrations were not different among the groups.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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, which shows
that this low level of zinc is possibly the minimum dietary zinc
requirement. However, zinc absorption and the concentrations of zinc in
the femur and pancreas increased gradually upon consumption of diets
containing higher levels of zinc and reached a plateau at 0.229 mmol/kg
diet. Serum zinc concentrations increased substantially as the dietary
zinc levels were increased from 0.076 to 0.153 mmol Zn/kg diet and did
not change as the dietary levels were increased from 0.153 to 0.229
mmol Zn/kg diet. These results suggest that rats fed the diet
containing 0.153 mmol Zn/kg diet were marginally zinc deficient even
though their body weight gain was the same as that of rats fed diets
containing > 0.153 mmol Zn/kg diet. These results agree with
those reported by Hunt and Johnson (1992)
. Prasad et al. (1993)
showed that zinc concentrations in granulocytes
and lymphocytes are diminished when the plasma zinc concentration is
normal in elderly subjects. Southon et al. (1988)
also
established that a diet containing 0.153 mmol (10 mg) Zn/kg was a diet
with a marginally deficient level of zinc. Very high absorptive
efficiencies were shown in rats fed low zinc diets (0.076 and 0.153
mmol/kg diet). This finding also suggests that these levels of zinc are
below zinc requirements and that the absorptive capacity adapts to the
low dose of zinc. Our results also support the view that serum zinc
concentration reflects intestinal zinc absorption and is a sensitive
indicator of the body zinc status, as shown by Wilkins et al. (1972)
.
Zinc absorption in the large intestine has been examined in in vitro
and in situ experiments, and it has been reported that the zinc
absorption capacity of the large intestine is high (Meneely and Ghishan 1982
, Seal and Mathers 1989
).
Meneely and Ghishan (1982)
showed that the large
intestine is the site showing the highest levels of zinc absorption in
the intestinal tract of rats. In this study, we examined the zinc
absorption capacity of the large intestine in vivo by direct
instillation of an insoluble zinc salt into the cecum under conditions
that prevented coprophagy. Absorption of cecally administered zinc was
only half of that observed when zinc was administered into the stomach
(Table 3)
. This was consistent with the decreased concentrations of
zinc observed in the serum and femur of rats in the group that received
cecally administered zinc vs. the group administered zinc by the
gastric route (Fig. 2)
. The amount of zinc absorbed when administered
into the cecum (µmol/d, Table 3
) was lower than that
observed in rats fed a diet containing 0.076 mmol Zn/kg diet (Table 2)
.
This indicated that rats of the cecally administered group had zinc
deficiency, which might cause growth retardation in this group. More
zinc absorption is required in these rats. This suggests that, at this
level of zinc, in spite of the high absorptive capacity of the large
intestine, the zinc absorption of the large intestine is insufficient
to meet the zinc requirement for maximum growth of the rats.
A possible factor contributing to the poor functional efficiency of the
large intestine in absorption of zinc is a low concentration of soluble
zinc in the luminal contents. The level of soluble zinc in the cecal
contents in the experiment shown in Table 4
was 100–200 mmol/cecum.
When the percentage of water in the cecal contents was taken to be 70%
(result of a separate experiment), zinc concentration in the cecal
contents was 75–150 µmol/L. This value is higher than the
Kt value of the saturable zinc
transporter in the small intestine (Blakeborough and Salter 1987
, Raffaniello and Wapnir 1989
) and much
higher than the serum zinc concentrations shown in Figure 2
. It is not
likely that zinc solubilization in the lumen of the large intestine is
the limiting factor for zinc absorption in the large intestine.
The luminal environment of the large intestine is influenced
considerably by dietary components, especially highly fermentable
indigestible substances. These dietary ingredients enhance absorption
of some minerals, e.g., calcium and magnesium salts (Ohta et al. 1997
, Younes et al. 1996
). The increase in
intestinal fermentation produces large amounts of organic acids, such
as short-chain fatty acids. These acids also promote calcium
absorption in the colon (Hara et al. 1999a
,
Trinidad et al. 1996
). Recently, Lopez et al. (1998)
showed that feeding resistant starch increases zinc
absorption; the authors suggested that intestinal fermentation may be
involved in the increment. We examined the effects of guar gum
hydrolysate, which is a highly fermentable dietary fiber
(Takahashi et al. 1994
), on zinc absorption in the large
intestine. However, in this study, we did not find that zinc absorption
was increased by feeding this source of highly fermentable dietary
fiber. In addition, we confirmed this result in a separate experiment
using fructooligosaccharides, that is, the feeding of highly
fermentable oligosaccharides did not increase zinc absorption in rats
(unpublished results). Our results suggest that zinc absorption in the
large intestine is not influenced by intestinal fermentation.
In Experiment 3, we demonstrated that the large intestine contributes
to zinc absorption in rats treated with a proton pump inhibitor,
omeprazole. In this experiment, we could not collect feces because of
severe diarrhea, and serum zinc concentration was used as an indicator
of zinc status. The zinc concentration in the diet was at a marginally
deficient level as described above, and serum zinc concentrations
changed sharply to a level below that of the minimum requirement for
zinc in the diet (Fig. 1)
. Suppression of gastric acid secretion by
omeprazole treatment reduces insoluble salt absorption in the small
intestine (Hara et al. 1999b
). Sturniolo et al. (1991)
reported that suppression of gastric acid secretion
reduced zinc absorption. In this study, omeprazole treatment
significantly reduced serum zinc concentrations compared with vehicle
treatment in cecocolonectomized rats, but not in sham-operated
rats. This result suggests that impaired zinc absorption induced by
omeprazole is compensated for by an elevated efficiency of zinc
absorption in the large intestine, and also that such compensation was
lost as a result of cecocolonectomy. In Experiment 1, we showed that
the serum zinc concentration reflects intestinal zinc absorption (Fig. 1
and Table 2
). It has been reported that serum zinc concentrations may
be decreased temporarily as a result of infection or drug stress, and
it is suggested that the serum concentration is not an appropriate
indicator of zinc status (Lowe et al. 1991
, Sato et al. 1984
). However, omeprazole treatment did not influence
zinc concentration in the sham-operated rats, and the rats that
underwent cecocolonectomy recovered completely from surgical damage
before the start of consumption of the test diet in our experiment.
Drug and surgical damage probably did not affect the results of this
study.
In conclusion, the cecum and colon do not show sufficient zinc absorptive efficiency; however, these sites of the intestine compensate for impaired zinc absorption in the small intestine.
Manuscript received May 3, 1999. Initial review completed June 30, 1999. Revision accepted August 30, 1999.
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