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*
Laboratory of Nutrition, Division of Life Science, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan and
Ishinomaki-Senshu University, Ishinomaki 986-8580, Japan
2To whom correspondence should be addressed. E-mail: gtomoko{at}biochem.tohoku.ac.jp
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • zinc deficiency • chorda tympani nerve • taste abnormality • NaCl preference • rats
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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. Zinc
deficiency also leads to hypogeusia (decreased taste acuity) in both
humans and rats, and these symptoms can be reversed by the
administration of zinc (2
3
4)
. As a way of examining the
role of zinc in taste, assessments have been of the effects of zinc
deficiency on taste preference in rats. McConnell and Henkin
(5)
, for example, demonstrated that within 3 d of the
start of feeding, the intake of 0.30 mol/L NaCl (a normally aversive
concentration) was greater in rats fed a zinc-deficient diet than
in zinc-replete rats. Because NaCl intake can be influenced by
factors other than taste, Catalanotto and Lacy (6)
carried
out further investigations and demonstrated that severely
zinc-deficient rats also increase their intake of both 1.28
µmol/L quinine sulfate (at least after 18 d) and 1 mmol/L HCl
(at least after 24 d), tastants normally avoided by rats.
Moreover, when anatomical abnormalities and a delay in turnover were
observed in the taste buds of zinc-deficient rats (7
8
9)
,
many investigators hypothesized that the altered preferences for
normally avoided tastants were the result of decreases in taste
sensitivity. Brosvic et al (10)
, using an operant
discrimination conditioning procedure in rats, examined the NaCl
threshold and the ability to discriminate between NaCl and sucrose and
demonstrated that zinc deficiency does induce decrease gustatory
sensitivity.
Catalanotto and Frank (11)
mentioned in an abstract that
the integrated chorda tympani
(CT)3
nerve responses to tastant solutions were significantly weaker in
severely zinc-deficient rats (4–6 wk of feeding) than in the
control rats, although these data have not been published in full.
However, none of the reports cited above compared the timing of the
changes in taste preference and taste sensitivity with the time course
of any neurophysiological changes.
Jakinovich and Osborn (12)
found that the CT nerve
responses to saltwater were not impaired in zinc-deficient rats.
However, the zinc-deficient rats that they studied (they used adult
rats) did not exhibit overt symptoms of deficiency, which implies that
they may have had difficulty establishing a strict deficiency model (as
the authors admitted in their discussion). Therefore, the changes in CT
nerve responses shown by zinc-deficient rats would seem to still be
controversial. Consequently, we decided to examine the zinc
deficiency–induced changes in both preference rate (for NaCl and
quinine HCl solutions) and taste sensitivity (by recording CT nerve
responses) on a daily basis throughout a 42-d period of zinc
deficiency.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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We used male Sprague-Dawley rats (4 wk old and weighing 80–90 g at the time of delivery) (Japan SLC, Hamamatsu, Japan). The rats were fed a commercial pelleted diet (F-2; Funabashi Farms Ltd., Funabashi, Japan) for 3 d before starting on the experimental diets, and they were then divided into four groups: zinc-deficient (Zn-Def), low zinc (Low-Zn), zinc-sufficient (Zn-Suf) and pair-fed (see later). All rats were maintained on a 12-h light/dark cycle at 22 ± 1°C with constant humidity (50 ± 10%). The experimental plan of the present study was approved by the Animal Research-Animal Care Committee of the Graduate School of Agricultural Science, Tohoku University. The entire experiment closely followed the guidelines issued by that committee, which strictly follows government legislation in Japan (1980). The care and use of the rats involved in the present study were under the surveillance of the above-mentioned committee.
The compositions of the basal experimental diet are given in
Table 1
(13
, 14
). Three types of diets with different
zinc levels were used. By atomic absorption spectrophotometric analysis
(SAS-727; SEIKO Denshikogyo, Tokyo, Japan), the Zn-Def, Low-Zn and
Zn-Suf diets were found to contain 2.2, 4.1 and 33.7 mg of zinc/kg,
respectively.
|
, 15
). In
fact, Harper’s mineral mixture contains 0.2 g of
ZnCl2/kg of mixture (16)
, a level
well under the recommended dietary requirement in the AIN-93 diet (1.65
g of ZnCO3/kg of mixture) (17
,
18
). Rats consuming <12.0 mg of added zinc/kg should be
considered zinc deficient (19)
. The mineral mixture for
the Zn-Def diet was prepared using the same components as in
Harper’s mixture but with ZnCl2 excluded
completely. The mixture for the Zn-Suf diet was prepared by
supplementing the commercial Harper’s mixture with 1.6 g of
ZnCl2/kg, and this diet provides an adequate
amount of zinc for rats (17)
.
Biotin was further added to the basal diet (0.015 g/kg) because egg
white contains avidin, which combines tightly with dietary biotin and
reduces biotin absorption via the intestine (20)
. The
Zn-Def, Low-Zn and Zn-Suf rats were given free access to the
appropriate diet, but the pair-fed rats, which were fed the
Zn-Suf diet, were pair-fed with respect to the Zn-Def rats
(1 d later). The food consumption and body weight changes in the
various experimental groups were as shown in our previous report
(14)
.
Behavioral experiment.
The behavioral experiment for assessing taste preference was performed
using the 24-h, two-bottle preference test developed by Torii
(21)
. The five rats in each group were housed together in
a big stainless steel cage for 35 d. Two bottles were set up on
each cage, and the rats were allowed free choice of solution. One
bottle contained the test solution (0.15 mol/L NaCl or 0.01 mmol/L
quinine HCl), and the other contained distilled water. The daily
consumption was measured as follows: preference rate (%) = (volume of tastant solution consumed/total volume consumed) x 100. The 1st d of feeding was designated d 0 of the study.
Electrophysiological experiment.
An additional 156 rats were used in this experiment, and they were housed individually in stainless steel cages. The rats were maintained on the appropriate experimental diet until electrophysiological recordings were undertaken. We measured the CT nerve responses to taste stimuli on d 0 (n = 5) and after 4, 10, 14, 21, 28, 35 and 42 (Zn-Def, n = 4–12; Low-Zn, n = 4–9; Zn-Suf, n = 4–11; pair-fed, n = 4–10) d of the experimental diet.
In preparation for recording from the CT nerve, each rat was deeply
anesthetized with an intraperitoneal injection of sodium pentobarbital
(65 mg/kg body) and urethane (150 mg/kg body), and the trachea was
cannulated to facilitate breathing. Supplemental doses of anesthesia
were administered when the rat responded to foot pad pinching. Body
temperature was monitored and maintained with the aid of thermal pads.
Access to the nerve was obtained via a lateral approach to the junction
of the CT nerve. The nerve was exposed, cut and desheathed, and the
neural activity of the whole nerve was recorded with a
platinum/iridium electrode. The activity was amplified
differentially against an indifferent electrode attached to an exposed
muscle, passed through an integrator (time constant = 1.4 s)
and displayed on a pen recorder. In each test, 8 mL of stimulating
solution, with its temperature maintained at 28°C, was applied to the
anterior tongue through a supply tube over a 5-s period, and a nerve
recording was made that lasted 60 s. The tongue was rinsed with
deionized water after each stimulation, and 3 min was allowed to elapse
between stimulations. The NaCl test solutions were applied in an
ascending order of concentration (0.01, 0.05, 0.10, 0.15 and 0.20
mol/L). In addition, other basic taste solutions (0.02 mol quinine HCl,
0.01 mol L-glutamic acid, 0.01 mol HCl and 0.50 mol sucrose
per L) and 0.25 mol/L NH4Cl were applied. The peak height
of the integrated response recorded after the onset of stimulation was
measured to assess the magnitude of the response. Responses were
calculated by dividing the integrated response by the spontaneous
activity preceding the response (12
, 22
). In
addition, we measured the CT nerve responses to other salt solutions
(0.10 mol KCl, CaCl2, ZnCl2 or
MgCl2 per L). Furthermore, we measured the CT nerve
response to 0.10 mol/L NaCl after pretreatment with 0.10 mmol/L
amiloride HCl on d 42 of the experimental diet (the amiloride was
administered 2 min before the test solution) to assess the effect of
zinc deficiency on the density of sodium channels in the taste bud
cells.
Statistical analysis.
The results are expressed as means ± SEM. The data obtained from the behavioral experiment were analyzed statistically by means of a two-way analysis of variance (ANOVA). The data obtained from the electrophysiological experiment in the case of NaCl dose responses of the CT nerve were analyzed using a two-way repeated-measures ANOVA, and in the case of other studies of the CT nerve, responses were analyzed using a two-way ANOVA. All post hoc multiple comparisons were made with the Scheffé test. The StatView program (StatView J-4.5; Abacus Concepts, Berkeley, CA) was used for the analysis in each case.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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, 15
); these included anorexia and growth
retardation, as well as depletion of serum zinc. After the Zn-Def
diet was fed for > 21 d, we observed severe signs of zinc
deficiency (epilation, hyperkeratosis of oral mucosal tissues, scaly
encrustation of the paws and prolapsed penes). In contrast, none of
these changes was seen in the Low-Zn rats. Behavioral experiment.
The results of the two-bottle preference test with NaCl (0.15
mol/L) and water revealed that NaCl preference was greater in
Zn-Def and Low-Zn rats than in Zn-Suf and pair-fed rats
after 4 d (Fig. 1
). In the case of the quinine HCl solution (0.01 mmol/L), the preference
rate of the Zn-Def rats was greater than that of other groups after
9 d, although normal rats show a distaste for this bitter solution.
In contrast, the preference rate of the Low-Zn rats did not change
within the 35-d experimental period (Fig. 2
).
|
|
The data obtained by measuring the integrated responses of the whole CT
nerve to NaCl solutions of various concentration after 21, 28, 35 and
42 d of feeding are shown in Figure 3
. The time course of the responses to 0.15 and 0.20 mol/L NaCl are shown
in Figure 4
. There were no significant differences among the four groups in their
responses to various NaCl solutions in the first 14 d of feeding
(these data are not shown in Fig. 3
). In the Zn-Def
rats, the response to 0.20 mol/L NaCl was significantly less than that
in the control rats after 21 d, and the response to 0.15 mol/L
NaCl was significantly less than that in the control rats after 28 d. In the Low-Zn rats, the response to 0.20 mol/L NaCl was
significantly less than that in the control rats after 35 d, and
the response to 0.15 mol/L NaCl was significantly less than that in the
control rats after 42 d. This confirms that as time passes, taste
sensitivity decreases in the Zn-Def rats. There were no significant
differences among the four groups in their responses to various taste
solutions in the first 14 d of feeding (data not shown). After
42 d, the responses to quinine HCl (0.02 mol/L), HCl (0.01 mol/L),
L-glutamic acid (0.01 mol/L) and
NH4Cl (0.25 mol/L) solutions were significantly
weaker in the Zn-Def rats than in the Zn-Suf or pair-fed
rats, whereas the response to sucrose (0.50 mol/L) was not different in
the Zn-Def rats (Fig. 5
). The data obtained for the integrated responses of the CT nerve to
various salt solutions after 42 d of feeding are shown in
Figure 6
. The response to KCl (0.10 mol/L) was significantly weaker in the
Zn-Def rats than in the Zn-Suf rats, whereas those in the
Low-Zn and pair-fed rats were not. The mean responses to 0.10
mol ZnCl2, MgCl2 and
CaCl2 per L solutions tended to be weaker in the
Zn-Def rats than in the Zn-Suf (P = 0.36, 0.33,
and 0.29, respectively) and pair-fed (P = 0.06,
0.08, and 0.19, respectively) rats, although the differences
were not significant. Amiloride suppressed the NaCl response by 59.76
± 2.68% (Zn-Def), 62.55 ± 2.04% (Low-Zn), 57.39 ± 2.20% (Zn-Suf) and 57.04 ± 1.63% (pair-fed) (means ± SEM, data not shown). These results suggest that the
density of amiloride-sensitive sodium channels (amiloride-sensitive
component of the response to NaCl) was not influenced by dietary zinc
deficiency.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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,
6
, 12
, 13
, 23
).
However, those previous researchers reported the intake pooled every
few days, so none of these reports clarified the daily changes in
preference rate or, the relationship between taste preference
and taste sensitivity at different times (using electrophysiological
techniques). The present results suggest that daily changes in NaCl
preference could be used as a sensitive indicator of subclinical zinc
deficiency in rats (as can anorexia). In humans, it has been reported
that the ability to correctly discriminate salt concentrations shows a
significant positive correlation with plasma zinc (24)
. In
our electrophysiological analysis, however, there were no significant
differences among the four groups in the responses to NaCl solutions in
the first 14 d of feeding at the level of the CT nerve. Hence, our
time course data revealed for the first time that the change in NaCl
preference due to zinc deficiency occurs before any changes in NaCl
taste sensitivity can be detected (at least by our technique). On the
other hand, we also noted that as time passed, taste sensitivity
(especially to NaCl) in the Zn-Def rats gradually decreased, with
the extent of the decrease dependent on the dietary zinc content. We
also noted that an increase in quinine HCl preference occurred in the
Zn-Def rats after 9 d of feeding. This led us to think that a
decrease in taste sensitivity might occur in Zn-Def rats at that
time. However, the response to quinine HCl (0.02 mol/L) in the
Zn-Def rats did not become significantly less than that in the
control rats until d 42. It would be interesting to examine this issue
further by recording the electrophysiological responses of the
glossopharyngeal nerve, because the CT nerve is not particularly
suitable for measurement of bitter-taste sensitivity
(25)
. Interestingly, the quinine HCl preference rate in
the Low-Zn rats tended to be the lowest among the four groups
(P = 0.001, vs. Zn-Def), making us wonder
whether a change in taste quality might occur with subclinical zinc
deficiency. In the Zn-Def and Low-Zn rats after 42 d of feeding, the taste sensitivities to various taste solutions (except for sucrose) were significantly lower (relative to those of the control rats). In the case of KCl (0.10 mol/L), that in the Zn-Def rats was also significantly weaker than that in the Zn-Suf rats (although that in the Low-Zn rats was not). These results suggest that the taste sensitivities to a variety of taste stimuli mediated via the CT nerve are impaired in severely (long-term) zinc-deficient rats and that an increased intake of a normally avoided solution in such animals might be the consequence of a decrease in taste sensitivity. However, the increase in quinine HCl preference observed in the Zn-Def rats as early as d 9 of the feeding regimen is unlikely to be the result of such changes in taste sensitivity mediated by the CT nerve. The present findings suggest that although long-term zinc deficiency decreases the CT nerve responses to a variety of taste stimuli in rats, the change in NaCl preference that is associated with zinc deficiency occurs too early to be explained by the such changes in NaCl taste sensitivity.
If we had expressed the integrated CT nerve responses to NaCl solutions
relative to the response to 0.25 mol/L NH4Cl
solution, we would most likely have missed the effect of zinc
deficiency observed here, because the response to
NH4Cl solution in Zn-Def rats after 42 d
of feeding was also significantly reduced (Fig. 5
). Perhaps
for this reason, the changes in CT nerve responses shown by Zn-Def
rats have been controversial for a long time. The mechanism underlying
the decrease in taste sensitivity present in rats with long-term
zinc deficiency has yet to be clarified. In the present study, the NaCl
responses of the four groups were suppressed by amiloride to a similar
extent, suggesting that the decreased CT nerve responses seen in
long-term Zn-Def rats were not caused by a reduction in the density
of the amiloride-sensitive sodium channel.
Our hypothesis is that in long-term zinc-deficient rats, the
reduction in salivary carbonic anhydrase, a zinc enzyme, activity
(14
, 15
) is causally related to the decreased
taste sensitivity, as are anatomical abnormalities and a reduced
turnover in taste buds (7
8
9)
. Indeed, these changes may
be concurrent, because salivary carbonic anhydrase affects the
maintenance of taste sensation (26
, 27
, 28
). It may be relevant that
zinc is also important in the central nervous system, for example, in
zinc-containing neurons (29)
. Moreover, O’Dell et al.
(30)
demonstrated a decreased motor nerve–conduction
velocity in the sciatic nerve in zinc-deficient guinea pigs.
The mechanism underlying the increased salt preference seen here in
short-term zinc deficiency is still unclear. Tordoff
(31)
demonstrated that NaCl ingestion ameliorates the
effects on plasma ionized calcium and parathyroid hormone seen in
calcium-deficient rats and that there also is an increase in salt
preference within 3 d of starting of feeding of a
calcium-deficient diet. Because the food intake of the Zn-Def
rats decreased soon after feeding of the diet began (14)
,
the dietary signal of zinc deficiency may affect salt preference
through the central nervous system or through the mineral status in
organs such as bone, kidney or liver.
We suggest that taste abnormality due to zinc deficiency may be the result of a combination of a decrease in the sensitivity of the peripheral taste nerve (long-term effect) together with possible changes in the sensitivity of the central nervous system (short- and long-term effects).
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FOOTNOTES |
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3 Abbreviations used: CT, chorda tympani; Zn-Def, zinc deficient; Low-Zn, low zinc; Zn-Suf, zinc sufficient.
Manuscript received July 14, 2000. Initial review completed August 22, 2000. Revision accepted October 27, 2000.
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REFERENCES |
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6. Catalanotto F. A., Lacy P. Effects of a zinc deficient diet upon fluid intake in the rat. J. Nutr. 1977;107:436-442
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9. Ohki M. Turnover of taste bud cells in rats with taste disorder caused by zinc deficiency. J. Nihon Univ. Med. Assoc. 1990;49:189-199
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Contreras R. J., Frank M. Sodium deprivation alters neural responses to gustatory stimuli. J. Gen. Physiol. 1979;73:569-594
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