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Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA 95616 and * Waltham Centre for Pet Nutrition, Waltham-on-the-Wolds, Melton Mowbray, LE14 4RT, UK
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: • calcium • phosphorus • cats • osteocalcin • parathyroid hormone
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Nutritional secondary hyperparathyroidism has
been recorded in both domestic cats and other felids, including lions
kept in captivity (Fiennes and Graham-Jones 1960
),
but is unknown in felids in the wild (Jackson 1968
).
Roberts and Scott (1961)
measured the calcium and
phosphorus balance of kittens given a meat diet supplemented with
calcium carbonate and a stock diet. Presumably on the basis of these
calcium balance data, Scott (1965)
and Scott and Scott (1967)
stated that growing kittens required 200–400 mg
Ca/50 g diet and a Ca:P ratio of 1:1. This recommendation would be
equivalent to a dietary concentration of 4–8 g calcium/kg diet dry
matter; the higher value is proposed as the requirement by the
NRC (1986)
.
Because vitamin D plays a key role in the active absorption of calcium
from the gut and synthesis of vitamin D by cats is ineffective
(Morris 1999
), we (Morris et al. 1999
)
investigated the vitamin D requirement of growing kittens. A purified
diet containing 3.125 µg cholecalciferol/kg diet produced
an increase in plasma concentration of 25-hydroxyvitamin D over
pretreatment depleted levels and resulted in a mean concentration of
27.7 ± 2.1 nmol 25-hydroxyvitamin D/L. The objective of this
experiment was to use a purified diet containing 3.125 µg
cholecalciferol (125 IU) to determine the calcium
requirements of kittens.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Kittens were from domestic short-haired queens given a complete
commercial-type expanded (dry) diet that had no added vitamin D
beyond that present in the natural ingredients. This diet had
previously produced kittens with low, but not deficient levels of
circulating 25-hydroxyvitamin D (Morris et al. 1999
). At
4 wk of age, kittens were given a purified diet containing 7.2 g
calcium, 8.7 g phosphorus and 3.125 µg
cholecalciferol/kg; weaning commenced at 7 wk of age and was completed
at 9 wk of age. After weaning, the kittens were allocated to their
respective experimental diets and housed in individual enclosures (1.15
x 0.60 x 0.55 m) with food and water available at all
times with the exception of when the enclosures were cleaned and the
kittens socialized as a group. A temperature of 21 ± 2°C and a
12-h light:dark cycle were maintained in the room. The protocol
conformed to the guidelines of the NIH.
Diet.
A purified diet was prepared from the ingredients given in Table 1
. Animal fat (a source of arachidonate) was excluded from the diet
because it would have introduced vitamin D. Because synthesis of
arachidonate by cats is limited, evening primrose oil was added as a
source of 
-linoleic acid. Calcium in the diets for treatments 1–5
was supplied by a fixed amount of calcium carbonate and varying amounts
of calcium phosphate dibasic from mineral mixture B. Similarly, the
phosphorus in the diets was supplied by varying amounts of mineral
mixture B (containing calcium phosphate dibasic and potassium phosphate
dibasic). In the case of treatments 6 and 7, additional potassium
phosphate dibasic was added to these diets (Table 2
). With the exceptions of calcium, phosphorus and vitamin D, the basal
diet was formulated to provide all essential nutrients at levels in
excess of those recommended by the NRC (1986)
. All diets
were analyzed and the values for calcium and phosphorus are given in
Table 3
.
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At 9 wk of age, kittens were randomly assigned to the dietary
treatments given in Table 3
on the basis of sex, such that each
treatment group contained four female and three male kittens
(n = 7). Treatments 1–5 had increasing
concentrations of calcium in the diet from 3.8 to 8.1 g/kg with a
constant calcium to phosphorus ratio of ~1:1.25. These diets were
calculated to supply 0.75, 1.0, 1.25, 1.5, 1.74 and 2.0 times the
calculated accretion rate of calcium on the basis of the body
composition data of kittens and adult cats of Kienzle et al. (1991)
and the food intake and growth rate of kittens in the
study of Morris et al. (1999)
. Treatments 6 and 7 had
calcium contents similar to those of treatment 3, but with higher
levels of phosphorus, resulting in calcium to phosphorus ratios of
1:1.55 and 1:2.61, respectively. With the exception of treatment 1, all
diets equaled or exceeded the phosphorus concentration recommended by
the NRC (1986)
, and only treatment 5 equaled the
recommended calcium concentration. The metabolizable energy value of
the diets was ~ 20 kJ/g.
All kittens received the diets until they were 18 wk of age. Samples of blood were taken from kittens into heparinized syringes at weekly intervals according to the age of the kitten at the last week. For example, the 9-wk sample was taken between ages of 9 and 10 wk. The following measurements were made on the samples collected at wk 6, 7, 9, 11, 12, 13, 15 and 18: total calcium and phosphorus (except at wk 12) (Coulter CPA Analyzer, Coulter Electronics, Luton, UK); ionized calcium (Ciba-Corning 228 Analyzer, Ciba-Corning Medfield, MA); at all the above time points except 6 wk of age: hemoglobin, packed cell volume, red and white cell numbers (Serono-Baker Diagnostics System Analyzer 9000, Allentown, PA); at 6, 7, 9, 11, 12, 15 and 18 wk of age, total plasma protein, albumin, urea and cholesterol concentration; and alanine and aspartic aminotransferase activity (Coulter CPA Analyzer, Coulter Electronics). At 6 and 18 wk of age, plasma taurine concentration was measured by an amino acid analyzer; at 18 wk, creatine kinase (Sigma Chemical, St. Louis, MO) was measured. Body composition was measured by dual energy X-ray absorptiometry (DXA) using a Hologic 7 QDR-1000/W(S/N 1038P) densitometer (Hologic Waltham, MA) on 18-wk-old anesthetized kittens. Body weight was measured weekly, and food intake recorded daily.
Parathyroid hormone, osteocalcin and 25-hydroxyvitamin D assays.
Plasma concentration of intact parathyroid hormone concentration
(i-PTH) was measured using the Intact PTH-parathyroid hormone kit
(Nichols Institute, San Juan Capistrano, CA) on heparinized plasma
samples taken at 8, 13 and 18 wk of age. Plasma osteocalcin
concentration was measured using an antibody produced in rabbits to cat
osteocalcin, synthesized according to the structure of Shimomura et al. (1984)
when the kittens were 12, 13, 17 and 18 wk of
age. The concentration of 25-hydroxyvitamin D in the plasma, (the
preferred index of vitamin D status; Collins and Norman, 1991
, Holick, 1990
) was measured by a
protein-binding assay (Chen et al. 1990
) using a cat
binding protein, when the kittens were 17 wk old.
Statistical analysis.
Observations were subjected to two-way (sex, treatments) or a repeated-measures ANOVA using a General Linear Models procedure (SAS Institute, Cary, NC) and P < 0.05 was taken as significant. Pair-wise multiple comparisons were made by the Student-Newman-Keuls method when the ANOVA was significant. Log transformations of raw data were done in cases of unequal variances. Values in the text are means ± SEM.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Regular clinical examination of the kittens by a veterinarian who was
unaware of the treatments did not reveal any clinical abnormalities or
signs of calcium deficiency. Initial mean body weight was not
significantly different among the treatment groups. Treatments had no
significant effect on final body weight or body weight gain
(P = 0.68) (Table 4
) even though treatment 7 had the lowest least-squares group mean
body weight gain (919 ± 62 g) and treatment 2 had the
highest gain (1029 ± 62 g). Sex had a significant effect
(P < 0.001) on body weight gain and final body weight.
The mean treatment body weight gain was 82.4 ± 1.5% of the
colony average for kittens fed commercial-type diets. Similarly,
there were no significant differences due to treatments in food and
energy intakes and gain/MJ food ingested.
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Plasma total calcium was not significantly different (P = 0.3) among groups at 6 wk of age before treatments commenced, or at 9, 11, 15 and 18 wk of age (values not shown). At 18 wk of age, there was no significant difference among groups (P = 0.17) although kittens in treatments 1 and 7 had the lowest values, i.e., 2.71 ± 0.048 and 2.66 ± 0.048 mmol/L, respectively. At each sampling, males tended to have a lower concentration of plasma calcium than females, but sex was not significant in the ANOVA except for the 11-wk sampling (P < 0.04, males 2.67 ± 0.04, females 2.78 ± 0.04 mmol/L).
There was a significant treatment effect on plasma ionizable calcium at
13 wk of age (P < 0.026) (Table 5
). Kittens in treatment 5 had an ionizable calcium concentration of 1.45
± 0.019 mmol/L, which was greater than the concentrations in
kittens in treatments 1 (1.35 ± 0.021 mmol/L) and 7 (1.36 ± 0.019 mmol/L). In addition, at 18 wk of age, the concentration of
ionizable calcium in treatment 7 was 1.32 ± 0.015 mmol/L, which
was significantly less (P < 0.007) than the
concentration in those in treatments 4, 5 and 6 (1.39 ± 0.015,
1.40 ± 0.015, and 1.39 ± 0.017 mmol/L, respectively).
Treatment 1 kittens also had significantly (P < 0.04)
lower plasma ionized calcium values (1.35 ± 0.017 mmol/L) than
those in treatment 5 (1.40 ± 0.015 mmol/L).
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Phosphorus concentration in plasma was not significantly different at 6
wk of age before treatments commenced; however, by 9 wk of age, plasma
phosphorus was significantly lower in kittens in treatment 7 (those
receiving the highest concentration of phosphorus in the diet) than in
kittens in treatments 1, 2, 3 and 4 (Table 6
). Kittens in treatment 5 also had a lower concentration of phosphorus
in plasma than kittens in treatments 1 and 3. These differences
persisted through 18 wk of age when there was a significant negative
relationship (r 2 = 0.81, P
< 0.001) between dietary phosphorus concentration over the range
6.3–15.7 g/kg diet and plasma phosphorus concentration (Fig. 1
).
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Alkaline phosphatase activity was not significantly different among treatments at 6, 9, 11, 13 and 15 wk of age; at 18 wk of age, however, kittens receiving treatment 7 had significantly (P < 0.02) higher values (473 ± 40 U/L) than kittens in treatments 1, 2, 3 and 5 (300 ± 41, 318 ± 41, 315 ± 41 and 266 ± 41 U/L, respectively). Treatments 4 and 6 were not significantly different from the other treatments. Treatments had no significant effect on the activities of alanine or aspartate aminotransferase or creatine kinase.
Other measurements.
Treatments had no significant effect on the concentration of plasma proteins, urea or cholesterol, nor did they affect hemoglobin concentration, packed cell volume, or red or white cell numbers. There was no significant difference in plasma 25-hydroxyvitamin D concentration at 17 wk of age; the mean ± SEM was 28.2 ± 2.2 nmol/L. The plasma taurine concentration of kittens was >300 nmol/L at all times.
Plasma peptides.
Although the ANOVA of the effect of treatments on intact parathyroid hormone attained a significance of only P < 0.067, some of kittens in treatments 1 and 7 had individual values that were higher than those in all other treatments.
Treatments, but not sex or sampling times, had a significant effect
(P < 0.001) on plasma osteocalcin concentration of
kittens. Kittens in treatments 2 and 7 had significantly higher values
(P < 0.05) than kittens in treatments 5, 6, 4 and 1.
Kittens in treatment 3 had higher concentrations than those in
treatments 5 and 6, whereas kittens in treatment 4 had levels
significantly higher than kittens in treatment 5 (Table 4)
.
Body composition.
Although kittens in treatments 1 and 7 had numerically lower values for bone mineral content by DXA when expressed in g/kitten at 18 wk, there were no significant treatment effects in the ANOVA (P = 0.55). Sex had a significant (P < 0.0001) effect on bone mineral mass (males 40.0 ± 1.25 g; females 31.44 ± 1.08 g). There was no significant sex effect when bone minerals were expressed as a percentage of body weight. However, there was a significant (P < 0.0015) treatment effect in the ANOVA; values for kittens in treatment 1 were lower than those in treatments 3, 4, 5 and 6 (P < 0.03), treatment 7 kittens had lower values than those in treatments 3, 4, 5 and 6 (P < 0.05) and values for kittens in treatment 2 were lower than those in treatments 4 and 5 (P < 0.04).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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compared the performance of a large breed of dogs (Great
Danes) given diets containing either 5.5 or 11.0 g of calcium/kg
diet and a constant phosphorus content (9 g/kg dry matter). He reported
that puppies given the 5.5 g calcium/kg diet had abnormalities of
gait, a reluctance to move and compression fractures in the epiphyseal
and metaphyseal regions of the long bones as well as the vertebral
bodies. These dogs also had elevated i-PTH concentrations in
plasma; on some sampling occasions, they had significantly higher
concentrations of total calcium and phosphorus in plasma. He also
reported that dogs given high levels of calcium (33 g/kg) in the diet
developed abnormal alignment of the radius and ulna, posterior ataxia,
stunted growth, hypercalcemia, hyperphosphatemia, elevated alkaline
phosphatase, retained cartilage plates in the distal ulna and stenosis
of the spinal canal. In contrast to large-breed dogs, Nap (1993)
found that small-breed dogs tolerated a wide range
of calcium levels in the diet. He gave growing puppies (Miniature
Poodles) from weaning, diets containing 0.5, 3.3, 11 or 33 g
calcium/kg and a constant phosphorus content (9 g/kg dry matter) for 20
wk. There were no significant differences in response to calcium level
in the diet in total plasma calcium, but plasma phosphorus was lower in
puppies receiving the 33 g calcium/kg diet. Intact PTH was
significantly higher in the puppies in the group receiving the 0.5 g Ca/kg diet than in puppies given the 11 g/kg diet on five of eight
sampling occasions. In general, there were no significant differences
in the performance of dogs given diets containing 3.3 and 11 g
calcium/kg diet.
The response of our kittens to various levels of calcium in the diet
was more similar to that of the small-breed rather than the
large-breed dogs. For dietary calcium concentrations from 3.8 to
8.1 g calcium/kg diet, there were no adverse effects on gross
criteria, including clinical examination, total body weight gain, rate
of gain or energy intake. This lack of response indicates that
homeostatic mechanisms prevented perturbations over this range of
calcium intakes. The major adaptive mechanism of animals in response to
varying calcium levels in the diet is to change the efficiency of
calcium absorption from the gut. Petith and Schedl (1976)
demonstrated that when rats were restricted in calcium,
they adapted by a fourfold increase in net absorption of calcium in the
ileum and a nearly twofold increase in absorption in the duodenum.
There was also decreased calcium flux from plasma to lumen in the
duodenum in restricted conditions, but the main adaptation was the
enhanced flux in the ileum. Cats do not significantly change their
urinary output of calcium over a wide range of calcium intakes
(Pastoor 1993
); thus changes in urinary loss have only a
minor effect on calcium balance.
The minimum dietary level of calcium that we propose is greater than
that for mink, but similar to that for rats for growth (5 g calcium/kg
diet, NRC 1995
). Bassett et al. (1951)
conducted a factorial experiment with weaning mink that received four
dietary levels of calcium (3, 5, 6 and 10 g/kg diet) and of phosphorus
(3, 4, 6 and 8 g/kg diet). They concluded that the minimum calcium and
phosphorus requirements were < 0.3% of the dry diet. Humerus
bone ash was the main index used to assess adequacy. The NRC
(1982)
proposed 4 g/kg diet for both calcium and phosphorus for
weaning mink and 3 g/kg diet for adult mink. Similarly, 4 g
calcium/kg diet has been proposed by the NRC (1977)
as a
requirement for growing rabbits, which have a mature body weight
similar to that of cats.
Although our kittens adapted to the varying calcium levels in the diet,
differences in blood variables indicate that some of the diets,
particularly treatments 1 (the lowest level of calcium) and 7 (the
widest inverse Ca:P ratio), may be suboptimal. Ionized calcium was
significantly lower in kittens in treatments 1 and 7 than in those in
treatment 5 at wk 13, and was significantly lower in kittens in
treatment 7 than in kittens in treatments 4, 5 and 6 at wk 15 and 18.
The depressed ionized calcium is supported by elevated values for
i-PTH in these two groups of kittens. Ionized calcium is the
fraction in plasma that is most important physiologically
(Bringhurst 1989
) The rate of PTH secretion in response
to a decrease in plasma calcium follows a sigmoidal relationship
(Mayer and Hurst 1978
). Because the secretion of PTH is
pulsatile (Schmitt et al. 1996
) and because it has a
short half-life in plasma (of the order of minutes), the three
samplings we took may have been inadequate to demonstrate a
statistically significant difference.
The formation and resorption of bone in humans has been studied using
markers arising from bone synthesis or dissolution. Two of the serum
markers for bone formation are total (or bone-specific) alkaline
phosphatase and osteocalcin. Bone alkaline phosphatase is released by
osteoblasts during bone formation, whereas osteocalcin is a small,
noncollagenous protein synthesized predominately by osteoblasts with a
specific 
-carboxyglutamic acid–dependent Ca2+
binding site. Total serum alkaline phosphatase activity in most species
is a combination of isoenzymes from a number of tissue sources,
including intestine, kidney, liver and bone. Horney et al. (1992)
reported that the primary tissue source of the
isoenzymes in the serum of mature healthy adult cats was liver, but
immature cats (<1 y of age) had a greater proportion of the isoenzyme
from bone. Everett et al. (1997)
also reported that the
sera from kittens <15 wk old contained only the osseous alkaline
phosphatase isoenzyme. Therefore, our measurements of total alkaline
phosphatase activity should represent mainly activity of isoenzyme from
the osteoblasts. Because the activity of alkaline phosphatase was
significantly higher in kittens in treatment 7 (diet with the widest
inverse Ca:P ratio), we have interpreted this as indicating that bone
formation was highest in this treatment. Osteocalcin concentration in
plasma was also highest in kittens in treatment 7, which supports the
alkaline phosphatase data indicating higher rates of bone formation.
However, bone is continually being resorbed, as well as being formed in
response to hormonal and physical stimuli. Some of the indices of bone
resorption that have been used in humans are the urinary markers
pyridinoline and deoxypyridinoline (collagen cross-links),
hydroxyproline and hydroxylysine glycosides or the serum marker of
tartrate-resistant acid phosphatase (Delmas 1995
).
Unfortunately, we did not measure these markers, which, like those of
bone formation, give only the direction of the process and do not
measure bone mass.
For the measurement of bone mass we used DXA. Although there are
recognized problems with the accuracy of this method (Elowsson et al. 1998
), the precision in measurement of bone mineral mass
is in general superior to the measurement of fat mass and should give
comparative values among treatments. Wedekind et al. (1992)
reported that the precision of three DXA units in the
measurement of bone mineral content of cats was better than the
precision of chemical analysis. No significant differences were found
among treatments for bone mass expressed as g/kitten (Table 4)
.
However, there was a significant difference in bone mineral mass
expressed as a percentage of body weight. Kittens in treatment 1 had a
significantly lower percentage of bone mineral mass than those in
treatments 3, 4, 5 and 6, and the kittens in treatment 7 had a
numerically lower percentage bone mineral mass than those in treatments
2–6; however, the difference was not significant. Therefore it would
appear that in kittens in treatment 7, the rate of bone resorption may
have been higher than in the other kittens, which would nullify the
possible greater rate of bone deposition indicated by elevated
osteocalcin and alkaline phosphatase.
The mean concentration of 25-hydroxyvitamin D that we found in these
kittens at 17.2 wk of age (28.2 ± 2.2 nmol/L) was virtually
identical to that reported by Morris et al. (1999)
of
27.7 ± 2.1 nmol/L in kittens given the same diet containing 3.125
µg cholecalciferol. This lends support to the
suggestion that plasma concentration of 25-hydroxyvitamin D could be
used in a bioassay of the availability of vitamin D in foods.
The basis for the negative relationship of plasma phosphorus to
phosphorus intake over the range of dietary concentrations from 6.3 to
15.76 g/kg diet is not apparent. Because a fixed Ca:P ratio was used
for treatments 1–5, a similar negative relationship exists between
calcium concentration in the diet and plasma phosphorus for treatments
2–5. However, treatments 6 and 7 contained the same levels of calcium
as treatment 3, and kittens in these treatments had lower plasma
phosphorus concentrations than kittens in treatment 3, indicating that
the effect is related to phosphorus rather than to calcium
concentration in the diet. Pastoor (1993)
reported a
decline in blood phosphorus with increasing dietary phosphorus in adult
cats given diets with a fixed level of calcium and a variable level of
phosphorus. Nap (1993)
reported that plasma phosphorus
concentration in miniature poodle puppies given a fixed phosphorus
concentration in the diet was less in puppies when the diet contained
33 rather than 11 g calcium/kg. This indicates a reciprocal effect
of dietary calcium on blood phosphorus that could have been due to the
higher level of calcium depressing phosphorus absorption from the gut.
It has been generally recommended that diets for most animals,
including cats, contain a higher amount of calcium than phosphorus, on
the basis that the total body contains more calcium than phosphorus.
However, in the balance studies on cats reported by Roberts and Scott (1961)
, the retention of phosphorus was consistently
higher than the retention of calcium. From our study, it appears that
growing kittens tolerate an inverse Ca:P ratio of 1:1.55, but a ratio
of 1:2.61 results in some metabolic changes. Edfors et al. (1990)
reported that European ferrets (Mustela putorius
furo) given diets containing 6, 7 or 8 g calcium/kg dry
matter with Ca:P ratios of 1.3:1 or 1:1.3 grew normally and that diet
had no effect on plasma alkaline phosphatase activity or femur weight,
length diameter, maximum breaking force, or bending moment. However,
the dietary Ca:P ratios of 1.3:1 produced higher plasma calcium and
lower plasma phosphorus concentrations than the diets with a Ca:P ratio
of 1:1.3.
Although kittens adapted to the five levels of calcium in the
diet and the two Ca:P ratios, there were differences in measurements
that indicated that the diets with the lowest calcium concentration
(treatment 1) and the most extreme Ca:P ratio (treatment 7) were
suboptimal. Kittens in treatment 7 had significantly decreased plasma
ionized calcium and phosphorus and the highest osteocalcin levels. In
addition, although not statistically significant, these kittens had the
lowest body weight gain (ANOVA, P = 0.7) and
highest values for i-PTH, (ANOVA, P = 0.067).
Kittens in treatment 1 had significantly lower bone mineral percentages
and higher values for i-PTH than those in treatments 3–6. At no
time were there any significant differences among any of the
measurements taken on kittens in treatment 3, 4 and 5, which supports a
calcium requirement of no greater than 6 g/kg, and 5 g/kg diet may be
adequate. This value is similar to the calcium requirement of other
growing mammals ranging from rats to rabbits. The proposed requirement
is less than the NRC (1986)
recommendation of 8 g/kg
diet and the Association of American Feed Control Officials (1999)
allowance of 10 g/kg diet. Because the primary sources
of calcium in commercial cat foods are animal products such as bone,
which has a high bioavailability (Soares 1995
), this
allowance is excessive. Growing kittens do not appear to be sensitive
to mild inverse Ca:P ratios (1:1.55), provided adequate calcium is
present in the diet.
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ACKNOWLEDGMENTS |
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Manuscript received March 17, 1999. Initial review completed April 22, 1999. Revision accepted May 25, 1999.
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