OCR for page 4
4 Nutrient Requirements of Cats
(1985) remains unclear. However, since the various
breeds of domestic cats differ so little in mature size,
energy requirements listed in this publication will con-
tinue to be expressed per unit of body weight. Indeed
Kendall et al. (1983) found no extra precision when en-
ergy requirements of adult domestic cats were scaled to
mass exponents of body weight (kg) of either 0.75 or
0. 67, compared with unity.
Data from which estimates of energy requirements
can be made are available from two sources: short-term
measurements of gaseous exchange or heat production,
and longer-term measurements of food intake and body
weight or body energy changes. Theoretically, both ap-
proaches should give similar values. However, activity
is limited in a respiration chamber or metabolism cage,
and most studies in ' chambers have measured fasting
heat production rather than maintenance energy re-
quirements. Several previous estimates of energy re-
quirements from feeding trials with cats must be inter-
preted with caution, because dietary energy intakes
were based on Atwater factor calculations rather than
direct measurement (Miller and Allison, 1958; Scott,
1968~. Unless diets of very high digestibility are used,
these values are likely to be serious overestimates.
ReguirementsfoT Adult Maintenance
Energy requirements for maintenance of adults have
been estimated by several investigators. MacDonald et
al. (1984c), using the calorimetric data of Benedict
(1938) and Carpenter (1944), calculated the daily re-
quirement (1.5 times basal heat production) for the cat
as 87 kcal ME/kg body weight (BW).
Various estimations of energy requirements of cats re-
ported in the literature have been based on measure-
ments of food intake. Kreh} et al. (1955) reported dally
ME intakes of 65 kcal/kg BW for maintenance of young
adult cats. Daily maintenance energy estimates for ma-
ture adults in confined conditions range from 60 to 70
(Miller and Allison, 1958; Gisler and Ewing, 1964;
Skultety, 1969; Burger et al., 1984) to 80 kcal ME/kg
BW (Greaves and Scott, 1960~. The latter value may be
biased upwards because Atwater factors of 4 kcal/g for
protein and carbohydrate and 9 kcal/g for fat were ap-
plied to high-fiber canned diets containing 4 percent
sugar beet pulp and 20 percent potato flake as fed.
Kendall et al. (1983) reported a mean daily DE re-
quirement for maintenance of six adult cats in metabo-
lism cages of 76 kcal/kg BW, based on 6 months' contin-
uous measurement of DE intake and body weight
change. This value is equivalent to a daily ME require-
ment of 68 kcal/kg BW, assuming a urinary energy loss
of 1.2S kcal/g digestible crude protein intake. While no
definitive value for maintenance energy requirement
can be derived from the above data, it would appear
that a value of about 70 kcal ME/kg BW is reasonable
for inactive cats. Higher energy intakes are probably ap-
propriate for maintenance of active cats. Miller and A1-
lison (1958) reported that adult cats allowed to exercise
in runs increased their calculated daily energy intakes to
80 to 90 kcal/kg BW compared with 60 kcal/kg BW in
metabolism cages. When the above estimate is adjusted
downwards to account for the probable bias in ME in-
takes from the use of Atwater factors, a daily ME re-
quirement of about 80 kcal/kg BW is recommended.
Requirementsfor Growth
Miller and Allison (19S8) observed that the daily ME
requirements of growing kittens rapidly declined with
advancing age from about 250 kcal/kg BW at 5 weeks to
about 100 kcal/kg BW at 30 weeks of age. By 50 weeks of
age daily ME intakes stabilized at about 60 kcal/kg BW
for cats kept in metabolism cages and at about 85 kcal/
kg BW for cats allowed] to exercise in runs. Miller and
Allison (1958) used a purified diet in their studies. Com-
parable ME intakes for growing kittens have been subse-
quently reported by a number of investigators. Wa-
terhouse and Carver (1962) found mean daily ME
intakes of 128, 95, and 76 kcal/kg BW for kittens 18, 30,
and 56 weeks of age, respectively. Loveridge (1986a)
measured mean daily Atwater ME intakes of 220 and
145 kcal/kg BW at 10 and 20 weeks of age, respectively,
for 52 kittens fed commercial canned foods. In contrast,
Greaves (1965) observed lower daily ME intakes of 152,
114, and 102 kcal/kg BW for kittens 11, 17, and 21
weeks of age. The lower ME intakes reported by
Greaves (1965) are probably explained by a lower food
intake required to support somewhat smaller mean
daily body weight gains of 16 ant] 10 g per cat for male
and female kittens, respectively, from 12 to 20 weeks
compared with 18 and 16 g per cat reported by Lov-
eridge (1986a). Allison et al. (1956) suggested that daily
ME intakes of 160 kcal/kg BW may represent a lower
limit for satisfactory growth in young kittens.
Figure 1 outlines the growth response for 19 male and
37 female kittens from birth to 52 weeks of age (Lov-
ericige, 1986a). These kittens were raised in a specific
pathogen-free derived cat colony and were given com-
mercial canned diets.
Requirementsfor Gestation and Lactation
Queens appear to require about 25 percent more en-
ergy for gestation than for maintenance. Smith (1974)
observed mean daily ME intakes of approximately 90
OCR for page 5
Nutnent Requirements of Cats 5
4.
4.6
5)
I
by
~ 4.2
a
LL
o
I
o
m
4.4
4.0
Body Heights N ~ 64
Energy intakes N = 10
3.8 ~
3.6 ~F7
3.2
900
800
700
0 1
cat
600 Y
co
I
500 6
At
400 ~
Ct
At
300 uJ
1 1
~ _
5 6 7 8 9 1 2 3 4 5 6
2 3 4
Mating
WEEKS OF GESTATION
Parturition
WEEKSOF LACTATION
kcal/kg BW during gestation for queens fed a commer-
cial diet. Scott (1966) has suggested that average daily
ME requirements based on dietary Atwater ME concen-
trations are about 100 kcal/kg BW. This may be slightly
high when ME is based on direct in viva ME determina-
tion. More recently, voluntary energy intakes of cats
have been measured throughout gestation and lactation
by Loveridge (1986b). The pattern of body weight
change during gestation and lactation is outlined in Fig-
ure 2 based on data for 64 individual cats, together with
weekly averages of calculated (Atwater) ME intake for
10 of these cats. During gestation the mean body weight
of the queens increased from 3.4 to 4.7 kg, while calcu-
lated daily voluntary ME intakes showed a steady but
consistent increase from about 270 to 470 kcal ME per
cat. This level of calculated ME intake is equivalent to
93 to 109 kcal/kg BW and is in quite close agreement
with the earlier observations (Scott, 1966; Smith, 1974~.
It would appear from the postparturient weight loss of
the queens as seen in Figure 2 that for satisfactory repro-
ductive performance the body weight gain in pregnancy
should include net tissue accretion in preparation for
lactation, rather than gain in fetal and placental and
associated membrane weight alone.
Energy intakes for lactation increase substantially
and may exceed 250 kcal ME/kg BW at the peak of lacta-
tion (Smith, 1974), since food energy needs represent
that for the queen plus her kittens. Scott (1968) has
pointed out that female cats tend to lose body weight
during lactation even when allowed to eat palatable for-
mulated diets ad libitum. This is supported by the data
of Loveridge (1986b) outlined in Figure 2, which show a
drop in mean body weight of queens from about 4.2 kg
100
FIGURE 2 Weekly body weights and
mean metabolizable energy intakes of
queens during gestation and lactation.
Adapted from Loveridge (1986b).
postpartum to about 3.4 kg after 6 weeks of lactation.
Mean daily ME intakes for 10 queens showed an in-
crease from about 330 in the first week postpartum to
800 kcal per cat plus kittens in week 6 of lactation. These
values approximate to 90 to 270 kcal ME/kg maternal
BW/day, respectively.
More detailed data on mean daily calculated ME in-
takes of queens in lactation are outlined. in Table 1 by
litter size and week of lactation. These values are based
on the work of Loveridge (1986b) using a specific patho-
gen-free derived cat colony given canned foods that are
known to support satisfactory queen and kitten perfor-
mance.
Energy Allowances
Recommencled daily ME allowances for cats in vari-
ous physiological states are outlined in Table 1. These
allowances represent estimates of probable energy needs
of cats and are intended to serve as practical feeding
guides. They do not necessarily represent the precise en-
ergy requirement of a specific animal for optimum per-
formance. It should be recognized that the energy re-
auirements of cats vary with age, activity, body
condition, insulative characteristics of hair coat, envi-
ronmental circumstances, and temperature acclimati-
zation. In the case of lactating queens, allowances have
been detailed by litter size and week of lactation. The
values are based on total voluntary ME intake for queen
and kittens during the period shown, and thus ME in-
takes for the queen only will be lower than stated from
about weeks 4 to 6 of lactation.
OCR for page 6
6 Nutrient Requirements of Cats
CARBOHYDRATES
Although no known dieter,, carbohydrate require-
ment exists for the cat, dry commercial diets usually
contain 40 percent or more carbohydrate and are well
utilized. Based on research with chickens (Renner,
1964; Renner and Elcombe, 1964; Brambila and Hill,
1966; Edwards and Hart, 1971), rats (Goldberg, 1971;
Akrabawi et al., 1974), and dogs (Belo et al., 1976;
Romsos et al., 1976), it is probable that cats can be
maintained without dieter,' carbohv~rate if the diet Trudell and Morris (1975) estimated the apparent d~-
furnishes sufficient fat (and thus glycerol) and protein gestibilitv of individual carbohydrates using the feed-to-
(containing glucogenic amino acids) from which the fecal ratios of chromic oxide to carbohydrate. The basal
metabolic requirement for glucose can tee derived. ground beef and mutton diet was fed to near-mature
~ ' ^ -- -^^^ ~ ' ~' ~ ' ~ ~ ~ domestic short-haired cats with the test carbohydrates
constituting about 20 percent of diet dry matter. The
apparent digestibilities (percent) were: glucose, 99.8;
sucrose, 99.8; lactose, 99.1; dextrin, 97.6; starch, 96.1;
fmann, 1955; Carpenter, 1956; Zotterman, 1956),
perhaps because there are few sucrose-sensitive nerve
endings in feline taste buds. Nevertheless, interactions
between sucrose and other dietary components can af-
fect taste preference (Bartoshuk et al., 1971, 1975;
Frings, 1951~.
bereaves and bCOtt (1Ybd) noted that substitution of
dextrin for sucrose in a purified diet resulted in greater
food intakes by adult cats. Hardy et al. (1977) and Tee-
teret al. (1978b) have obtained excellent growth rates in
young kittens fed purified amino acid diets containing
carbohydrate as a 1:1 ratio of cornstarch to sucrose.
Trudell and Morris (1975) measured intestinal lactase
and sucrase activities up to 109 days of age in kittens
maintained from weaning (8 weeks) on either a basal
ground beef and mutton flint or the basal diet plus lac-
tose or sucrose (at 20 percent of diet ciry matter). There
was considerable individual variation in disacchariciase
activity, but it did not appear relater] to the presence of
carbohydrate in the diet.
The liver of most omnivorous animals has two en-
zymes, glucokinase and hexokinase, which catalyze the
phosphorylation of glucose to glucose-6-phosphate.
Hexokinase has a low Km for glucose, whereas gluco-
kinase has a high Km and operates mainly when the liver
receives a high load of glucose from the portal vein. The
activity of glucokinase in the liver of the cat is extremely
low, whereas the activity of hexokinase is in the normal
range (Ballard, 1965~. Carnivores with omnivorous die-
tary habits, e.g., domestic dog, possess both enzymes.
Therefore, one would] predict that they might have a
greater capacity to metabolize a high-glucose meal than
the cat, but this does not appear to have been tested.
Fiber is not generally considered essential for simple-
stomached mammals including cats, although includ-
ing some fiber in the diet is not uncommon in commer-
cial practice. Energy density of the diet is reduced by
fiber, and therefore including some fiber in the diet may
contribute to maintenance of ideal body weight in adult
sedentary cats fed ad libitum.
With the advent of semimoist cat foods there has been
renewed interest in the taste response of cats and their
tolerance for mono- and disaccharides, since these sug-
ars are important in the formulation of these diets. Su-
crose does not enhance diet palatability for cats (Pfaf-
cellulose, - 0.73.
Using the same technique and a ground meat basal
diet, Pencovic and Morris (1975) studied the apparent
digestibility of starch (added at 35 percent of diet dry
matter) found in corn or wheat grain. Apparent starch
digestibilities (percent) for coarsely ground, finely
ground, or coarsely ground and cooked grains were, re-
spectively: corn, 79, 94, and 88; wheat, 92, 97, and 96.
It was concluded that starch from corn and wheat, espe-
cially when finely ground, is well utilized by the cat.
Morris et al. (1977) studied the effects of age and the
addition of sucrose and lactose on the ,B-fructofurani-
dase (sucrase) and ,6-galactosidase (lactase) activities of
the small intestine. Intestinal ,B-galactosidase activity
decreased with age (71-106 days) in kittens. However,
the activities of neither enzyme were affected by addi-
tion of sucrose or lactose to the all-meat diet.
The apparent digestibilities of nitrogerl-free extract in
commercial cat foods (canned and dry type) ranged
from 82 to 87 percent (L. G. Miller, The Carnation Co.,
personal communication, 1985~. Apparent digestibili-
ties of "total carbohydrate', (assayed by the method of
Dubois et al., 1956) in dry-type commercial cat food
ranged from 90 to 95 percent (R. D. Kealy, Ralston
Purina Co., personal communication, 1985~.
The fiber contents of ingredients used in cat diets are
listed in Table 7 as crude fiber. It should be noted that
the crude fiber can be a very misleading parameter of
'4indigestible" fiber content, particularly with ingredi-
ents high in poorly soluble indigestible materials such as
cellulose, hemicellulose, lignin, and chitin. A more ap-
propriate criterion of insoluble fiber might be neutral-
detergent fiber (NDF). Unfortunately, NDF values for
common ingredients used in feline diets are not avail-
able at present.
OCR for page 7
Nutrient Requirements of Cats 7
FAT
Dietary fat functions as a concentrated energy source,
serves as a carrier for fat-soluble vitamins, provides es-
sential fatty acids, and influences diet acceptance by the
cat.
Analytical Procedures
Materials extracted from cat food with anhydrous di-
ethyl ether are termed crude fat and include primarily
glycerides of fatty acids, although small amounts of
other substances such as cholesterol, chlorophyll, or
xanthophylis, which have no known nutritional signifi-
cance for the cat, may also be included. In expanded or
baked cat foods, complete release of glycerides will not
result unless ether extraction is preceded by acid hydro-
lysis. Thus, using crude fat, levels for low fat diets may
underestimate total fat by more than 50 percent (Budde,
1952; Hoffman, 1953~. The fat (including phospholi-
pids) in certain animal products is extracted more com-
pletely by a chloroform-methanol mixture. Thus, use of
fat content derived from ether extraction may lead to
underestimates of the calculated energy potential in
these diet ingredients so that acid hydrolysis followed by
chloroform-methanol extraction is the preferred ap-
proach (Cox and Pearson, 1962~.
Digestibility
Morris et al. (i977) reported apparent digestibility of
crude fat in a diet of beef and mutton to be 99 percent,
and M. A. Norvel1 (personal communication, 1976)
found that apparent digestibilities of crude fat in several
commercial cat foods ranged from 85 to 94 percent (see
Table 3, page 43~. Kane et al. (1981a) found that the
apparent digestibility of fat was 90 percent when fed at
10 percent of the dry matter but was 97 to 99 percent
when fed at 25 or 50 percent of the dry matter. Hum-
phreys and Scott (1962) have shown that dietary fat con-
centration could be raised to 64 percent (dry matter ba-
sis) without an increase in the proportion of fecal fat,
commonly fed, whereas dry, commercial cat foods usu-
ally contain ~ to 12 percent fat. Generally, high-fat diets
appear to be more palatable than low-fat diets
(Greaves, 1965; Kendall, 1984~.
Both the amount and source of dietary fat influence
food acceptance and growth in kittens (Kane et al.,
1981a; MacDonald et al., 1983~. Diets containing 25
percent hydrogenated coconut oil were found to be un-
palatable and failed to support growth. Even when ac-
ceptance was improved by adding small amounts of es-
sential fatty acids as safflower of] or chicken fat, normal
growth was not restored. By contrast, hydrogenated
beef tallow did support growth in kittens, although
tested for only 7 weeks. This difference between fats was
attributed to palatability, since the hydrogenated beef
tallow diet was consumed at almost five times the level
of the hydrogenated coconut oil diet. Further studies by
the Davis group (MacDonald et al., 1985) indicate that
diets containing medium-chain triglycerides are poorly
accepted by cats and that caprylic acic] as low as 1 g/kg
diet causer] the diet to be unpalatable. Similarly, kittens
chose beef tallow (nonhydrogenated) over chicken fat
(3:1), although no significant difference in choice was
noted between diets containing 35 percent fat as hydro-
~enated tallow and those containing regular beef tallow
(MacDonald et al., 1983~. Other results (Kane et al.,
1981a) indicate that diets containing 25 percent fat are
selected over those containing 10 percent or 50 percent
fat. Beef tallow was selected over butter and chicken
fat, but no preference was apparent among beef tallow,
lard, or partially hydrogenated vegetable oil. Scott
(1966) found satisfactory performance in kittens fed di-
ets containing 22 percent fat.
Schneck and Cumberland (1968) observed that grow-
ing kittens responded to a 10 percent dietary fat addition
with a reduction in dry matter intake relative to the un-
supplemented control group. Total energy consumption
for the experimental period was about the same for both
groups, and weight gain as a percentage of the original
body weight was not significantly different. This sug-
gests that energy intake of the cat is maintained with
~ ~ diets of varying dietary energy densities.
indications of ketonuria, or significant pathological Because the metabolizable energy concentration of
changes in the cardiovascular system. These observa- fat is approximately 2.25 times that of protein and car-
tions suggest that cats have the capacity to tolerate and bohydrate, changes in fat level alter the caloric density
utilize high levels of dietary fat. of the diet. This may necessitate adjustment of other nu-
trient concentrations, particularly proteins, vitamins,
and minerals, in order to maintain appropriate intakes
of these nutrients. For example, if proportions of other
Dietary Fat Concentration
Relatively high dietary fat concentrations, from both
animal and plant sources, have been routinely used in
feeding experiments with cats. Purified diets composed
of 25 to 30 percent fat and 30 to 40 percent protein are
nutrients are not increased as the dietary caloric density
increases, energy intake may be adequate but intake of
proteins, vitamins, and minerals may be inadequate
(Elvehjem and Krehl, 1947; Crampton, 1964~.
OCR for page 8
Nutrient Requirements of Cats
Fat is a good energy source, provides a vehicle for car-
rying fat soluble vitamins and essential fatty acids into
the diet, and may improve palatability. A need for fat
above and beyond that required as essential fatty acids
has not been demonstrated.
Essential Fatty Acids (EFA)
Investigations of the essential fatty acid needs of two
Felidae species have been reported. Most studies of the
metabolism of polyunsaturated fatty acids (PUFA) have
been conducted on rats, which have relatively high ~6-
and ^5-desaturase activities associated with the ability
to convert linoleic acid (18:2n6) to the prostaglandin
precursors dihomo-~-linolenic acid (20: 3n6) and arachi-
donic acid (20:4n6), respectively. It had been assumed
that other species can desaturate polyunsaturated fatty
acids equally well. However, Rivers et al. (1975,
1976a,b,c) and Hassam et al. (1977) originally pre-
sented evidence that cats fail to convert linoleic (~6-de-
saturase) to~y-linolenic acid (18:3n6) or dihomo--y-lino-
lenic acid (~5-desaturase) to arachidonic acid,
implicating the need for dietary 20:4n6, which is avail-
able only from animal sources. Subsequent studies by
MacDonald et al. (1983, 1984a,b,c,3) demonstrated the
essentiality of dietary linoleate (5 gtkg diet), in its own
right, as a factor affecting skin water permeability, as
well as the failure of the cat to convert 18:2n6 to 18:3n6,
20:3n6, or 20: 4n6 due to a presumed lack of both A6-
and A5-desaturase activities. In addition their data sug-
gested a selective ability of the hepatic ^5-desaturase
to convert 20:2n6-11,14 to 20:3n6-5,11,14, but not
20:3n6-8,11,14 to 20:4n6-5,8,11,14. However, feeding
cats evening primrose oil, rich in 18:3n6 (Franker and
Rivers, 1978), improved the physical status of cats fed
safflower oil, but failed to enhance conversion of 18:3n6
to 20: 4n6 as evidenced by plasma phospholipid fatty ac-
ids. It was concluded that ~5-desaturase was absent but
that 18:3n6 and/or 20:3n6 were biologically important
fatty acids since they improved physical condition. In
contrast, Sinclair et al. (1979) fed the methyl ester of
18:3n6 to kittens consuming no PUPA or injected ra-
diolabeled 18:2n6 or 20:3n6 into kittens fed safflower oil
and found evidence for conversion of 18:3n6 and 20:3n6
(but not 18:2n6) to 20:4n6, concluding that ^5-(lesa-
turase was active, whereas the A6-clesaturase was not.
A requirement for dietary 18:2n6 and 20:4n6 in cats
was established with studies of reproductive function in
both sexes by MacDonald et al. (1984d). By feeding lino-
leate with or without arachidonate it was possible to
demonstrate that 20:4n6 was required by female cats to
deliver viable kittens, whereas 18:2n6 alone was suffi-
cient to maintain seminiferous tubule architecture and
spermatogenesis in males. Furthermore, conversion of
linoleate to arachidonate by the testes was evident from
phospholipid fatty acid profiles, indicating at least some
^5- and ~6-desaturase activity in the testes, in contrast
to the questionable ~5 and lack of ~6 activity in liver.
These reproduction studies demonstrated that 0.04
percent of the energy (200 mg/kg diet) supplied as
20:4n6 was adequate for assuring pregnancy and lacta-
tion except when additional fish oil (tuna oil) was fed
(MacDonald et al., 1984d). The latter contains n3 fatty
acids (20: 5n3, 22: 6n3), which both compete with
20:4n6 for incorporation into glyceryl lipids and may
depress the ^5-desaturase activity, as well.
It seems prudent to recommence including both
18:2n6 and 20:4n6 in any diet intended for cats. Five
and 0.2 gof lineolate and arachidonate/kg diets, respec-
tively, are recommended as the minimum require-
ments.
Signs of Deficiency
Rivers (1982) listed several changes attributed to EFA
deficiency in cats (listlessness, dry hair coat with dan-
druff, poor growth, and increased susceptibility to in-
fection), and MacDonald et al. (1984a) have detailed
the pathology involved after 1.5 to 2.5 years of EFA-
deficient diets. EFA-deficient cats develop reduced feed
efficiency without changing body weight gain. Scaly
skin and markedly increased water loss through the skin
were accompanies] by alopecia and focal exudative der-
matitis on the flanks and ventral surfaces of selective fe-
males. Livers were enlarged and fatty, and kidneys also
revealed histologic evidence of fatty infiltration. These
changes were corrected by feeding 18:2n6 alone, but
prevention of mild mineralization of kidneys (Mac-
Donald et al., 1984a) and changes in platelet aggrega-
tion (MacDonald et al., 1984b) depended on 20:4n6
supplementation. They concluded that dietary linoleate
probably provides for functions dependent on physical
properties of membranes, whereas arachidonate was
needed in processes requiring eicosanoid formation,
such as reproduction and platelet aggregation.
The variation in diet composition, age and sex of cats,
tissues examined, and method of assessment have all
served to complicate interpretation of the several studies
cited. Kittens have been raised and maintained for up to
2 years on purified diets containing vegetable oil (Hayes
et al., 1975a; Schmidt et al., 1976) without observed
differences ire growth or overt signs of EFA deficiency
(reproduction not studied), which suggests that cats can
be maintained without dietary 20:4n6. Furthermore,
undiscovered nutrient interactions presumably vary the
demand or in viva synthetic capacity of the various
EFA.
OCR for page 9
Nutnent Requirements of Cats 9
PROTE IN
Cats require protein in the diet to supply amino acids
that cannot be synthesized at a rate commensurate with
optimal performance (essential amino acids) and to sup-
ply nitrogen requires] for synthesis of dispensable amino
acids and other nitrogenous compounds such as purines,
pyrimidines, heme, and creatine. The following 10 al-
pha-amino acids were shown by Rogers and Morris
(1979) to be essential for the growing kitten.
· · .
Arglnlne
Histidine
Isoleucine
L.
euclne
Lysine
Methionine
Phenylalanine
Threonine
Tryptophan
Valine
When any one of the above 10 amino acids was de-
leted from an otherwise complete purified amino acid-
based cliet, food intake decreased and body weight loss
occurred. Returning the amino acid to the diet restored
food intake and body weight gain. The minimal re-
quirements for these 10 essential amino acids have been
determined only for growing kittens (generally between
10 and 20 weeks of age). Younger and older kittens may
have different requirements. With the exception of
methionine, no values are available for minimal essen-
tial amino acid requirements of adult cats for mainte-
nance or for pregnancy and lactation.
The minimal requirements were cletermined using
purified diets. These diets had an ME value about 4.7 to
5 kcal/g and nitrogen was supplied as crystalline amino
acids.
When diets are formulated from natural ingredients
the quantities of amino acids in the diet should be
greater than those listed in Table 2. These greater quan-
tities are necessary because digestibility (availability) of
amino acids in natural ingredients is less than that from
free amino acids.
Nitrogen Requirements of Cats
Published studies prior to the 1980s on the protein re-
quirements of the growing kitten and adult cat were
clone without knowledge of the quantitative require-
ments for essential amino acids. Therefore, no differen-
tiation could be made between a response to an essential
amino acic] and to protein (nitrogen) per se. In the last
edition of Nutrient Requirements of Cats (NRC, 1978a),
the protein requirement was set at 280 g/kg diet. The
sum of the nitrogen of the current minimal essential
amino acid requirements of the growing kitten (Table 2)
times 6.25 is equivalent to about one-fourth to one-fifth
of this quantity of protein. It would, therefore, appear
that a high proportion of the protein requirement of the
growing kitten and adult cat must be for amino nitrogen
for synthesis of dispensable amino acids and other com-
pounds containing nitrogen.
Several estimates have been made of the nitrogen re-
quirements of the growing kitten. Anderson et al.
(1980b) gave kittens diets varying from 21.5 to 29.4 g of
nitrogen/kg diet (134 to 184 g crude protein/kg diet). In
one experiment they found a linear growth response to
level of nitrogen in the diet and in the other essentially
no response.
Smalley et al. (1985) gave growing kittens either
amino acid-based diets or casein-based diets supple-
mented with essential amino acids. All diets exceeded
the essential amino acid requirements. They suggested
that 180 to 200 g of protein equivalent (N x 6.25/kg
diet was required to maximize both body weight gain
and nitrogen retention. When all the data are pooled for
the growing kitten, the relationships between growth
(gain in body weight and nitrogen retention) and pro-
tein content of the diet gradually approach a plateau
without a clefinite"breakpoint." Recently, Rogers and
Morris (personal communication, 1985), in studies in
which all the essential amino acids were added at their
minimum requirements (MacDonald et al., 1984c) plus
tryptophan at 1.5 g/kg diet, and total dispensable amino
acids added to bring the protein content (N x 6.25) to
200 g/kg diet, a substantial growth response was ob-
tained by the addition of dispensable amino acids equiv-
alent to 40 g crude protein/kg diet. These results indi-
cate that a higher concentration of nitrogen is required
for maximal growth if the essential amino acids are not
present in excess of their requirements as in the diets
used by Smalley et al. (1985~. A minimum requirement
of protein (N x 6.25) of 240 g/kg diet is recommended.
Burger et al. (1984) reported that most adult cats
could maintain good health and condition when given a
diet containing about 120 g crude protein/kg diet that
included all essential amino acids at the minimal re-
quirements for growth suggested by Anderson et al.
(1980b). There are no proteins known that supply the
essential amino acids at the concentration used by
Burger et al. (1984) when the diets contain 120 g protein
(N x 6.25/kg. Aclult cats (like kittens) might also re-
spond to a higher concentration of dietary nitrogen if
the essential amino acid concentration were not in ex-
cess of minimal requirements. This may account in part
for the higher requirement suggested by NRC (1978a)
for the adult cat when protein per se was used. If an
additional quantity of nitrogen is added to the diet con-
taining 120 g protein equivalent/kg diet in proportion to
that suggested for kittens (see above), the minimum pro-
tein (N x 6.25) requirement would be 144 g/kg diet.
Rounding this value, a minimum protein (N x 6.25) of
140 g/kg diet is recommended for the adult cat.
Both the growing kitten and adult cat have higher ni-
OCR for page 10
10 Nutrient Requirements of Cats
trogen requirements than most other domestic mam-
mals (Rogers and Morris, 1982a, 1983~. Cats (and pre-
sumably other strict carnivores) have a reduced capacity
to regulate the activity of the transaminases and urea-
cycle enzymes (Rogers et al., 1977) with change of die-
tary protein intake. Thus, cats require a relatively high
intake of nitrogen to accommodate this high obligatory
nitrogen loss.
A· ~
Anne
Morris and Rogers (1978a7b), using a purified diets
demonstrated that arginine was an essential amino acid.
When near-adult cats were given a diet containing 16.6
g ~-arginine/kg they grew normally. However, when
arginine was omitted from the diet, clinical signs of hy-
perammonemia appeared within 3 h of ingestion of a
single meal. These signs included vocalization (moan-
ing), emesis, ptyalism, hyperactivity, hyperesthesia,
ataxia, tetanic spasms, emprosthotonus, extended limbs
with exposed claws, apnea, and cyanosis, which in some
cases led to death. When arginine was substituted with
isomolar quantities of ornithine, near-adults cats did
not develop hyperammonemia. However, Morris et al.
(1979) demonstrated that while kittens given an argi-
nine-free diet containing ornithine were protected from
hyperammonemia, even high concentrations of or-
nithine did not support growth. Normal growth oc-
curred when citrulline replaced arginine, but the effi-
ciency of utilization of citrulline was less than that of
arginine (C. Johanssen, I. G. Morris, and Q. R. Rogers,
University of California, Davis, personal communica-
tion, 1985~.
Dietary arginine is required for optimal growth in
rats (Borman et al., 1946), and in its absence, growth
rate is reduced to about half maximal (Miiner and Vi-
sek, 1974) . This indicates that rats are capable of synthe-
sizing some arginine de nova, but the rate of synthesis is
suboptimal. In contrast, cats given an arginine-free diet
not only do not grow, but they also lose body mass at a
rate greater than when given diets devoid of any other
essential amino acid. This observation indicates that the
capacity of cats to synthesize arginine is much less than
that of rats. The metabolic basis for this difference be-
tweien species appears to be primarily due to the low
activity of the enzyme pyrroline-S-carboxylate synthase
in the intestinal mucosa. Rogers and Phang (1985)
showed that the specific activity of this enzyme in the
cat is only about 18 percent of that in the rat and only
about S percent as active per kilogram body weight. A
second factor limiting ornithine synthesis in the small
intestine is the low activity of the enzyme ornithine
amino transferase (Morris, 1985), which is also about 20
percent that of the rat.
The requirement of the kitten for arginine for maxi-
mal growth does not appear to exceed 8.3 g/kg diet (An-
derson et al., 1979a; Costello et al., 1979, 1980~. How-
ever, Costello et al. (1979) showed that at this level of
dietary arginine, urinary arctic acid excretion was ele-
vated, and they suggested that 10.5 g arginine/kg diet
was necessary to normalize both growth and orotic acid
excretion. A value of 10 g of arginine/kg diet is recom-
mended for the minimum requirement.
Histidine
The histidine requirement of the kitten was shown by
Rogers and Morris (1979) to be no greater than 6 g/kg
diet. Anderson et al. (1980a) gave kittens diets contain-
ing 0, 3.0, 6.0, and 9.0 g histidinelkg and on the basis of
growth rate, suggested a requirement of 3 g histidine/kg
diet. Quam et al. (1986) reported that food intake, rates
of body weight gain, and nitrogen retention attained
plateau values at 2.1 g histidine/kg diet. However,
weanling kittens given diets containing either 2.0 or 2.5
g histidine/kg diet later developed bilateral cataracts, a
histidine concentration of 3 g/kg diet was required to
support normal hematological values in young kittens.
A requirement of 3 g histidine/kg diet is therefore rec-
ommended for the minimum requirement of growing
kittens.
Isoleucine
Rogers and Morris (1979) reported that isoleucine was
an essential amino acid for the growing kitten and that a
diet containing 9.0 g isoleucine/kg would support
growth rates similar to those occurring in kittens receiv-
ing a diet containing 18 g isoleucine/kg. Anderson et al.
(1980c) did not observe a significant growth response in
kittens fed levels of isoleucine above 3 g/kg diet.
Hargrove et al. (1984a) measured growth rate, nitro-
gen retention, and plasma amino acid concentrations of
kittens given diets containing various levels of iso-
leucine. Using an asymptotic curve-fitting method,
maximal growth and nitrogen retention occurred at 6.2
and 8.4 g isoleucine/kg diet, respectively. However, kit-
tens given the diet containing 4.6 g isoleucine/kg diet
gained 30 g/day, and the authors suggested the require-
ment may not exceed this level. Kittens given diets con-
tainingsuboptimal levels of isoleucine (less than 3.8 g/kg
diet) had crusts of dried exudate around the eyes. Cul-
tures from the conjunctive of these kittens indicated the
presence of staphylococcal organisms, and the authors
suggested that a deficiency of isoleucine may have in-
duced a lack of membrane integrity or impaired immu-
nity. Clinical signs disappeared when the dietary con-
centration of isoleucine was increased.
OCR for page 11
Nutrient Requirements of Cats Il
J
Hargrove et al. (1984a) also observed that isoleucine
concentration in plasma was not a useful indicator of the
dietary requirement. Moreover, dietary concentrations
of isoleucine did not affect the concentrations of the
other branched-chain amino acids (valine and leucine)
in plasma.
A minimum requirement of 5.0 g isoleucine/kg diet is
recommended for the growing kitten.
Leucine
Rogers and Morris (1979) reported similar growth
rates in kittens receiving purified diets containing either
12 or 24 g leucineIkg diet. Anderson et al. (1980c), on
the basis of feed intake and rate of weight gain, sug-
gested a minimal leucine requirement for growth of 12 g
leucine/kg diet. Hargrove et al. (1984a) reported re-
quirements of 7.8 g and 10.6 g for maximal weight gain
and nitrogen retention respectively, of growing kittens.
However, levels as low as 5 g leucine/kg diet gave gains
and nitrogen retentions two-thirds of maximal. Increas-
ing the dietary concentration of leucine from 5 g to 20 g/
kg diet resulted in a decrease to about one-third in the
concentrations of the other branched-chain amino acids
in plasma. The rate of catabolism of isoleucine and
valine may be a function of the leucine concentration in
the diet.
A dietary concentration of 12.0 g leucine/kg diet is
recommended as the minimum requirement for the
growing kitten.
Lysine
Jansen et al. (1975) demonstrated that the rate of
body weight gain of cats given a diet based on wheat
gluten could be increased by a lysine supplement. Rog-
ers and Morns (1979), using crystalline amino acid di-
ets, showed that lysine was an essential amino acid for
the growing kitten, and the requirement (as lysine HC1)
did not exceed 14 g/kg diet. Anderson et al. (1979a) also
using crystalline amino acid diets indicated that the re-
quirement did not exceed 8 g/kg diet. This dietary con-
centration is in agreement with that found by J. O'Don-
nell, Q. R. Rogers, and I. G. Morris (University of
California, Davis, personal communication, 1985),
who used both gain and nitrogen retention as criteria of
adequacy. A minimum requirement of 8 g lysine/kg diet
is recommended.
Methionine
Early studies on the methionine requirement of the
kitten by Dymsza and Miller (1964) and Rambaut and
Miller (1965, 1967) led these authors to suggest that the
young and adult cat had a very low requirement for
methionine. In 1974, Bitter and Owens reported that
the addition of methionine to a diet based on casein and
gelatin increased the growth rate of cats. They inferred
from these observations that methionine was essential
for the cat and suggested a requirement of 9 g
methionine in the presence of 0.6 g cystine/kg diet (F. N.
Owens, Oklahoma State University, personal commu-
nication, 1985~.
Teeter et al. (1978a), using a purified amino acid diet
containing high concentrations of cystine, taurine, and
sulfate, demonstrated that methionine was an essential
amino acid for the growing kitten and adult cat. In an-
other study, also with amino acid diets, Teeter et al.
(1978b) showed that the methionine requirement of the
kitten in the presence of excess cystine was 4.5 g/kg diet.
When cystine was added to a diet containing 4.5 g
methionine/kg, growth rate plateaued at 4.5 g cystine/
kg diet. These results indicated that cystine may supply
about half the sulfur amino acid requirement of the
growing kitten and that the total sulfur amino acid re-
quirment was 9 g/kg diet, half of which must be
methionine.
The methionine requirement of the growing kitten
given purified amino acid diets was also studied by
Schaeffer et al. (1982a). They reported that in the ab-
sence of cystine, growth rate and nitrogen retention at-
tained maximal values at 7 g and 7.5 g methionine/kg
diet, respectively. In a diet containing adequate cystine
(6.0 g/kg), growth and nitrogen retention plateaued at
3.3 and 3.9 g/kg, added methionine, respectively (Smal-
ley et al., 1983~.
The slightly different estimates of requirements in the
above studies arise from the different increments of
methionine tested by both groups of researchers. Be-
cause Schaeffer et al. (1982a) and Smalley et al. (1983)
used smaller increments than Teeter et al. (197Ba,b),
these values are suggested as the minimum requirements
for growth, i.e., a total methionine plus cystine require-
ment of 7.5 g/kg diet of which 4.0 g/kg must be supplied
as methionine. These requirements for methionine are
based on a diet containing adequate levels of choline (3
g/kg diet). If the diet contains suboptimal levels of cho-
line (or other methyl donors3, the requirement for
methionine will be greater. The D isomer of methionine
is utilized by the cat (Teeter et al., 1978a; K. A. Smalley,
Q. R. Rogers, and J. G. Morris, University of Califor-
nia, Davis, personal communication, 1985~. The latter
authors fed growing kittens diets containing 5.5, 7.0, or
15 g/kg of either the D or the ~ isomer of methionine.
Nitrogen retention values indicated that when
methionine was growth-limiting the efficiency of utili-
zation of D-methionine varied from 73 to 89 percent of
that for Methionine
OCR for page 12
12 Nutrient Requirements of Cats
The calcium salt of D~-OH-methionine appears to be
poorly utilized by the growing kitten given an amino
acid-based diet. When added as a supplement to a soy-
based diet its efficiency of utilization was greater than
with an amino acid diet, but still not equal to ~-
methionine (Teeter et al., 1978a).
The reason for the high-sulfur amino acid require-
ment of the cat, compared to other mammals, e.g., the
dog (Burns and Milner, 1981; Blaza et al., 1982; Hira-
kawa and Baker, 1984), is not readily apparent. The
urine of the cat contains the branched-chain sulfur
amino acid felinine (Datta and Harris, 1951; Westall,
1953), which may be a territorial marker. However, its
synthesis in the male cat should not require more than
0.5 g of methionine or cystine/kg diet (MacDonald et
al., 1984c). Methionine and cystine may act to a limited
extent as precursors for synthesis of the beta sulfonic
amino acid taurine, which is discussed in a later section.
However, the quantity of sulfur amino acids equivalent
to the taurine requirement of the cat does not exceed 0.5
g/kg diet.
Limited data are available on the sulfur amino acid
requirements of the adult cat for maintenance. Studies
of Burger (I. lI. Burger, Pedigree Petfoods, personal
communication, 1985) suggest that the total sulfur
amino acid requirement for maintenance was greater
than 2.4 g, but less than 4.0 g/kg diet. Subsequent work
indicates the requirement to be 3 g total sulfur amino
acids/kg (lies.
Phenylalanine
Rogers and Morris (1979) using crystalline amino acid
diets demonstrated that phenylalanine was an essential
amino acid for the growing kitten and suggested that the
requirement for phenylalanine was not greater than 7.5
g/kg diet when the diet contained 10 g tyrosine/kg diet.
These authors also showed that tyrosine was a dispensa-
ble amino acid.
Anderson et al. (1980a) gave kittens crystalline amino
acid-based diets with varying phenylalanine and tyro-
sine concentrations. On the basis of body weight gain,
they showed that the total aromatic amino acid require-
ment (phenylalanine plus tyrosine) of the kitten dial not
exceed 10 g/kg diet, of which half could be supplied by
tyrosine. Morris and Rogers (1983) determined the re-
quirement for these amino acids in growing kittens. In
the absence of tyrosine, growth rate and nitrogen reten-
tion were maximized at 8.5 g/phenylalanine/kg diet,
whereas when tyrosine was present in the diet in excess
(10 g/kg diet) growth rate and nitrogen retention were
maximized at 3.5 g phenylalanine/kg diet.
A minimum requirement of phenylalanine plus tyro-
sine of 8.5 g/kg diet is recommended for the growing
kitten. Half of this requirement should be provided by
phenylalanine.
Threonine
Rogers and Morris (1979) demonstrated that
threonine was an essential amino acid for the growing
kitten and that the requirement did not exceed 7 g/kg
diet. Anderson et al. (1980c) in two experiments gave
kittens amino acic] diets with varying levels of
threonine. In the first experiment, 8.0, 11.0, and 14.0 g/
kg diet were used, and, in the second experiment, 6.0,
7.0, and 8.0 g/kg were tested. However, significant dif-
ferences were not observed in rates of body weight gain
in either experiment.
Titchenal et al. (1980) gave kittens threonine-imbal-
anced and -deficient diets. They suggested that the re-
quirement was between 7 and 10 g threonine/kg diet.
Near maximal weight gains were observed at 6 g
threonine/kg diet. Kittens fed threonine-deficient diets
grew suboptimally and developed neurological dysfunc-
tions. Clinical signs included ataxia, incoordination,
dysequilibrium, and a defective righting reflex. Carpal
joints were affected, resulting in abnormal conforma-
tion of the forelimbs. Also, reduced flexion and exten-
sion of the hip, stifle, and hock resulted in stilted pelvic
limb movements. Evidence of necrologic dysfunction
appeared as early as the fifth day of ingestion of the im-
balanced diet. The clinical signs and absence of histo-
pathological changes in the carpal joints, peripheral
nerves, spinal cord, or brain suggested that the defi-
ciency of threonine induced cerebellar dysfunction.
A minimum dietary requirement of 7 g threonine/kg
diet is recommended for the growing kitten.
Tryptophan
Rogers and Morris (1979) demonstrated the essential-
ity of tryptophan for the growing kitten and they indi-
cated that the requirement was no greater than 2 g/kg
diet. Anderson et al. (1980a) suggested a requirement of
1 .5 g/kg diet, although kittens in their study grew rather
poorly. Hargrove et al. (1983), on the basis of rate of
body weight gain and nitrogen retention, reported a
minimum requirement of 1.1 g tryptophan/kg diet.
However, Q. R. Rogers and J. G. Morris (University of
California, Davis, personal communication, 1985) have
found that when all the essential amino acids are present
in the diet at their minimum requirements (tryptophan
1.1 g/kg diet) total amino acids provided a protein
equivalent (N x 6.25) of 200 g/kg diet, tryptophan se-
verely limits growth. Therefore, a minimum require-
ment of 1.5 g tryptophan/kg diet is recommended.
. . .
OCR for page 13
Nutnent Requirements of Cats 13
Vatine
Hardy et al. (1977) demonstrated that valine was an
essential amino acid for the growing kitten. Growth rate
and nitrogen retention of kittens given a diet containing
6 g valine/kg was the same as when the diet contained 18
g valine/kg. Anderson et al. (1980c), using a similar
amino acid mixture to that used by Hardy et al. (1977),
also reported a minimum requirement of 6 g valine/kg
diet. P. Wright, J. G. Morris, and Q. R. Rogers (Univer-
sity of California, Davis, personal communication,
1985) found that 4 g valine/kg diet was suboptimal for
kittens given an amino acid diet. However, 6 g valine/kg
diet gave maximal weight gain and nitrogen retention.
A minimum dietary requirement of 6 g valine/kg diet
is recommended for the growth of kittens.
Amino Acid Availabilityfrom the Diet
While the amino acid composition of dietary protein
is a useful index of nutritive value, not all the amino
acids in the ingested food are absorbed. A variable pro-
portion of dietary protein is indigestible, and processing
methods may result in changes in digestibility and struc-
ture of individual amino acids. Processing may enhance
or reduce the nutritive value of proteins. Some raw
plant products contain inhibitors of proteolytic diges-
tion, e.g., soybeans contain trypsin inhibitors, which
are inactivated by cooking, which also enhances digest-
ibility. In contrast, the nutritional value of protein in
the diet may be lowered as a result of heat damage either
to the dietary ingredients in the course of their manufac-
ture as in drying meat meals or during preparation of
the complete diet in the process of extrusion or retorting.
Some of the major types of processing damage that
may occur to proteins are:
1. Excessive heat, especially in the presence of sugars
or oxidized lipids, can induce cross linkage of amino ac-
icis and render proteins resistant to digestion. The avail-
ability of all amino acids in these proteins is decreased.
This type of heat damage is encountered in the manu-
facture of dried animal tissue meals.
2. Mild heat treatment of proteins or free amino ac-
ids in the presence of reducing sugars can reduce the
availability of amino acids. The epsilon amino group of
lysine reacts with the reducing sugar to form compounds
that are resistant to digestion, thereby rendering lysine
unavailable.
3. Exposure of proteins to strong alkali solutions can
result in racemization of -amino acids and formation of
compounds such as lanthionine and lysinoalanine. The
latter is absorbed from the gut and in high concentration
can result in damage to the kidney.
4. Oxidative damage of proteins may occur when
proteins are stored with polyunsaturated lipids. Oxida-
tion products of lipids react with methionine, tryp-
tophan, and histidine reducing their bioavailability.
In the formulation of diets, allowances should be
made for the amino acid composition of the proteins in
the dietary ingredients and the digestibility and avail-
ability of the amino acids in the proteins. For high-qual-
ity natural ingredients a value of 80 to 90 percent avail-
ability is suggested, whereas for low-quality proteins a
value of 60 to 70 percent should be used.
Amino Acid Interactions
Little work has been done on the effect of dispropor-
tionalities among dietary amino acids in the cat. The rat
and cat appear to have similar sensitivities to a dietary
excess of methionine. A methionine concentration of 25
g/kg diet was reported by Fau et al. (1983) to cause ~le-
pres$ion in food intake and growth in kittens. Kittens
were capable of exhibiting some adaptation to diets con-
taining up to 35 g methionine/kg diet. However, Fau et
al. (1984) showed that the cystathionase activity in the
liver of the cat was less than that in the liver of the rat
ant] was probably the limiting step for transsulfuration
in the cat.
Intolerance of growing kittens to glutamic acid in the
diet at 90 g/kg diet or higher has been reported by Deady
et al. (1981a). High concentrations of glutamic acid ap-
peared to increase the requirement of the kitten for thi-
amin. Titchenal et al. (1980) reported that growing kit-
tens given threonine-imbalanced diets had depressed
food intakes and body weight gains compared to kittens
given balanced diets. Threonine-imbalanced or -defi-
cient diets both resulted in the development of neurolog-
ical lesions that were resolved when dietary threonine
was increased.
The growing kitten appears relatively less sensitive to
antagonisms among the branchecI-chain amino acids
than the rat. Hargrove et al. (1984b) was unable to dem-
onstrate a depression of feed intake or body weight gain
resulting from the addition of 100 g branched chain
amino acids/kg diet. From the limited data available, it
appears that the cat may be less sensitive to imbalances
and antagonisms than the rat.
Taurine (Feline Central Retinal Degeneration)
In 1964 Scott et al. reported corneal and retinal le-
sions in cats given a vitamin A-deficient purified diet
based on 350 g casein/kg diet. Supplemental vitamin A
gave remission of the cornea!, but not the retinal lesions.
A similar vitamin-A deficient diet based on meat protein
OCR for page 18
IS Nutnent Requirements of Cats
Based upon results with other species, however, it seems
likely that (a) heme (i.e., from meat sources) iron is well
utilized; (b) iron sulfate may be assimilated twice as effi-
ciently as iron carbonate; and (c) iron oxides have very
little if any iron bioavailability for animals.
Requirements of 80 mg Fe/kg diet and 5 mg Cu/kg
diet are recommended for growing kittens.
iodine
REQUIREMENTS
Iodine (I) serves as a component of the thyroid hor-
mones thyroxine and triiodothyronine, which are in-
volved in the control of the rate of cellular metabolism.
An interaction with calcium metabolism has been de-
scribec] by Scott (1959), Scott and Greaves (1961), and
Roberts and Scott (1961~.
Recommended iodine levels in published literature
range from 1.4 to 4.0 mg/kg dry diet (Scott, 1964~. Data
from other species suggest that the minimum require-
ment would not exceed 350 ~g/kg diet for the kitten.
SIGNS OF DEFICIENCY OR TOXICITY
Although the reported incidence is rare, iodine defi-
ciency has been observed in zoo felids (Ratcliff, 1956;
Fiennes and Graham-Iones, 1960) as well as in domestic
cats (Greaves et al., 1959~. Clinical signs include thyroid
hypertrophy, alopecia, abnormal calcium metabolism,
and death. Further, Scott (1960) reported that iodine
deficiency caused fetal resorption, while estrus and li-
bido were unaffected.
Scott (1964) stated that relatively high doses of iodine
(up to 5 mg I/day) are tolerated by euthyroid cats, but
hypothyroid individuals subjected to these amounts
show toxic signs, which include anorexia, fever, and
weight loss.
It is worth noting that in recent years (first reported in
1980) a substantial number of adult cats, typically be-
tween 6 and 20 years old, have been diagnosed with hy-
perthyroidism and elevated circulating thyroxine and
triiodothyronine levels (see Peterson et al., 1983~.
Whether this is related to a dietary factorks), including
an increase in iodine intake or its metabolism, is pres-
ently unknown and awaits further investigation.
Zzinc
REQUIREMENTS
Zinc (Zn) is found in trace amounts, but is widely dis-
tributed throughout the body. Certain tissues (e.g.,
male reproductive tissue, pancreas, choroid tissue of the
eye) contain relatively high concentrations of zinc, but
tissues such as bones, teeth, and skin account for a far
larger total quantity of zinc in an animal's body. As a
component or activator of numerous body enzymes, it is
important in the metabolism of nucleic acids, carbohy-
drate, protein, and fat. The zinc requirement of wean-
ling kittens fed a soy-based purified diet was found by
Kane et al. (1981c) not to exceed 15 mg Zn/kg diet based
upon growth and lack of gross deficiency signs. Male
kittens, however, showed evidence of impaired testicu-
lar function when fed 15 mg Zn/kg over an 8-month pe-
riod. This suggests that during growth, male kittens
have a higher requirement for zinc than females. Male
kittens fed 67 mg Zn/kg diet showed no evidence of tes-
ticular degeneration.
Kane et al. (1981c) also fed kittens a diet based upon
EDTA-washed soy protein isolate in an attempt to pro-
duce severe zinc deficiency signs. The basal diet in this
study contained only 0.7 mg Zn/kg diet. Although clas-
sic zinc deficiency signs were produced in kittens fed this
diet for 8 weeks, the parakeratosis and other dermal le-
sions were less severe than that which has been observed
previously in zinc-deficient pigs and dogs. Good weight
gains and no zinc deficiency signs were observed in kit-
tens fed the EDTA-treated soy diet containing 52 mg
zinc/kg diet.
Excess dietary calcium when provided in phytate-
containing diets is known to antagonize zinc via forma-
tion of an insoluble Zn-Ca-phytate complex in the gut.
Kane et al. (1981c) added excess calcium (2 percent
added CaHPO4) to their soy protein isolate-based diets
containing 15 mg Zn/kg and still failed to observe either
reduced weight gains or skin lesions. In a preliminary
report, however, Aiken et al. (1978) reported skin le-
sions and reduced growth when a vegetable protein-
based diet containing 40 mg Zn/kg was fed to young kit-
tens. Whether breed differences or some other factor
accounts for the disparity between the Kane et al.
(1981c) and Aiken et al. (1978) results cannot be deter-
mined.
The minimal requirement of zinc for gestation and
lactation has not been determined. A high dietary zinc
requirement (50-100 mg/kg diet) is known for several
species for fetal development. A deficiency causes sev-
eral congenital abnormalities (e.g., cleft palate, hair-
lessness).
Coccidiosis has been shown to increase the zinc re-
quirement of chickens (Southern and Baker, 1983a,b).
Whether a similar effect would occur in coccidial-in-
fected cats remains problematic. Excess dietary cad-
mium has also been shown to exacerbate a zinc defi-
ciency in chicks (Bafundo et al., 1984b), while excess
inorganic lead, iron, or copper ingestion seemed to have
OCR for page 19
Nutrient Requirements of Cats 19
little or no effect on zinc status (Bafundo et al., 1984a,c;
Southern and Baker, 1983b).
A minimum requirement of 15 mg zinc/kg diet is rec-
ommended for kittens fed diets containing a low quan-
tity of compounds known to decrease zinc bioavailabil-
ity, e. g., phytate and fiber, under which conditions 50
mg/kg diet should suffice.
SIGNS OF DEFICIENCY OR TOXICITY
Signs of zinc deficiency include emaciation, para-
keratosis, achromotrichia, testicular dysfunction, gen-
eral debility, and retarded growth. Although zinc toxic-
ity has not been reported in the cat, levels of 2000 mg/kg
or more have been observed to produce iron- or copper-
deficiency anemia in other species (Balundo et al.,
1984a).
Manganese
REQUIREMENTS
Manganese (Mn) is an essential factor for several en-
zymes and is necessary for proper bone formation and
reproduction. Satisfactory performance of kittens has
been obtained by feeding levels of ~ mg/kg dry diet
(Scott, 1960, 1964~. This level is recommended with an
appropriate increase for a diet of higher caloric density
than that fed by Scott (1960, 1964~; that is, 5 mgmanga-
nese/kg diet.
Cobalt
Cobalt (Co) is an integral component of vitamin Bit.
Other functions of cobalt in the tissues have not been
identified. A deficiency of vitamin BY is characterized
by anemia, poor growth, and lack of resistance to infec-
tions. Based on research with other species, there is no
evidence that cobalt is needed when adequate vitamin
BY is present in the diet, and therefore no requirement is
recommended.
Selenium
Selenium (Se) deficiency in cats has not been ob-
served, although it would appear likely from work with
other species that a specific dietary requirement does ex-
ist. Much of the selenium present in common feed ingre-
dients used in cat foods exists as selenomethionine. This
compound provides a readily bioavailable source of sele-
nium, except under conditions of dietary methionine de-
ficiency. Inorganic salts of selenite or selenate are good
sources of selenium. Some fish products are very rich in
selenium. Levels of selenium in excess of 5 mg/kg diet
are toxic for many animal species, but have not been
reported to be toxic to the cat. Based on the requirement
of selenium in other species, a minimal requirement of
100 fig Se/kg diet is recommencled.
Sulfur, Fluorine, Molybdenum, Tin, Silicon, Nickel,
Vanadium, and Chromium
There are no published data on the requirements of
cats for sulfur, fluorine, molybdenum, tin, silicon,
nickel, vanadium, and chromium, although a physio-
logical need for these elements has been demonstrated in
other species.
EFFECT OF ACID-BASE BAI~ANCE ON
NUTRIENT BE QUIREMENTS
The mineral composition of the diet dictates the acid-
base status of the animal. The effects of diet composition
on acid-base balance have generally not been consid-
ered when diets are formulated for cats, and this inat-
tention may be a major factor contributing to the cur-
rent high incidence of feline struvite urolithiasis, which
represents the majority of cases reported under the gen-
eral term FUS (feline urological syndrome) (Fishier,
1955; Carbone, 1965; Rich and Kirk, 1969; Lewis and
Morris, 1983, 1984; Taton et al., 1984a,b; Buffington et
al., 1985~.
Large quantities of acid are normally formed from
carbon dioxide generated during metabolic processes
(Albert) and Cuthbert, 1982~. Pulmonary excretion, the
primary mode of excretion of the carbon dioxide, main-
tains pH homeostasis related to this source of acid. Un-
less metabolic disturbances such as keto- or lactic-acido-
sis occur, no net acid is produced or consumed during
the complete catabolism of neutral lipids and carboby-
drate. The catabolism of phospholipids may affect acid-
base balance, depending on the quantity of phosphate
hydrolyzed and extent of profanation of free phosphate
groups (i.e., pH of the ingested phospholipid). Catabo-
lism of amino acids from proteins to urea, carbon diox-
ide, sulphate, and water generates net acid (acid form-
ing) clue to production of sulfates during oxidation of the
sulfur amino acids (Hunt, 1956~. Carnivores eating
high-protein diets thus produce net amounts of acid
(from sulfur amino acid catabolism), which results in an
acid urine. Excretion of excess acid in the urine restores
proper tissue hydrogen ion and electrolyte concentra-
tions.
In contrast, herbivores ingest largely vegetable mate-
rials, which contain large amounts of potassium and or-
ganic anions. The organic anions are protonated during
catabolism and then oxidized to carbon dioxide and wa-
OCR for page 20
20 Nutrient Requirements of Cats
ter (base forming), leaving an excess of potassium and
base (bicarbonate ion) to be excreted. An alkaline urine
results, and homeostasis is likewise restored.
The influence of dietary mineral composition (ash) on
overall acid-base balance was recognized in the nine-
teenth century by documenting the "acid-forming" ef-
fects of dietary chloride, phosphorus, and sulfur and the
"base-forming" effects of dietary sodium, potassium,
calcium, and magnesium (see Hills, 1973~. Lack of com-
plete absorption of magnesium, calcium, and phos-
phate, however, precludes prediction of urinary pH
from dietary mineral composition. Thus, to fully assess
the net acid-base effect of a given foodstuff, it must be
fed under a standard set of conditions and the net acid
(base) excretion measured (see Camien et al., 1966,
1969; Gonick et al., 1968~.
Homeostatic mechanisms (primarily renal) that en-
able the animal to excrete either acid or base (resulting
in either acidic or alkaline urine) allow regulation of
blood pH over a wide range of net acid or base intake (or
production). If, however, the capability of the animal
to excrete acid or base is exceeded, acidemia or alkale-
mia develops. The medical treatment of acid-base ab-
normalities commonly present in certain diseases is dealt
with in detail in the physiology and medical literature
(Porter and Lawrenson, 1982~. Minimal research has
addressed the question of diet-incluced acidemia and al-
kalemia and their impact on nutrient requirements of
the cat. For example, these conditions influence calcium
and potassium balance.
Acidemic kittens avoid high-protein diets in favor of
low-protein diets (Cook et al., 1985~; avoidance of the
high-protein diet lessens the acid load. Indeed, it has
been shown that when offered a choice, the cat (N.
Cook, Q. R. Rogers, and ] . G. Morris, University of Cal-
ifornia, Davis, personal communication, 1985) and the
rabbit (Hermus et al., 1983) will correct an acid-base
deficit (or excess) by selecting the proper diet.
A major nutritional factor contributing to feline uro-
lithiasis appears to be ingestion of abnormally large
quantities of base-forming elements in the diet, which
result in an alkaline urine. In the normal situation, a
feral cat eats a carnivorous diet ant] produces a urine
with a pH of 6.0 to 7.0. Since the cat evolved as a desert
animal, it has the capacity to produce high urinary con-
centrations of many waste products in order to conserve
water (Schmidt-Nielsen, 1964~. These waste products
include magnesium, ammonium, and phosphate ions
that may crystallize in neutral and alkaline urine to
form struvite uroliths (Fishier, 195S; Carbone, 1965;
Rich and Kirk, 1969; Lewis and Morris, 1983~. Below
6.6, struvite remains largely in solution, while if the uri-
nary pH rises above 7.1, the formation product is ex-
ceeded and crystallization may occur spontaneously.
FUS includes various clinical signs, but is often charac-
terized by dysuria, hematuria, cystitis, and urinary
tract obstruction (Osbaidiston and Taussig, 1970; Os-
borne and Lees, 1978; Lewis and Morris, 1984~. This
term has been used and applied to the domestic cat as a
broad descriptor for urethral obstruction arising not
only from the formation of calculi, but also from the
presence of sabulous and matrix plugs. The common le-
sion in the female is vesicular calculi, while in the male
urethral obstruction by either microcalculi, sabulous
plugs, or matrix plugs is more common (Carbone, 1965;
Rich and Kirk, 1968; Sutor et al., 1970; Jackson and
Colles, 1974~.
The reported incidence of FUS in domestic cats
appears to have increased from a low incidence in
the 1950s to around 0.6 percent of the population in the
mid-1970s (Willeberg, 1984) and 0.85 percent in the
mid-1980s (Lawler et al., 1985~. About 3 to 7 percent
(Willeberg, 1984) or even a higher percent (Reif, 1977)
of cats presented at veterinary clinics are diagnosed as
having FUS.
For several decacles the etiology of FUS has been elu-
sive (Willeberg, 1984~. Numerous potential causative
factors have been suggested, including infection, both
bacterial and viral; alkaline urine; castration; endo-
crine imbalance; high ash level of the diet, high dietary
magnesium, phosphate, and nitrogen; low water in-
take; obesity; dry cat foods; stricter confinement of cats;
less frequent urination, e. g., during rainy weather) (see
extensive reviews by Finco et al., 1975; Greene and
Scott, 1983; Lewis and Morris, 1984; Obsorne et al.,
1984~. There has been great difficulty in attempting to
determine the primary cause and in reproducing experi-
mental results from one laboratory to another.
Environmental changes affecting the cat population
during the last 30 years include more strict confinement
and a greater dependence on commercial foods. Com-
mercial cat foods, especially dry cat foods, contain sig-
nificant amounts of vegetable-based ingredients. Unless
special precautions are taken, vegetable ingredients in
cat foods can result in the production of neutral or
slightly alkaline urine.
Although it has been known for decades that urinary
pH is one factor involved (Vermeulen et al., 1951), dif-
ferences found in urinary pH of affected cats were often
ascribed to urinary stasis or infection rather than to the
mineral composition of the diet. This has resulted in
most experimenters not reporting the urinary pH caused
by the specific diet fed. Most of the dietary effects stud-
ied were in association with diets that produced a uri-
nary pH around neutrality, and with the alkaline tide
the pH of the urine would often reach 7.3 to 8.0 (Lewis
and Morris, 1984; Taton et al., 1984a,b). Under dietary
conditions that produce a urinary pH around neutral-
OCR for page 21
Nutrient Requirements of Cats 21
ity, high dietary magnesium is one factor that contrib-
utes to high incidence of FUS (Jackson, 1972; Rich et al.,
1974; Lewis et al., 1978; Kallfeiz et al., 1980; Lewis and
Morris, 1984~. Lack of recognition of the base-forming
properties of magnesium oxide appears to have resulted
in an inordinate emphasis being focused on magnesium
as an etiologic agent. Recent experiments using magne-
sium chloride as the form of acIded magnesium have
shown that high dietary magnesium does not result in
any signs of FUS if an acid urine is produced (Buffington
et al., 1985~. Uncler conditions in which the urinary pH
is around neutrality, water intake, water and high salt
intake (therefore urinary volume), frequency of urina-
tion, and calcium and phosphate levels may also be im-
portant in decreasing or enhancing crystallization of
struvite in the urinary tract. (See Osborne and Kruger
[1984] for a discussion of initiation and growth of uro-
liths.) Some of these variables, plus others such as infec-
tion and level of ash (depending upon composition),
could also affect urinary pH.
It has been demonstrated that dropping the urinary
pH not only prevents FUS, but also causes formed stones
to dissolve (Taton et al., 1984a,b), ant] since struvite
plugs will form at low dietary magnesium concentra-
tions if the urinary pH is 7.5 or higher (Cook, 1985), the
most important dietary factors in the etiology of FUS
appear to be those that affect urinary phi. The recent
work of Taton et al. (1984a,b) and Buffington et al.
(1985) has therefore re-emphasized the role of urinary
pH on the development of FUS in an animal that has
been evolutionarily adapted to produce acidic urine.
This evidence suggests that special attention should be
given to the mineral composition of cat foods in order to
assure the consistent production of cat urine at a pH be-
low6.6.
A word of caution is appropriate on the possible con-
sequences of chronic acidemia to such a degree that the
urinary pH is kept consistently near 5.5. Chronic acido-
sis mobilizes bone to provide phosphate for hydrogen
ion buffering (Brosnan and Brosnan, 1982~. Steenbock
et al. (1914) described this type of bone dissolution in
pigs and calves, and Jaffe et al. (1932) found in all age
groups of dogs studied that the acidifying effect of am-
monium chloride administration on bone calcium con-
centrations was strongly associated with calcium intake.
That is, dogs receiving adequate calcium showed less
decalcification than those receiving a low-calcium diet.
As might be expected, since calcification of bone is aci
forming, the acidifying effect of ammonium chloride
was more pronounced in younger dogs. More recently,
in rats (Beck and Webster, 1976) and humans (Wach-
man and Bernstein, 1970) metabolic acidosis increased
calcium and phosphate mobilization mediated by an in-
crease in parathyroid hormone activity. Since there is no
experimentally published work on the cat concerning
the effect of chronic aciclemia on bone density or on cal-
cium requirement, the acid-forming constituents in the
diet should be limited to the production of urine at a pal
above the minimal urinary pH obtainable (the average
minimal urinary pH obtainable in cats is about 5.5 tTa-
ton et al., 1984a,b; Buffington et al., 19853~. Long-term
experiments are essential to determine the minimal cal-
cium requirement for maintaining optimal calcium ho-
meostasis in various age groups when feeding diets that
produce urine at a pH between 5.5 and 6.6. While long-
term studies have not been published, it appears that for
minimum FUS risk, the urinary pH shouIcl be less than
6.6.
VITAMINS
Very limited research has been conducted on vitamin
requirements of the cat. Recommendations of quantita-
tive needs are based on both published and unpublished
research with cats and extrapolation from data on other
species. Since several vitamins are rather unstable, and
their destruction may be promoted by light, heat, oxida-
tion, moisture, rancidity, or certain mineral elements,
sufficient amounts should be provided to ensure that the
recommended concentrations will be present when the
diet is consumed. Just as important is recognition that
excessive intake of vitamins A and D may be harmful.
Vitamin A
REQUIREMENTS
Cats require preformed vitamin A in their diet since
they lack the ability to effectively convert ,B-carotene to
vitamin A (Ahmad, 1931; Rea and Drummond, 1932;
Gershoff et al., 1957a). This is true whether ,B-carotene
is presented in the diet or intravenously. Carotenoid
pigments are not normally found in plasma or other tis-
sues.
Lowe et al. (1957) found, and Moore et al. (1963)
confirmed, that the kidney of the cat contains much
higher concentrations of vitamin A than do the kidneys
of other species~cats, >lOOIU/g;hens, >3;dogs, >12;
pigs, 5; rabbits and sheep, 4; cattle and goats, >1. One
retinal equivalent equals 3.3 IU of vitamin A). Never-
theless, liver vitamin A appears to constitute the pri-
mary vitamin A reserve, and liver concentrations tend
to be related more closely to dietary intake than do kid-
ney concentrations. Vitamin A depletion may result in
exhaustion of both liver and kidney levels, but not infre-
quently, some kidney vitamin A is detectable when liver
vitamin A can no longer be measured. When liberal
OCR for page 22
22 Nutrient Requirements of Cats
amounts of vitamin A were included in the diet, liver
vitamin A concentrations (mean of 3,500 IU/g) were
many times those in the kidney (mean of 77 IU/g)
(Moore et al., 1963~.
Scott and Thompson (1969) found that the vitamin A
concentration in the diet of the queen influenced the
concentration of vitamin A in the liver and kidneys of
the unsuckled newborn kitten. However, when the
mother's diet contained adequate vitamin A, suckling
produced a marked increase in liver vitamin A levels as
compared to the effect on kidney levels.
Liver, cod liver oil, and retinyl acetate or palmitate
are satisfactory sources of vitamin A for the cat. Within
limits (1-26 percent fat in the diet), vitamin A absorp-
tion, as estimated by serum vitamin A levels, appears
positively related to dietary fat concentration (Gershoff
et al., 1957a).
Although Scott and Scott (1964) concluded that cats
required 1,600 to 2,000 IU/day, studies designed to de-
fine the vitamin A requirement have not been pub-
lished. Unpublished data (K. Knox, University of Con-
necticut, 1982) suggest that 64 fig of retinol/kg of body
weight daily maintains adequate plasma vitamin A con-
centrations (greater than 40 ~g/61) in weaned kittens.
The next level studied (256 fig retinol/kg body weight)
appeared more than necessary.
In long-term studies (Rogers and Morns, personal
communication, 198S) 4,000 IU (1.2 ma) retinol/kg diet
was not adequate for pregnancy in that several kittens
were born hairless or afflicted with cleft palate. An in-
take of 6,000 IU (1.8 ma) retinol/kg diet prevented de-
formities and provided for normal kitten development
during lactation. From these data one would predict
that 1 mg retinol/kg diet should satisfy the minimum
requirement for growth in kittens, whereas 1.8 mg/kg
should meet the minimum needs [or pregnancy and lac-
tation.
SIGNS OF DEFICIENCY
While Scott et al. (1964) reported conjunctivitis,
xerosis with keratitis and vascularization of the cornea,
photophobia, delay in the papillary response to light,
retinal degeneration, and the formation of cataracts in
cats fed semipurified diets for 6 to 20 months, oral sup-
plements of vitamin A did not prevent all of these le-
sions. These workers concluded that the continuous
feeding of casein interfered with proper utilization of
dietary vitamin A. Morris (1962), feeding a similar diet,
noted that the histological lesions of the retina were
"somewhat similar to, but not quite identical with, the
lesion shown in vitamin A deficiency by other species."
Since neither diet contained taurine, the retinal lesions
presumably were complicated by taurine deficiency
(Rabin et al., 1973; Hayes et al., 1975a,b).
Gershoff et al. (1957a) observed squamous metapla-
sia in the respiratory tract, conjunctive, salivary glands,
and endometrium. Subpleural cysts without apparent
bronchial communication and lined by keratinizing
squamous epithelium were also seen. Extensive infec-
tious sequelae were common in the lung and occasion-
ally in the conjunctive and salivary glands. Local dys-
plasia of pancreatic acinar tissue and marked
hypoplasia of the seminiferous tubules, depletion of ad-
renal cortical lipid, and focal atrophy of the skin were
also observed. Skeletal and neurological lesions were not
demonstrated, due apparently to the failure to induce
the deficiency early enough to retard bone growth.
Bartsch et al. (1975) described ataxia, "star gazing,"
blindness, and intermittent convulsions in African lion
cubs presumed to be vitamin A-deficient. There was se-
vere thickening of the cranium, compression of the
brain, and partial herniation of the cerebellum.
SIGNS OF TOXICITY
Deforming cervical spondylosis in cats has been at-
tributed by Seawright et al. (1967) to prolonged, exces-
sive intake of vitamin A. The naturally occurring disease
is associated with the near-exclusive feeding of raw liver
and milk, and it can be duplicated by large supplements
of vitamin A in a lean beef and milk diet. The levels of
dietary vitamin A supplied by liver, which induced skel-
etal lesions, ranged from 17 to 35 ,ug retinol/g body
weight, while IS ,ug retinol/g body weight added to the
meat diet over 41 weeks produced no effect. The next
higher level of supplemental vitamin A (30,ug retinol/g
body weight) produced lethargy after 10 weeks and
spondylosis after 24 weeks. The primary lesions con-
sisted of an extensive osseocartilagenous hyperplasia
about the first three diarthroidal joints of the cervical
vertebrae. There was also a marked lipid infiltration of
the reticulohistiocytic cells of the liver, lungs, spleen,
and hepatic lymph node and of the tubular epithelium
of the renal cortex. Plasma vitamin A levels ranged from
452 to 1,281 fig retinol/dl in affected cats. Liver and kid-
ney vitamin A concentrations were 15,442 to 39,750 and
100 to 4,083,ug/g, respectively.
In subsequent work, Clark et al. (1970a) verified that
these lesions could be produced by excessive vitamin A,
even when dietary concentrations and the ratio of cal-
cium and phosphorus were optimum. These workers
(Clark, 1970, 1973; Clark et al., 1970b) also found that
abnormalities in long bone morphology could be pro-
duced when kittens were dosed with high levels of vita-
min A at the time of most active bone growth. The long
bones were shorter than normal, osteoporotic, and the
car~tilagenous epiphyseal plates suffered extensive dam-
age, resulting in reduced endochondral bone growth.
Seawright and Hrdlicka (1974) described a proliferative
OCR for page 23
Nutnent Requirements of Cats 23
gingivitis, retarded development of the osseous alveolar
processes, and tooth loss due to excess vitamin A.
Vitamin D
REQUIREMENTS
Vitamin D is involved in the metabolism of calcium
and phosphorous, and probably magnesium. In the rat
and chick it has been shown that cholecalciferol (vita-
min D3) is absorber] in the small intestine, hydroxylated
in the liver to 25-hydroxycholecalciferol and in the kid-
ney to 1,2S-dihydroxycholecalciferol. The latter com-
pound appears to play a significant role in promoting
calcium absorption. Both ergocalciferol (vitamin D2)
and cholecalciferol have been used successfully in the
diet for growth and reproduction of confined cats (R. D.
Kealy, personal communication, 1985~.
Gershoff et al. (1957b) found that 250 IU of cholecal-
cifero} given orally, twice a week, prevented the devel-
opment of rickets in kittens fee] a semipurified diet from
3 to 6 months of age to 21 months of age. The exacerba-
tions and remissions of rickets in unsupplemented cats,
which survived longer than 12 months, suggest that the
vitamin D requirement of older cats is low. The latter
conclusion is supported by the observation that no signs
of deficiency occurred in adult cats fed a vitamin D-free
diet for a year in the absence of sunlight (Rivers et al.,
1979~. For kittens, the minimal requirement should be
provided by 500 IU (12.5 ,ug) of vitamin D per kg of diet.
SIGNS OF DEFICIENCY
Severe rickets in kittens was produced using vitamin
D-deficient diets containing either 1 percent calcium
and 1 percent phosphorus or 2 percent calcium and 0.65
percent phosphorus (Gershoff et al., 1957b). Weight
gain was less with the latter diet, and rickets was less
severe. Serum alkaline phosphatase activity increased
markedly in the third month, peaked during the fifth to
seventh months, and decreased through the twenty-first
month. Serum calcium and inorganic phosphorus con-
centrations decreased markedly cluring the acute phase
of rickets in cats fed 1 percent calcium and 1 percent
phosphorus. The cats that died during acute rickets had
a lower percent femur ash than cats supplemented with
vitamin D. The deficient cats had enlarged costochon-
dral junctions ("rachitic rosary") with disorganization
in the region of new bone formation and excessive os-
teoid.
SIGNS OF TOXICITY
Effects of overdosage of vitamin D were observed at
necropsy in a cat that had been given 5 million IU of
vitamin D3 and 2.5 million IU of vitamin A by mouth
over a 6-month period. The cat received these vitamins
as treatment for a skin ailment, but gradually lost
weight and died suddenly. The great vessels, including
aorta and the carotid arteries, ant] the adrenals were
heavily calcified, and calcium was deposited in the
stomach wall and parathyroids. No increased fragility
of bones was noted (Suter, 1957~.
Vitamin E
REQUIREMENTS
The need for vitamin E in the diet of cats is markedly
influenced by dietary composition. Cordy (1954), Cof-
fin and Ho~zworth (1954), Munson et al. (1958), and
Griffiths et al. (1960) have noted an association of
steatitis (yellow fat disease presumed vitamin E defi-
ciency) with consumption of fish-based diets, particu-
larly red tuna.
Cordy (1954) fed a commercial cat food containing
mostly fish, but including about 10 percent cereal prod-
ucts, to weaned kittens from 6 to 8 weeks of age for 16
weeks. In addition, each cat was given, orally 6 days a
week, 1 ml of fish-liver oil containing 1,500 IU vitamin
A and 200 IU vitamin D. One of the kittens receiving no
supplemental vitamin E died at 30 days. The remaining
animals appeared healthy and were sacrificed after 16
weeks. At necropsy all four unsupplemented kittens and
one of two receiving 10 mg D~-~-tocopherol per day
shower] signs of vitamin E deficiency. The kittens re-
ceiving 20 or 40 mg/day were normal (see below).
Gershoff and Norkin (1962) fed a semipurified diet,
with or without S percent tuna oil, to 3- to 6-month-old
kittens for periods up to 13.5 months. Basal diet compo-
sition (in percent) was: caseinj 32; vitamin E-free lard,
20; sucrose, 42.7; Hegsted salts IV, 4; cod liver oil, 1;
and a vitamin mix. Steatitis was not observed in any of
the cats receiving the basal diet without tuna oil, even in
the absence of vitamin E supplementation. However,
four out of six of these cats exhibited focal interstitial
myocarditis, focal myositis of the skeletal muscle, and
periportal mononuclear infiltration in the liver. When
17 IU of vitamin E (as ma-tocopheryl acetates per kilo-
gram of diet was provided, one out of four cats exhibited
myositis. Supplemental vitamin E at 34 or 68 IU/kg of
diet prevented all lesions. When S percent tuna oil was
substituted for S percent of the lard, steatitis was severe
in cats unsupplemented with vitamin E. The severity of
steatitis was diminished by supplemental vitamin E, but
was not entirely preventer] by 34 IU/kg of diet. When
136 IU/kg of diet were provided, no lesions were seen.
Despite the awareness of the relationship between vita-
min E intake and steatitis, cases in cats still occur occa-
sionally (Gaskell et al., 1975~.
OCR for page 24
24 Nutnent Requirements of Cats
Tocophero! is found in eight isomeric forms (four
tocols, four tocotrienols) in nature, but it is agreed that
a-tocophero} is the biologically important isomer.
Gamma-tocopherol, found in considerable quantity in
soybean oil, has considerably less (only 10 percent) of
the biological activity attributed to a-tocopherol and is
not typically included in the dietary allowance. HPLC
is currently the preferred method of analysis, and,
unlike the original colorimetric assay, it readily dis-
tinguished among isomers (Bier) et al., 1979~. The
minimum requirement for cats is set at 30 mg
cx-tocopherol/kg diet, but it is presumed that a relatively
low-fat diet ~ < 10 percent dry weight) containing anti-
oxidants and adequate selenium would greatly reduce
this requirement. High-PUFA diets, especially those
containing fish oil, may increase the suggested mini-
mum three- to four-fold.
SIGNS OF DEFICIENCY
Steatitis has been noted when sources of highly unsat-
urated fatty acids have been fed in the absence of ade-
quate supplemental vitamin E. The adipose tissue is yel-
low to orange-brown and very firm. Microscopically,
the fat shows focal neutrophilic infiltration with some
mononuclear cells. Acid-fast ceroid pigment is present
as globules and as peripheral rings in the fat cell vacu-
oles.
While gross fat pigmentation was not seen by
Gershoff and Norkin (1962) in cats not fed tuna oil, some
cats unsupplemented with vitamin E exhibited micro-
scopic changes in the subcutaneous adipose tissue. These
consisted of focal cuffing of capillaries and arterioles
with mononuclear cells. Some of the fat cells had fine
yellowish granules in thickened rims of cytoplasm, and
similar granules were seen in some interstitial cells,
probably macrophages or fibroblasts. Also seen were fo-
cal interstitial myocarditis and rarely muscle fiber de-
generation, focal myositis of the skeletal muscle, and
periportal mononuclear infiltration in the liver.
In a preliminary report, Stephan and Hayes (1978)
induced severe vitamin E deficiency with hemolytic
anemia and steatitis by feeding a diet containing IS per-
cent stripped safflower oil without cr-tocopherol. Clini-
cal signs of deficiency were prevented by supplementing
with c`-tocopheryl acetate at 100 IU/kg diet.
Vitamin K
REQUIREMENTS
Presumably the cat, like other higher vertebrates that
have been studied, has a metabolic vitamin K require-
ment for the carboxylation of certain glutamyl residues
of specific proteins such as prothrombin. Neither vita-
min K absorption nor function has been studied in cats.
Reber and Malhotra (1961) found that an irradiated
beef diet, which caused hemorrhages in weanling rats,
did not cause death, loss of weight, or prolonged pro-
thrombin times when fed to cats for 40 weeks. The con-
centration of vitamin K in the diet was calculated to be
60 ~g/kg of solids. Although a minimum requirement
has never been demonstrated for cats, a level of 100 fig/
kg is suggested. In other species, on a weight basis,
menadione is about as effective as phylloquinone in pre-
venting prolongation of clotting time, whereas it may
take several times as much menadione as phyIloquinone
to cure an existing deficiency Cohn W. Suttie, Univer-
sity of Wisconsin, personal communication, 1986~.
SIGNS OF DEFICIENCY
Vitamin K deficiency has not been reported in the
cat, but hypoprothrombinemia and hemorrhage might
be expected.
Thiamin
REQUIREMENTS
Odom and McEachern (1942) produced thiamin defi-
ciency in cats by giving them the same diet that Cowgill
(1921) used to induce thiamin deficiency in dogs. Ever-
ett (1944) provided a detailed account of thiamin defi-
ciency in the cat. He showed that daily injections of 0.5
mg thiamin would prevent neurological disorders and
maintain weight (or produce gains) in adult cats given
an autociaved dog food diet. This diet was supple-
mented with riboflavin, pyridoxine, and calcium pan-
tothenate. Loew et al. (1970) calculated that the thi-
amin requirement for maintenance of a cat weighing
about 3 kg was about 0.36 mg/day or 0.1 mg/50 kcal
ME. Deady et al. (1981a) gave kittens purified amino
acid diets containing 4.4 mg thiaminikg diet. When the
diet contained high levels of glutamic acid (90 followed
by 120 g/kg diet or vice versa), kittens developed severe
neurological signs of thiamin deficiency, which re-
sponded to parenteral thiamin.
A functional inadequacy of thiamin may be induced
either by consumption of a thiamin-deficient diet or by
ingestion of uncooked food containing the enzyme
thiaminase. Some species of fish contain thiaminase
(Smith and Proutt, 1944; Jubb et al., 1956; Loew et al.,
1970~. Carp and saltwater herring, but not perch, cat-
fish, butterfish, or spots, may produce thiamin defi-
ciency. Thiamin is readily destroyed by heat, especially
under neutral or alkaline conditions, and extensive
losses may occur in canned cat foods during processing
OCR for page 25
Nutnent Requirements of Cats 25
and storage (Baggs et al., 1978~. Sufficient thiamin has
to be present in the food before processing to ensure that
adequate amounts are present after processing and rea-
sonable storage.
A requirement of 5 mg thiamin/kg diet is suggested as
the minimal requirement for growth. This concentra-
tion appears adequate for gestation and lactation a G.
Morris and Q. R. Rogers, University of California,
Davis, personal communication, 1985~.
SIGNS OF DEFICIENCY
Everett (1944) described three stages of thiamin defi-
ciency in cats: (1) induction, characterized by anorexia;
(2) critical, characterized by sudden appearance of
neurological disorders, particularly of the postural
mechanisms, and by short tonic convulsive seizures;
(3) terminal, characterized by progressive weakness,
prostration, and death. The anorexia of stage (1) fre-
quently appears within 1 to 2 weeks of ingestion of a
deficient diet and may be accompanied by emesis (Jubb
et al., 1956; Deady et al., 1981a,b). Neurological disor-
ders in the critical stage (2) include impairment of laby-
rinthine righting reactions, as shown by ventroflexion of
the head, loss of righting in the air, and defective con-
scious proprioception. Affected cats, when suspended
by their hind limbs, keep their heads ventroflexed on the
sternum instead of the normal dorsoflexion. In addition,
ventroflexion of the head causes cats to somersault as
they jump from a table Uubb et al., 1956~. The impaired
vestibulolocular reflexes observed include decreased
nystagmus time and an impaired or slow papillary light
reflex. Affected kittens also have dilated pupils.
Electrocardiographic changes due to thiamin defi-
ciency have been described by Toman et al. (1945~.
These included sinus bradycardia, which developed as
early as the second week. Tachycardia was less frequent
and seen later. Disorders in rate regularity and impulse
formation responded promptly to thiamin treatment.
Changes in the ventricular complex (QRS prolongation
and other changes and T wave) were slower to respond.
Cats affected with thiamin deficiency may exhibit
spontaneous seizures, which may be accompanied by
brief periods of tachycardia followed by severe brady-
carclia.
A number of pathological changes of the central ner-
vous system have been described. In acute cases, bilat-
eral symmetrical hemorrhages of the brain in the
periventricular gray matter have been recorded. Con-
siderable variation occurred in the number of nuclear
masses of the brain involved. The main nuclei involved
in order of frequency were: inferior colliculi, medial
vestibular, lateral geniculate, habenular and occulomo-
tor nuclei in the accessory vestibular, cuneate and red
nuclei (Jubb et al., 1956; Deady et al., 1981a,b).
The measurement of erythrocyte transketolase stimu-
lation by thiamin pyrophosphate (Brie and Vincent,
1965) has been used in the diagnosis of thiamin defi-
ciency in the cat (Baggs et al., 1978; Deady et al.,
1981a,b). However, a decrease in the concentration of
thiamin pyrophosphate in the blood of rats has been
shown to precede changes in transketolase activity
(Warnock et al., 1978) and may be a superior test for the
cat. Thiamin and its phosphate esters in tissues may be
conveniently measured by high-performance liquid
chromatography (Ishii et al., 1979~.
Riboflavin
REQUIREMENTS
Microbial synthesis of riboflavin occurs in the gastro-
intestinal tract of a number of animal species. However,
the extent of synthesis appears to depend on the animal
and the type of carbohydrate in the diet. In the cat, the
contribution of symbiotically synthesized riboflavin is
not known. This vitamin loses biological activity when
exposed to light.
Leahy et al. (1967), using 6- to 8-week-old kittens
(about 700 g body weight) and a semipurified diet (con-
taining 35 percent vitamin-free casein, 50 percent su-
crose, 5 percent cellulose, 4 percent peanut oil, and 6
percent minerals (which did not include a source of cop-
per or zinc) and vitamins, concluded that riboflavin re-
quirements for growth did not exceed 100 Gay, or
approximately 1 mg/kg of diet. The authors reported
similar concentrations of riboflavin in the liver and mus-
cle of kittens given the high fecal residue diet with and
without supplemental riboflavin. Intestinal synthesis of
riboflavin by microorganisms may have contributed to
the daily intake of the vitamin and resulted in an artifi-
cially low estimate of the requirement.
Gershoff et al. (1959a) studied the effects of a low-
carbohydrate, high-fat diet (46 percent of the ME from
fat) or a high-carbohydrate, low-fat diet (11 percent of
the ME from fat) on the riboflavin requirements of 3- to
6-month-old kittens. Casein provided 25 percent of the
ME in both diets. The authors concluded that a high-
carbohydrate, low-fat diet favored synthesis of ribofla-
vin by intestinal microorganisms as indicated by greater
urinary and fecal excretion. The high-carbohydrate diet
may also have favored utilization or retention of ribofla-
vin. Although these authors reported that two cats were
maintained in excellent health for more than 34 months
on the high-carbohydrate diet plus 3 mg riboflavin/kg
diet. Cats were routinely reared in their laboratory on
the low-carbohydrate. hi~h-fat diet Dlus 4 mg ribofla-
, ~ ,
OCR for page 26
26 Nutrient Requirements of Cats
vin/kg diet for up to 2 years. A minimal requirement of 4
mg riboflavin/kg diet is suggested for growth.
SIGNS OF DEFICIENCY
Gershoff et al. (1959a) reported that in acute ribofla-
vin deficiency, cats exhibited anorexia, loss of weight,
and periauricular alopecia with epidermal atrophy. In
chronic riboflavin deficiency, cats developed cataracts,
fatty livers, and testicular hypoplasia. Erythrocyte glu-
tathione reductase activity is currently the preferred test
for diagnosis of riboflavin deficiency in man. Factors
affecting the assay are described by Thurnham and Ra-
thakette (1982~.
Vitamin Be
REQUIREMENTS
Carvalho da Silva et al. (1959b), using 3- to 4-month-
old kittens fed a semipurified Juliet, reported that 1 mg of
pyridoxine given orally, three times per week, would
prevent signs of deficiency and would support satisfac-
tory growth and a normal hemogram. Vitamin B6-defi-
cient cats resumed growth and attained normal weights
for age when given oral doses of 1 to 10 mg pyridoxine
per day. One animal given 0.5 mg per day recovered,
but another given 0.25 mg per day did not. Gershoff et
al. (1959b) using 3- to 6-month-old kittens fed a semi-
purified diet, reported that 1 mg of pyridoxine HCl/kg
diet was not adequate for all cats, but a 2 mg pyridoxine
HCl/kg permitted normal growth and hematology.
However, urinary excretion of oxalate was greater in
cats given a diet containing 2 mg pyridoxine/kg than
those receiving a diet containing 4 mg pyridoxine/kg
diet. A minimal requirement of 4 mg pyridoxine/kg diet
is recommended for growing kitten.
SIGNS OF DEFICIENCY
Carvalho da Silva et al. (1959b) reported growth de-
pression, a mild microcytic, hypochromic anemia with
elevated serum iron; convulsive seizures; and irrevers-
ible kidney lesions consisting of areas of tubular atrophy
and dilatation, fibrosis, and intratubular deposits of bi-
refringent crystals in cats receiving a vitamin B6-defi-
cient diet. Tissue pyridoxine levels were 50 percent of
supplemented controls. Gershoff et al. (1959b) reported
similar signs and identified the birefringent crystals as
calcium oxalate monohydrate. He also showed that the
urine of vitamin B6-deficient cats contained large
amounts of oxalate.
Niacin
REQUIREMENTS
The niacin requirement of many animal species can
be satisfied by synthesis of the vitamin from tryptophan.
The cat liver has all the enzymes for niacin synthesis.
However, the rate of removal of an intermediate in the
pathway (alpha-amino-beta-carboxymuconic epsilon
semialdehyde) is so rapid that virtually no niacin is pro-
duced (Suhadolnick et al., 1957; Ikeda et al., 1965~. In
whole animal studies, Carvalho da Silva et al. (1952)
showed that administration of a tryptophan load to cats
did not result in increased urinary nicotinamide excre-
tion. Heath et al. (1940) described lesions of feline pel-
lagra that responded to daily oral doses of 80 to 100 mg
of nicotinic acid. After a few days of treatment with this
level, the daily oral dose was lowered to 30 ma. Car-
valho da Silva (1950) reported that supplementation of a
purified diet (containing all vitamins except vitamin BY
and niacin) with 2.5 mg of nicotinic acid three times a
week produced satisfactory growth, a normal hemo-
gram, and good health for at least 12 months. However,
in a later publication Carvalho da Silva et al. (1952),
when referring to their earlier paper, stated 4 mg of nic-
otinic acid three times a week maintained good health.
In cats made niacin deficient, Carvalho da Silva et al.
(1952) found that periodic subcutaneous injections of 1
to 3 mg of nicotinic acid or nicotinamide produced a
favorable response. They concluded, however, that the
optimum parenteral dose was about 10 ma. In short-
term studies with growing cats weighing 800 to 900 g,
Braham et al. (1962) found that an oral intake of 5 mg of
nicotinic acid per day was adequate as measured by N-
methy} nicotinamide excretion. They also reported that
the cat is able to utilize the niacin from raw and lime-
treated corn to an equal extent. In the absence of further
information, the minimal requirement of 40 mg niacin/
kg diet is suggested.
SIGNS OF DEFICIENCY
Heath et al. (1940) observed weight loss, anorexia,
weakness, and apathy in deficient cats. Thick saliva
with a foul odor drooled from the mouth. The oral cav-
ity was characterized by ulceration of the upper palate,
the tongue was fiery red in color and had an area about 1
cm wide of ulceration and congestion along the anterior
border. Carvalho da Silva et al. (1952) noted unkempt
fur and diarrhea but no buccal lesions. An association
with respiratory diseases was common and contributed
to early death.
Supplemental niacin activity can be provided as ei-
OCR for page 27
Nutnent Requirements of Cats 27
ther niacin or niacinamide. Either source of niacin ac-
tivity is acceptable. Work with the chick has indicated
that niacinamide contains somewhat more niacin activ-
ity per unit weight than niacin (Baker et al., 1976~. No
comparable studies have been done on the cat.
Pantothenic Acid
REQUIREMENTS
Gershoff and Gottlieb (1964) fed 3-month-old kittens
a purified diet (32.1 percent casein, 37.6 percent su-
crose, 12.5 percent corn oil, 12.5 percent hydrogenated
fat, 1.0 percent cod liver oil, and mineral and vitamins).
Based on weight gain, freedom from deficiency signs,
and the efficiency with which p-amino-benzoic acid
was acetylated, these workers concluded that 3 mg of
calcium pantothenate/kg diet was inadequate, but 5 mg
of calcium pantothenate/kg diet was sufficient for the
period of the test (nearly 2 years). A minimum require-
ment of 5 mg of pantothenate/kg diet is suggested. Only
the dextrorotatory form of the vitamin (D-pantothenic
acid) has vitamin activity.
SIGNS OF DEF ICIENCY
The terminal stages of acute pantothenic acid defi-
ciency were observed after 2.0 to 4.5 months in kittens
fed an unsupplemented semipurified diet (Gershoff and
Gottlieb, 1964~. The deficiency state was characterized
chiefly by emaciation. Moderate to marked fatty meta-
morphosis of the liver was noted, with both fine and
coarse vacuolar formation. Giant, blunted villi were
seen in some areas of the jejunum and upper ileum with
the tops of the villi in some animals showing infarct ne-
crosis. No losses or graying of hair and blood dyscrasias
were observed.
Fotacin
REQUIREMENTS
Carvalho da Silva et al. (1955) were not able to in-
duce folacin deficiency in 2- to 3-month-old-kittens
with a purified diet containing no added folic acid or
vitamin B~2 unless 0.6 to 2.0 percent of sulfaguanidine or
sulfathalidine was included. A growth response was ob-
tained in sulfa-treated, deficient kittens with either two
oral doses of 0.8 mg of folic acid administered 24 hours
apart or with one oral dose of 1.0 mg of folic acid. The
latter treatment produced a response that persisted for
about a month.
Amyes et al. (1975) determined the folic acid concen-
trations of cat erythrocytes, plasma, and liver and found
that these values declined from birth to 32 days. How-
ever, no information was presented on the diet of queens
that gave birth to and nursed the kittens.
Thenen and Rasmussen (1978) demonstrated that
weanling kittens fed a purified diet based on casein and
lard without added folacin (diet prov~ded o~y 2 ,ug/kg
BW/day) for 10 weeks developed megaloblastic erythro-
poiesis and marked depletion of plasma and liver folic
acid. Control kittens receiving 1.36 mg total folacin per
kilogram of diet were normal.
In the absence of an experimentally determined value
for the cat, a minimal requirement of 800 ~g/kg diet as
suggested for swine (NRC, 1979) as adjusted for dietary
energy density.
SIGNS OF DEFICIENCY
W>en a deficiency was induced by adding sulfa drugs
to a purified diet, affected cats exhibited weight loss,
anemia (with macrocytic tendencies), and leucopenia.
Blood clotting time was increased, and plasma iron con-
centrations were elevated (Carvalho da Silva et al.,
1955) . Schalm (1974) has described a megaloblastic ane-
mia in an adult cat that responded to vitamin B~2 and
folic acid administration.
Biotin
REQUIREMENTS
Carey and Morris (1975, 1977), using 3-month-old
kittens, fed a purified diet containing 32 percent of a
protein source, 38 percent sucrose, 25 percent animal
and vegetable fat, and minerals and vitamins (except
biotin). When the protein source was vitamin-free ca-
sein, sign-e of biotin deficiency were not seen, even when
the diet contained 2 percent succinyl sulfathiazole to
limit microbial synthesis in the intestine. Replacement
of 58 to 100 percent of the vitamin-free casein with dried
egg white and including 2 percent succinyl sulfathiazole
resulted in deficiency signs that disappeared when 0.25
mg of D-biotin was administered subcutaneously every
other day. Presumably, avidin in the egg white rendered
biotin unavailable. Cats probably do not require a die-
tary source of biotin except under abnormal conditions
(diets containing raw egg white or antimicrobials or if
animals are germ-free). A purified diet containing 60 ~g
biotin/kg supported pregnancy and lactation in queens
and normal growth in kittens (Kang, Morris, and Rog-
ers, personal communication, 1985~. Therefore, with
adjustment for dietary caloric density, a requirement of
70 ,ug/kg diet is recommended.
OCR for page 28
28 Nutnent Requirements of Cats
SIGNS OF DEFICIENCY
Carey and Morris (1975, 1977) produced biotin defi-
ciency by including 18.5 to 32.0 percent egg white in a
purified diet for kittens. Growth was normal to about
150 days, but by this time dried secretions were evident
around the eyes, nose, and at the angle of the mouth.
Also seen were scaly dermatitis of the nasolabial-man-
dibular region, general alopecia, and hypersalivation.
These signs increased in severity and were later accom-
panied by bloody diarrhea and marked anorexia and
emaciation. There was also a decrease in the activity of
hepatic propionyl CoA carboxylase.
Vitamin BE
REQUIREMENTS
A neec] for vitamin BE in a purified diet fed to weaned
kittens has been established (Keesling and Morris, 1975;
Morris, 1977~. However, the quantitative requirement
has not been determined.
A purified diet containing 20 fig vitamin B~2/kg sup-
ported pregnancy and lactation in queens and growth in
kittens. This diet also maintained a normal concentra-
tion of hemoglobin in blood (Kang, Morris, and Rogers,
personal communication, 1985~. A minimal require-
ment of 20 fig vitamin B~2/kg diet is suggested.
SIGNS OF DEFICIENCY
Morris (1977) reported that kittens given a vitamin
B~2-deficient diet at first grew normally for 3 to 4
months, after which growth ceased. Subsequently,
body weight was lost at an accelerating rate until sup-
plementation was initiated with parenteral vitamin BE
which restored weight gain. Hemoglobin, hematocrit,
and bone cytology remained normal, probably because
of high concentrations of folio acid in the diet (10 mg/kg),
which overcame the consequences of folate "trapped" as
methyl folate (Shane and Stokstad, 1985~.
Choline -
REQUIREMENTS
Carvalho da Silva et al. (1959a) reported that a diet
containing 420 g casein and 240 g hydrogenated coconut
fat/kg diet and a supplement of 1 g choline/kg diet pro-
duced some growth in young cats but did not prevent
fatty infiltration of the liver. When the choline was in-
creased to 5 g/kg diet, rate of growth was increased and
fat content of the liver decreased.
Anderson et al. (1979c) used an amino acid-based diet
containing 4.5 g methionine, 4.5 g cystine, 1.0 g
taurine, and 250 g of turkey fat/kg diet. They found that
rate of growth was maximized at 1 g choline/kg diet, but
liver lipid concentration was still elevated. Increasing
the choline to 3 g/kg reduced liver lipids. They also dem-
onstratec] that methionine was an effective methyl do-
nor for the cat. Methionine provided in excess of its die-
tary requirement as an amino acid can totally replace
the dietary need for choline on an iso-methyl basis.
Schaeffer et al. (1982b) investigated the effect of five
dietary concentrations of choline between O and 3 g/kg
diet on rate of body weight gain and liver lipids. The
diet used was based on soy protein and contained 4 g
methionine/kg diet (which approximates the kittens'
minimal requirement), and additional cystine. They
suggested the requirement for maximal growth and
minimal liver lipid was 2.4 g choline/kg diet. This value
has been used as the minimal requirement.
SIGNS OF DEFICIENCY
Decreased food intake and growth rate and increased
lipid content of the liver have been reported (Carvalho
da Silva et al., 1959a; Anderson et al., 1979c; Schaeffer
et al., 1982b). Perilobular infiltration of the liver has
been described by Carvalho da Silva et al. (1959a). Hy-
poalbuminemia was reported by Mansur Guerios and
Hoxter (1962), but was not found by Schaeffer et al.
(1982b).
Ascorbic Acid
Repeated trials have failed to demonstrate a need for
dietary ascorbic acid in cats (Carvalho da Silva, 1950~.
Successful growth and reproduction are routinely ob-
tained with commercial and purified (Kang, Morris,
and Rogers, personal communication, 1985) diets con-
taining no supplemental ascorbic acid.
Representative terms from entire chapter:
purified diet
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