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Ann. Rev. Nutr. 1984.4:521-62

Copyright 1984 by Annual Reviews Inc. All rights reserved.

NUTRITION OF THE

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DOMESTIC CAT, A
MAMMALIAN CARNIVORE
M. L. MacDonald and Q. R. Rogers
Department of Physiological Sciences , School of Veterinary Medicine, University
of California, Davis, California 95616

J. G.

Morris

Departments of Physiological Sciences and Animal Sciences , University of California,

Davis, California 95616

CONTENTS
INTRODUCTION.....................................................................................
EATING AND DRINKING BEHAVIOR ........................................................
Rhythms in the Cat ...............................................................................
Feeding Patterns and Food Intake Regulation . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Water Requirements and Drinking Patterns..................................................

522
524
524
525
528

Carbohydrates.....................................................................................
Lipids ... ......... .. ........ ... ........ . . . ........ .. ... ..... ......... ... . . .. .. ... .. . . . .... ... . ... ..

529
530
532

PROTEIN AND AMINO ACIDS .... . . . .. . .... . . ....... . . .. ...... ..... . . . ... ..... ...... . ..........

533

Protein Requirement..............................................................................
Amino Acid Requirements .......................................................................
Amino Acid Intolerance ..... .......... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

533
535
542

ENERGY REQUIREMENTS .......................................................................

.

MINERALS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
VITAMINS........... .......... ........................................................................
Fat-Soluble Vitamins ..... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Water-Soluble Vitamins..........................................................................

OTHER FOOD CONSTITUENTS ................ .................................................

ESSENTIAL FATTY ACIDS.. .....................................................................

543
545
545
546
547

Metabolism.........................................................................................
EFA Deficiency in Cats. . ... ... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . . .
EFA Requirements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . .

547
547
550
551

SUMMARy................. ...........................................................................

552

1 41

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MacDONALD, ROGERS & MORRIS

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INTRODUCTION
Wild or domesticated carnivores belonging to the family Felidae were kept in a
captive or semidomesticated state by the Egyptians at least 3000 years ago
(264). Despite this long association between humans and carnivores, precise
infonnation on the nutritional requirements of these mammals has been lacking
until relatively recently. This review focuses on unique aspects of the nutrition
of the domestic cat (Felis domesticus), the most thoroughly studied mammalian
carnivore. It is our thesis that the domestic cat is a good model for studying the
peculiarities in the nutrition of carnivores.
The ancestral origin of the domestic cat F. domesticus and the precise date of
its domestication are open to dispute. Resolution of both of these questions is
hampered by the fact that there were relatively few skeletal changes in the cat
after its domestication. The cat may have been domesticated by the Egyptians
as early as 3000 Be, but Zeuner (264) considers the evidence ambiguous. hi any
case, the cat was clearly domesticated and regarded as a sacred animal by 1600
Be. Cats were sacred to the Egyptian goddess Bast of Bubastis and were
regarded as her incarnation (35). According to the Roman historian Diodorus
(circa 100 Be), the Egyptians fed their cats on bread, milk, and slices of Nile
fish, and they called their animals to their meals by special sounds (35). On the
basis of mummified embalmed cat bodies recovered in recent times, the
number of cats kept by the Egyptians must have been prolific . During the latter
part of the nineteenth and early twentieth centuries, mummified cats were
excavated at Bubastis and other places in Egypt and were spread on the land as
fertilizer. They were so numerous that they were also exported; one consign
ment sent to England for fertilizer weighed nineteen tons (170).
The Egyptians collected and kept various recognizable species of cats
including F. chaus, the jungle cat, and F. iybica, the African wild cat.
However, most of the mummified skulls referred to above (170) were found on
examination to be smaller than F. chaus but larger than F. lybica and the
domestic cat. It has been suggested that the present domestic cat may have been
derived from interbreeding of F. silvestrus, the European wild cat, and F.
lybica (202).
In classifying the cat, Carl Linne named the domestic cat F. catus, which he
described as having blotched tabby markings; apparently he neglected or was
oblivious to the equally common mackerel type (202), which came to receive
the designation of F. torquata. Thus, the specific name F. domesticus appears
to be the most appropriate and all-inclusive name to describe the domestic cat.
The Feloidae (Viverrids, Hyaenids , and Felids) diverged from the other
members of the order Carnivora relatively early in their evolutionary develop
ment, i.e . , during the late Eocene to the early Pleistocene . After the Felids
diverged from the Viverrid ancestry, they underwent rapid evolution to fully
specialized forms, which have not changed for millions of years (48).

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FELINE NUTRITION

523

The closest relatives of the Feloidae, the Canoidae (which include Pro
cyonids , Ursids, Ailurides, Canids, and Mustelids) exhibit much greater di
versity than the Feloidae. The Ursids (bears) are well recognized as omnivores.
The molar teeth of the Ursids are elongated, and the enamel of the crowns is
fissured, a characteristic which indicates an omnivorous or herbivorous diet.
The Procyonids, of which the raccoon is a typical member, are also omnivo
rous. The Ailurids , which probably are an offshoot of the Ursids, are repre
sented by the lesser and greater pandas, which are strict herbivores.
In contrast to the Canoidae, all members of the Feloidae are flesh-eaters, i.e.
strict carnivores, so it is clear that the order Carnivora contains mammals with
widely divergent dietary patterns. The order may also provide researchers with
an opportunity to determine whether adherence to a specialized diet during
evolution induced or contributed to changes in metabolic pathways and nutri
tional requirements. One could anticipate that these changes might be ex
pressed in the Feloidae but not in the Canoidae.
A comparison of the nutritional requirements of the cat and the dog as
representative members of the Feloidae and Canoidae supports the thesis that
FELOIDEA

CANOIDEA

' 't:7
Raccoon

RECENT

Bear

Panda
I

Weasel

Genet

Cat

PLIOCENE

MIOCENE

OLIGOCENE

EOCENE

PALEOCENE

Figure 1
210).

The relationship of the cat to other members of the order Carnivora. (After Refs. 165,

524

MacDONALD, ROGERS & MORRIS

specialization consistent with the evolutionary influence of a strict carnivorous

diet has occurred in the cat. Examples of this specialization, which will be
discussed more fully later, are: (a) The cat has limited ability to regulate
catabolic enzymes of amino acid metabolism, which causes the cat to require a
higher level of dietary protein for maintenance than the dog. (b) The cat does
not synthesize niacin from tryptophan because of a very active alternate
degradative pathway. (c) The dog (but not the cat) converts carotene to vitamin
A and may therefore obtain its vitamin A requirement from plants. (d) The dog
(but not the cat) can convert enough linoleic acid to arachidonic acid, and may

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therefore meet its arachidonic acid requirements from plant sources. (e) The
dog can synthesize sufficient taurine from cysteine and can conserve taurine
when limited by using glycine conjugation. The cat has a lower capacity to
synthesize taurine than the dog and is unable to use the alternate glycine
conjugation. Thus, unlike the cat, the dog can meet its taurine requirement
from dietary sulfur amino acids supplied from plant sources. All the above
nutrients that the cat cannot synthesize are found in a carnivorous diet.

EATING AND DRINKING BEHAVIOR

Rhythms

in

the Cat

Many biological variables that exhibit rhythmicity in most mammals (15, 160)
do not appear to do so in the domestic cat (102, 189, 241). The behavior
patterns that do not show daily rhythmicity include feeding and drinking (131,
171,246), activity (102), and sleep-wake (159). Thus, if the domestic cat is
allowed to eat ad libitum, it will eat many (12-20) small meals per day, and
these will be approximately evenly distributed between the light and dark
periods (131,171, 246) . Core body temperature is normally circadian in most
mammals, but it does not appear to vary on a daily basis in the cat (102). This
virtual absence of circadian rhythmicity appears to be a function of the eat's
natural behavior as a predator; circadian rhythmicity is also absent in certain
other felines, such as the bobcat. There is some evidence that these rhythms are
also less rigid in the dog, which is a less strict carnivore than is the cat (160).
The lack of many of the usual circadian rhythms does not mean, however, that
cats have no biological clocks. Instead, it appears that many of their activities
simply are not coupled to their biological clocks. Cats' reproductive cycles
depend upon day length to trigger the female estrus cycle (19, 63) . It has been
shown that the most pronounced estrus in the cat is induced by a period of
extended daylight (more than 12 hours) after a period of short days (19). In
nature this occurs with the change of seasons, which establishes the breeding
season in the late winter and early spring; however, it can be induced in the
laboratory during any season by lighting manipulations (119). Also, cerebro
spinal fluid (CSF) vasopressin concentration varies as a circadian rhythm of

FELINE NUTRITION

525

slightly greater than 24 hours. This rhythm is characterized by high daytime

values and low night values (189).
As in other mammals (190), melatonin concentrations in cat CSF exhibit a
prominent daily rhythm that is characterized by high levels during the dark
period and low levels during the light hours (189). However, the CSF melato

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nin pattern splits into several components as the time in constant light is
increased. The fact that the melatonin rhythm in the cats persisted during
exposure to constant light is somewhat enigmatic, because in most mammals
artificial light of moderate intensity suppresses melatonin production so that no
rhythm exists (190). The splitting of the CSF melatonin into at least two distinct
components during constant light may represent the disassociation of multiple
circadian oscillators normally involved in the generation of this hormone
. rhythm. More work on the circadian rhythms of cats needs to be done to
establish which rhythms are intrinsically linked to feeding behavior and to
establish whether they exert the driving force for the behavioral patterns that
result in their natural predatory behavior.

Feeding Patterns and Food Intake Regulation

The predatory behavior of the cat has been studied and described in great detail
(145). The feral cat (Felis domesticus) eats a wide variety of prey, which varies
seasonally and includes mice, rats, rabbits, birds, lizards, insects; and other
animals (51, 72, 74, 154). Most wild felids (the lion is one exception) are
solitary hunters that rely on craftiness and speed to catch their prey (25, 74,
219). It is easy to see that the caloric content of each of their meals may vary
considerably. Mice are the most common prey for the domestic cat (51, 7 2) ,
and an average mouse consists of about 30 kcal (171) . Thus, the average cat
would require 12 meals of one mouse each per day. It is often thought that
domestic cats would naturally eat large infrequent meals, as do lions (74, 219) .
Grouping all cat families together, researchers usually described the cat
feeding pattern as intermittent or occasional (225) . It has now been shown,
however, that uncaged cats (133) or caged cats fed purified diets (131) or
commercial diets (128, 131, 171, 172) will eat 10-20 times a day if they are
given the food free-choice. As many of these meals will be eaten during the
dark period as will be eaten during the light period ( 131, 172). Normally a
slightly greater quantity of food and a slightly larger number of meals are eaten
during the period when the animals are given fresh food, whether it is light or
dark (131, 172).
It has been shown for both caged (50, 128) and uncaged (133) cats that
the more work a cat must do to obtain a meal, the fewer meals and the larger
the meal size it will eat. This same phenomenon occurs in other species (49,

132).
Adamec (1) showed that predatory behavior takes precedence over con
summatory behavior; cats will stop eating highly palatable food to go kill a rat,

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MacDONALD, ROGERS & MORRIS

even though they will then go back to their initial food rather than eat the rat.
This behavior appears to have the functional value of increasing food input by
providing for multiple kills when the opportunity arises.
Kanarek (128) and Hirsch et al (112) reported that when cat diets were
diluted with celluflour (128) or kaolin (I12) the cats ingested a constant
quantity of food (and therefore fewer calories) rather than ingesting more food
so that they would obtain a constant quantity of calories. Kanarek (128)
concluded that this might be true because cats are carnivores and the caloric
content of their food supply would not vary greatly in nature. She suggested
that cats may therefore regulate their food intake on the basis of bulk rather than
calories. Although both studies considered palatability as a possible factor, it
was dismissed because total food intake did not decrease when there was
increased nondigestible material in the diet. Careful examination of the results
of Hirsch et al (112), however, shows that the cats' food intake decreased on the
ftrst day after they received the higher levels of kaolin more than it did on
subsequent days. Also, food intake was greatly increased the first day after the
cats were returned to the kaolin-free diet, which indicates that palatability
certainly was one factor. Most prey animals contain at least 4. 5 kcallg dry
weight; therefore , the basal diet of dry cat food which contains 3.4 kcal/g dry
weight should be considered already calorically dilute for the cat, which has a
short gastrointestinal tract and therefore a rapid transit time. It is possible that
the total volume of diet ingested was becoming somewhat limiting before the
diets were calorically diluted. Mugford & Thome (172) showed that when cats
are fed isocaloric diets, they decrease their intake of a diet that is low in
palatability by decreasing both meal size and meal frequency. Castonguay (42)
showed that cats compensate effectively for water dilution of the diet by
increasing their intake of the calorically dilute diets . Kane et al (131) used both
purifted and commercial diets of good palatability but with different caloric
contents and showed that cats quickly adjust the quantity of food they ingest to
maintain a quite constant caloric intake. Although there is high variability in
eating patterns among cats and although the cat is more sensitive to the physical
form and taste of its diet than are the rat, dog, and many other animals, the cat
does have mechanisms to control caloric intake . This is consistent with reports
that cats have fewer problems with obesity than dogs when both are given
highly palatable diets (116, 171).
Anand & Brobeck (6) showed that cats that are bilaterally lesioned in the
ventromedial hypothalamus (VMH) become hyperphagic and obese , whereas
those lesioned in the lateral hypothalamus (LH) become aphagic. Other work
ers have shown that lesions in the VMH (233 , 235),periaqueductal gray matter
(234), rhinencephalon (161),and dorsal periaqueductal gray matter (236) result
in hyperphagia in cats. Thus, the neuropathways involved in the control of food
intake in cats appear to be similar to those of other animals. One might expect,

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FELINE NUTRITION

527

however, that some of the metabolic cues would be different in the cat , a
carnivore, than in the rat , an omnivore . Although little is known about metabo
lite mediation of satiety in the cat , it has been shown that low doses of
2-deoxy-o-glucose (50-100 mg/kg body weight) increased short term (1-3
hour) food intake fourfold (213), which suggests that the cat may have glu
costatic, short-term controls of feeding as do other mammals. It appears , in
fact, that lower doses are required to produce this effect in the cat than in other
animals; administration of 2-deoxY-D-glucose at the dose levels used for the rat
(200-750 mg/kg) caused vomiting (213) and produced a soporific effect (121),
which resulted in a decrease in food intake.
Cats respond classically to a learned-aversion paradigm using lithium chlor
ide (171) but appear to be generally neophilic rather than neophobic like the rat.
Cats will eat a novel diet rather than a familiar diet unless they are put in a new
environment or a stressful situation, in which case they will choose the familiar
diet ( 172).
As a carnivore, the cat might be expected to have taste preferences that differ
from those of omnivores and herbivores . Indeed, early smdies indicated that
the cat did not detect (185) or select (40) sweet solutions. Other studies
indicated that cats would select sweet substances only if they were in diluted
milk (82) or in saline solutions (22), because the cat has a negative response to
pure water solutions (22, 82). Although it was reported that saccharin solutions
were selected by cats (263), Bartoshuk et al (23) found that cats rejected both
saccharin and cyclamate solutions. The work by Beauchamp et al (24) supports
the idea that cats are neutral to sugars whether in water or saline. These workers
also found that cats show a preference for sucrose and lactose in a diluted milk
solution, but a mechanism for this phenomenon has not yet been elucidated.
Beauchamp et al (24) confirmed and extended the work of Boudreau and
coworkers (32, 257) by showing that the cat has a positive taste preference for
protein hydrolyzates , meat extracts , and certain free amino acids such as
alanine, proline, lysine, and histidine. This demonstrated the practical signifi
cance of the elegant work of Boudreau and coworkers , who showed that amino
acids that elicit an increase in spike output from geniculate ganglion che
moresponsive group II units were preferred in a preference test, while amino
acids that decreased group II discharge were avoided (32 , 257).
Animal lipids improve the palatability of cat diets ( 128). Acceptance by cats
of diets containing 25% fat derived from different sources was reported (129).
These authors tested bleached tallow versus six alternate fats in a two-choice
test. All cats preferred diets based on bleached tallow to those made with butter
oil or chicken fat. There was a tendency for cats to prefer unbleached tallow and
yellow grease over bleached tallow , but cats showed no preference between
partially hydrogenated vegetable fat and bleached tallow. When purified diets
containing 10 , 25 , and 50% yellow grease were presented to cats , they showed

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MacDONALD, ROGERS & MORRIS

a preference for the diets containing 25% yellow grease over either 10% or 50%
yellow grease. The level of fat in purified diets has a marked effect on texture of
the diet, however, so the cats may have preferred diets containing 25% fat
partly because these diets have a more desirable texture than those containing

10% fat, which are powdery in nature, or those containing 50% fat, which are
greasy (129) . In a subsequent study, these authors found that cats consumed
more of a diet made with 40% bleached tallow than of those made with either 12
or 25% bleached tallow.
Experimental diets based solely on coconut oil as a fat source have been

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found to be aversive to cats. Similarly, diets containing medium-chain tri

glycerides are aversive, and the aversion is stronger for triglycerides with

C8-1O fatty acids than for those with e12 fatty acids. The aversive nature of
these diets may be related to an ability of the cat to detect and avoid low levels
of mdium-chain fatty acids that are normally present in these fats (M. L.
MacDonald, unpublished results).

Water Requirements and Drinking Patterns

The cat is thought to have evolved as a desert animal, in part because it can
concentrate its urine more than the dog or man can (43). This enables the cat to
survive on less water, but the physiologic processes involved may also contrib
ute to the cat's susceptibility to feline urological syndrome (FUS). Even though
the cat is able to overcome a previous water deficit when given sea water to
drink (262),the cat will spontaneously drink considerably less pure water under
the same conditions than the dog will. A dog will accurately replenish a water
deficit up to 8% of its body weight in just a few minutes; the cat will not
immediately make up a water deficit of as little as 4% of its body weight (2) .
Although the minimum water requirement for survival is less for the cat than for
the dog, the weaker thirst drive of the cat results in an ad libitum intake of water
that is often too low to prevent crystallization of struvite in the urine, which
makes the cat particularly susceptible to FUS. Although the actual course of
FUS may differ from case to case, it is clear that increased water intake helps
prevent recurrences. The only effective way to increase the cat's water intake is
to feed a high-protein and/or a high-salt diet or to put water in the diet. Because
a high salt level (4% or more) is needed in the diet to provide a substantial
increase in water intake (13,36,97),the only practical way to increase water
intake is to add water to the food. If fed a normal dry cat food, cats will drink
about 1.5-2.0 ml of water for each gram of dry food (36, 131). This proportion

(2:1) is near the proportion of water in the animals that are prey for carnivores.
Thus, cats need or drink very little water if they are fed other animal tissues and
probably seldom drink if they are fed canned food that is 75-80% water (131) .
Indeed, the most effective way to treat FUS in cats is to feed nothing but canned
cat food, because this increases water intake and thereby increases urine

FELINE NUTRITION

529

volume. A nutritionally complete canned food that contains 85-90% water

should be even more effective in controlling FUS in susceptible cats, although
no such food is currently on the market in the US.
The dog drinks only during the day unless it is dehydrated, but the cat drinks
during both the light and dark periods (131). Although the number of drinking
bouts are about the same as the number of meals eaten, no correlation has been
found between eating and drinking patterns (131) unless the cat was eating only
one or two meals a day (128).

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ENERGY REQUIREMENTS
The mature body size of members of the genus Felis ranges from 5 kg or less for
the black-footed cat (F. nigripes), domestic cat (F. domesticus), and the
African wild cat (e.g. F.lybica) to more than 100 kg for the puma (F. concolor)
(57). Other members of the family Felidae, e.g. lions (Panthera leo) and tigers
(P. tigris), may attain mature body weights in excess of 200 kg. To our
knowledge, there have been so few estimates of energy requirements over this
range of body weights, especially at the upper end, that no generalized rela
tionship between body mass and energy requirements can be made.
Measurements from which estimates of energy requirements can be derived
are available from two sources: short-term measurements of gaseous exchange
and longer-term measurements of food intake and body weight changes.
Theoretically, either approach should give similar values for maintenance
energy requirements, but activity is extremely limited in a respiration chamber
or cage and animals must be acclimated to the chamber before reliable measure
ments can be obtained. Further, most measurements on cats in chambers have
been of fasting (basal) heat production, not of maintenance energy require
ments.
Haldane (96) described a new apparatus for measuring respiratory exchange
in animals and reported data on a single 2.5-kg cat of unspecified age or
physiological state. When the usual thermal equivalent values are applied to the
CO2 production, the calculated heat production was 79 kcallkg body weight/
day.
In 1938, Benedict (30) compiled all measurements on basal heat production
of cats up to that time (38, 191), which yielded a total of 30 individual
measurements from five sources. The regression of basal heat production on
body weight approximated linearity and gave a mean value of 57 kcal/kg body
weight/day for cats with weights ranging from 1. 9-3.7 kg. This mean value is
similar to the heat production value we calculated from the respiratory ex
change data of Carpenter (41) for cats in the postabsorptive state. The mean
SE was 52.2 2.8 kcallkg body weight/day. A somewhat higher value of 66.1
2.8 kcallkg body weight/day was found by E. Kane, J. G. Morris, and Q. R.

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MacDONALD, ROGERS & MORRIS

Rogers (unpublished data). The reason for the latter value being greater than
that reported by Carpenter is not apparent.
All the measurements discussed above refer to fasting (basal) heat produc
tion, which is only one component of maintenance. If these data are to be
applied in a feeding system, the other components of maintenance energy,
activity and heat increment, must be included. The maintenance energy re
quirement is generally on the order of 1.5-2 times the basal heat production. If
the approximation of 1. 5 times basal heat production (58 kcallkg body weight/
day) is taken for the cat, the maintenance energy requirement is 87 kcal/kg body

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weight/day.
Various estimates of the cat's energy requirements based on measurement of
food intake and frequently calculated energy values of foods (usually physio
logical fuel values) have been reported in the literature. Typical values (in
kcallkg body weight/day) are 61-67 (138), 80 (5), 66-88 (168), and 60 (85,
155) for mature cats; 76 for 13-month-old cats (252); 129 for 3.5-month-old
cats (252); and 160 (5) and 250-(85, 155) for kittens. The upper estimates for
mature cats are in reasonable agreement with the value of 87 kcallkg/day
calculated from basal heat production. It is difficult to reconcile the lower
values, which approach basal energy expenditure.
Recently Kendall and coworkers used 143 digestibility trials to calculate the
digestible energy (DE) requirements of six adult cats for maintenance (136).
When energy intake for maintenance was expressed as a mass exponent of
unity, the mean value was 76 kcal/day. When the mass exponents of body
weight (kg) were 0.75 and 0.67, the coefficients were 104 and 114 kcal.
Although no definitive value for maintenance energy requirement can be
derived from the foregoing data, a value of about 80 kcal DE/kg body weight/
day appears reasonable. Compared to other mammals, the difference between
the cat's maintenace and basal heat production (i.e. energy required for activity
and heat increment) appears excessively small. As the cat's heat losses in the
digestion, assimilation, and metabolism of food probably do not differ mate
rially from other mammals, it appears that the activity of the cat used in the
measurements must have been similar under the basal and maintenance condi
tions. Certainly adult cats give the impression of not engaging in unnecessary
exercise, but whether this is an impression or fact remains to be investigated.

Carbohydrates
The milk of the queen contains about 3-5% carbohydrate as lactose, which
accounts for about 20% of the metabolizable energy of its milk (123, 134), so
carbohydrate is a major component of a kitten's diet. However, the adult cat
that consumes only an animal tissue diet ingests little carbohydrate. Morris et al
(167) reported that adult cats efficiently utilized most common isolated car
bohydrates that were added to a meat diet. Apparent digestion coefficients were

FELINE NUTRITION

531

0.88 for raw com starch, 0.87 for lactose, and more than 0.91 for glucose,
sucrose, and dextrin. High concentrations of lactose produced diarrhea in some
cats, presumably because they had inadequate lactase activity. Part of the
disappearance of lactose may have been the result of fermentation in the lower
gut, because the apparent digestibility coefficient of protein was reduced with
lactose. Utilization of starch in the cereal grains, wheat and com, was signifi
cantly greater when these grains were finely ground rather than coarsely
ground; cooking also increased utilization (167). The digestibility coefficients
of partially decomposed potato flour and wood cellulose were measured by

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deWilde & Huysentruyt (67) and found to be 0.95 and 0.31 respectively. The
value for potato flour is in agreement with that previously cited for starch (167),
but the wood product, because of partial hydrolysis, was digested to a greater
extent than unhydrolysed cellulose, which was found to be totally indigestible.
The livers of most omnivorous animals have two enzymes, glucokinase and
hexokinase, that catalyze the phosphorylation of glucose to glucose-6phosphate. Hexokinase has a low Km for glucose, whereas glucokinase has a
high Km and operates only when the liver receives a large 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 (18). Carnivores
with omnivorous dietary habits, e.g. domestic dogs, possess both enzymes, so
it seems likely that they have a greater capacity to handle a high glucose meal
than the cat; however, it does not appear that this has been tested.
In omnivorous animals, maximal gluconeogenesis occurs in the postabsorp
tive state, which occurs some hours after a meal; in carnivores ingesting diets of
animal tissue, maximal gluconeogenesis occurs in the absorptive phase im
mediately following a meal because the capacity to store protein per se is
minimal. The relationships between maximal gluconeogenesis and meals are
similar in carnivores and ruminants; also, gluconeogenesis is more or less
permanently "switched on" in both groups of animals (146, 147, 165). There
may also be differences between cats and omnivores in the relative importance
of various gluconeogenic pathways. Beliveau & Freedland (27) showed that
inhibition of cytosolic phosphoenolpyruvate carboxykinase depressed glu
coneogenesis from serine in rat hepatocytes but not in cat hepatocytes. This
finding suggests that in the cat, serine is converted to glucose by a route that
does not involve pyruvate and the enzyme serine dehydratase. Low activity of
serine dehydratase in the liver of the cat has been reported (209, 214), which
provides support for the notion that there is an alternate pathway to pyruvate
that probably involves hydroxypyruvate. Rowsell et al (214) suggested that
high activity of the first enzyme of this pathway (L-serine-pyruvate aminotrans
ferase) in mammals is associated with diets of animal flesh.
No dietary requirement for carbohydrate has been demonstrated for the cat.
Growing kittens and adult cats at maintenance probably do not require dietary

532

MacDONALD, ROGERS & MORRIS

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carbohydrate if their diets furnish triglycerides and adequate concentrations of

glucogenic amino acids. A need for dietary carbohydrate has been demon
strated in pregnant Beagle bitches given a carbohydrate-free diet containing
26% of energy from protein and 74% from fat (211). Bitches fed this diet
became hypoglycemic at whelping and had depressed concentrations of lactate
and alanine (glucose precursors) in plasma. Puppies from hypoglycemic bitch
es had a low survival rate, which may have been at least in part because of
reduced mothering ability of the dams. Whether the queen requires a source of
dietary glucose under comparable conditions has not been determined.

Lipids
Fat in the diet has three major functions: It provides a concentrated source of
energy, it supplies essential fatty acids, and it serves as a carrier for fat-soluble
vitamins. Fat may also have other roles related to the acceptability of food and
to the provision of sensory (textural and organoleptic) cues for cats.
Dry commercial diets intended for cats usually contain 9-15% crude fat on a
dry-matter basis (129). However, experimental diets ranging from less than 1
to 64% fat in the dry matter have been fed to cats. Similarly, a wide variety of
animal and vegetable fats and oils have been incorporated in experimental diets
(118). Cats have the ability to digest and utilize high levels of dietary fat. Most
of the measurements reported on apparent digestibility of fat by cats have been
derived from measurement of crude fat. Crude fat is the material extracted with
anhydrous diethyl ether; it is represented in cat foods primarily by triglycerides
but can also include other lipid-soluble substances of little or no nutritional
value, such as plant pigments, sterols, and waxes. In expanded or baked cat
foods, not all of the glycerides may be extracted with diethyl ether (34, 113)
unless ether extraction is preceeded by acid hydrolysis (16). Therefore, ether
extraction may not provide adequate measurement of all of the triglyceride in
these diets.
Apparent digestibility coefficients of crude fat in commercial cat foods
marketed in the US have been reported to range from 0.85 to 0.94 (179). These
values are similar to those reported from the United Kingdom for apparent
digestibilities of acid ether extract in commercial cat foods, which were 0.79 in
dry foods, 0.88 in canned foods, and 0.92 in semimoist foods (137). Apparent
digestibility coefficients of crude fat in experimental diets that did not involve
extruding or baking generally have been higher than those reported for com
mercial diets. Mean values of 0.99 for beef and mutton fat (167) and 0.98 for
butter, lard, unbleached and bleached tallows, chicken fat, and yellow grease
have been reported (129). In one study (129), no significant differences were
found between the apparent digestibility coefficients of individual fatty acids
ranging from C12:0 to C18:3 for adult cats.

FELINE NUTRITION

533

PROTEIN AND AMINO ACIDS

One of the most striking aspects of protein and amino acid nutrition is that the
same amino acids are essential for virtually all animal species across the whole
scale of the phylogenetic tree. Our emphasis, however, is on what makes the
cat different or unique in its protein and amino acid nutrition.
The essentiality of the amino acids has been determined in the growing
kitten. As expected, the essential amino acids include arginine, histidine,
lysine, leucine, isoleucine, valine, methionine, threonine, tryptophan, and

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valine (206). Dietary asparagine is required for maximal growth in the early
post-weanling kitten (E. M. Kamikawa, J. G. Morris, Q. R. Rogers, unpub
lished results) but is not necessary after the first few weeks. Taurine is a dietary
essential for the cat in order to prevent central retinal degeneration (CRD), but
because this amino acid is not an a-amino carboxylic acid, is not found in
proteins, and is a metabolite of cysteine, it is discussed in the section on
Sulphur Amino Acids below. From a qualitative point of view then, nothing
appears unique about the essentiality of these amino acids. From a quantitative
viewpoint, however, several interesting differences have been found.

Protein Requirement
An animal's protein requirement normally reflects both its minimal nitrogen
requirement and its essential amino acid requirements. If the amino acid
requirements are known, the researcher can formulate the diet so that even the
lowest level of protein tested meets all the essential amino acid requirements;
under these conditions the minimal protein requirement becomes a measure of
the nitrogen requirement of the animal. Likewise, to determine the essential
amino acid requirements, the nitrogen requirement must be met in all diets so
that the only limiting factor is the amino acid being examined.
The earliest experiments in determining the protein requirements of kittens
and adult cats used foodstuffs (68, 92, 93) or purified components (5,79, 122,

155) and were done without any knowledge of the amino acid requirements.
Under those conditions the protein requirement was shown to be about 30% of
the diet for the growing kitten and about 20% of the diet for the adult cat.
Anderson et aI (9) used amino acid diets in which the amino acid requirements
were met and concluded that 16% of the dietary calories as protein meets the
nitrogen requirement. When the data from the latter study are plotted, there are
no break-points on the curves, so it is not obvious how the authors arrived at
their interpretation. After ensuring that all amino acid requirements were met,
Burger et al (37) estimated the adult cat protein requirement for maintenance to
be about 12% of the diet; K. Smalley, Q. R. Rogers and J. G. Morris
(unpublished results; see also Ref. 208) have estimated the protein requirement

534

MacDONALD, ROGERS & MORRIS

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of growing kittens to be about 18-20% of the diet whether the increments of

nitrogen in the diet were provided by free amino acids or by casein.
All purified diets used recently for determining protein and amino acid
requirements of the cat have had about 4.7 kcallg of diet. Using the above
results and the standard assumption that protein and amino acid requirements
vary directly with the energy content of the diet, we find that adult cats would
require about 10% of dietary energy as protein and growing kittens would
require about 17% of dietary energy as protein. Because cats accept high-fat
diets better than low-fat diets (especially with purified dry diets), the require
ments for protein and amino acids have not yet been determined with low-fat
diets. If comparisons are made of the nitrogen requirements (listed as the
protein requirements in Table 1) of several domestic mammalian species, it is
apparent that they fall into two groups: carnivores and omnivores. Herbivores
would be part of the group of omnivores with respect to protein requirements.
. Nutritionally the dog is a member of the group of omnivores even though it is
a member of the order Carnivora. The cat and other true carnivores have
substantially higher protein requirements than do omnivores. This higher
requirement is primarily an increased requirement for maintenance rather than
for growth. For example, the rat requires three times as much protein for
growth as for maintenance, but the cat requires only 50% more. If one
examines the increased increment for growth as an absolute increase in protein
need above maintenance, the amount is quite similar for cats and rats. The
metabolic reason for the high protein requirement of the cat is the high activity
of the nitrogen catabolic enzymes in cat liver (209). These enzymes are
nonadaptive, so the obligatory nitrogen loss is high even when cats are fed
low-protein diets (207).
Table 1

Protein requirement (% of diet) for adult and. growing animals of several mammalian

species'
Species
Dog
Rat
Man
Cat
Catb
Mink
Fox

Young

12
12

Reference

Adult

4
4.2

14, 90, 124, 13

178
176

29
17

19
10

31
24

20

175

16

1 75

68, 92, 93,

9,37; K.

155, 177

Smalley, Q. R. Rogers &

J. G. Morris, unpublished results

"Ideal protein, i.e. meeting all the known essential amino acid requirements. This may not be true for the data
for the mink and fox.
b
Values expressed as percentage of dietary energy.

FELINE NUTRITION

535

Amino Acid Requirements

A summary of the amino acid requirements of the growing kitten
is presented in Table 2. The arginine requirement is listed as 1.05% of the diet,
the dietary level of arginine required to prevent an increase in orotic aciduria,
which occurs when an arginine-deficient diet is fed (56).
Arginine deficiency causes the most dramatic response to any nutrient
deficiency in the cat. The feeding of a single meal of an arginine-devoid diet
may result in hyperammonemia in less than one hour and causes such severe
hyperammonemia within two to five hours that the cats exhibit severe symp
toms of ammonia intoxication, which include lethargy, emesis, vocalization,
hypersalivation, hyperactivity, hyperesthesia, ataxia, emprosthotonos, ex
tended limbs, and exposed claws. The most severely affected cats show

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ARGININE

Table 2

Current estimate of amino acid requirements of growing kittens

Amino acid

Reference

Requirement

Arginine

1.05b

7,56

Histidine

0.30c

10;

Isoleucine

0 .50

11;

Leucine

1.20

11; D. M.

Lysine

0.80

7;

Methionine (with excess

c ys tine)

0.40

237,245

Methionine + cystine

D. Quam, J. G. Morris, Q. R. Rogers,

unpublished results

D. M. Hargrove, Q. R. Rogers, J. G.
Morris, submitted for publication

Hargrove, Q. R. Rogers, I. G.
Morris, submitted

J. A. O'Donnell, Q. R. Rogers, J. G.
Morris, unpublished results

0.75

217,245

0.40

10;

Phenylalanine + tyrosine

0.90

10;

Threonine

0.70

11,206,247

Tryptophan

0.11

10,99

Valine

0.&

11,98

Phenylalanine (with excess

tyrosine)

J. Williams, Q. R. Rogers, J. G. Morris, unpublished results

J. Williams, Q. R. Rogers, J. G. Morris, unpublished results

aBased on experimental diets containing about 4.7 kcal!g diet. No work has been done to determine whether it
would be valid to express amino acid requirements of kittens as a percentage of a diet based on a standardized 4.0
kcaJ/g diet. Unless otherwise stated, each requirement is based on the minimal quantity of each amino acid
required in the diet to give maximum weight gain and maximum nitrogen retention.
bBased on minimizing orotic acid excretion in the urine. Maximum weight gain is sustained by 0.8-0.9%
arginine in the diet.
"Based on the dietary level of histidine required for the prevention of cataracts after several months. Histidine at
0.25% of the diet is sufficient to maximize nitrogen retention.
"The minimal requirement could be
have not been tested.

0.4 or 0.5% of the diet; increments between 0.3 and 0.6% dietary valine

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536

MacDONALD, ROGERS & MORRIS

hypothermia and bradypnea cyanosis, whiCh are followed by death in a low

percentage of cats (162, 163, 166, 207). This raises the question of why the cat
is so much more sensitive to arginine deficiency than are other mammals, such
as rat or man. Animals are more sensitive to ammonia load when they are in the
postabsorptive state (254), and the administration of arginine greatly decreases
the ammonia intoxication under these conditions (95). The generally accepted
explanation for the prevention of hyperammonemia by arginine is that it acts
anaplerotically to stimulate urea synthesis by providing an intermediate of the
urea cycle, as the intermediates are all depleted during the postabsorptive state.
The reason for the high sensitivity of the cat to arginine deficiency is related to
the metabolism of the urea cycle intermediates. A summary of the differences
between the cat and the rat is shown in Figure 2.
There appear to be at least two reasons for the differences between the
responses of the cat and those of the rat: (a) The cat apparently is less able to
synthesize ornithine and (b) the cat may be less able to provide citrulline to the
kidney for conversion to arginine . Several lines of evidence point to impaired
ornithine synthesis in the cat. Dietary ornithine completely prevents the hyper
arnmonemia of arginine deficiency in cats, although the animals still lose
approximately the same amount of weight as they would if any other essential
amino acid were omitted from the diet (163, 166, 206). Rats, in contrast, will
grow without any dietary arginine, although not maximally; yet the addition of
ornithine to an arginine-free diet does not improve weight gain in rats (156)
or in cats. Stewart et al (242) measured ornithine , citrulline, and arginine in
the livers of cats fed an arginine-free diet. They confirmed that the cats

GLN
+
CIT-GL U
t*
+*
GSA-ORN+
P5C-PRO

SMALL INTESTINE

o
o
o
...J
III

o
o
o
...J
III

LIVER

o
o
o
...J
III

KIDNEY

Metabolism of urea-cycle intennediates in the rat and cat. Enzymes that have been
shown or are presumed to be missing in the cat are marked with an asterisk (*). GLN= glutamine,
GLU= glutamic acid, GSA= glutamic semialdehyde, P5C= pyrroline-5-carboxylate, PRO=
proline, ORN= ornithine, CIT= citrulline, ARG= arginine.

Figure 2

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FELINE NUTRITION

537

showing severe hyperammonemia were the ones that were most severely
depleted of liver ornithine. The concentrations of ornithine in liver were lower
in cats than in rats fed arginine-free meals. However, the authors found no
difference between the cat and the rat in terms of the activity or kinetic
constants of ornithine aminotransferase ( O AT) or in terms of N
acetylglutamate concentrations of liver mitochondria.
The de novo synthesis of ornithine in rats appears to occur primarily in the
intestine. By measuring arterio-venous (A-V) differences across the perfused
rat intestine, Windmueller & Spaeth (259, 260, 261) showed that glutamine
and glutamic acid are converted to ornithine, citrulline, and proline. Herzfeld
& Raper ( 1 09) showed that OAT isolated from rat intestine could be made to act
in the ornithine-forming direction; OAT from rat liver could not. Furthermore,
the intestine has the enzyme glutamic acid reductase, which forms glutamic
acid semialdehyde that can be converted to ornithine and proline ( l08, 2 1 2) .
These authors did not find glutamate reductase i n any other rat tissues ex
amined, including the liver ( l 08, 2 1 2). In contrast, the cat may lack glutamic
acid reductase in both the intestine and the liver. Costello et al (55) have not
been able to detect this enzyme in cat intestine or liver, thus verifying that the
cat cannot make ornithine from glutamate (see Ref. 1 64) .
Citrulline can completely replace arginine in the diet of the cat ( 1 66) as in the
rat, but a higher dietary concentration of citrulline is needed for an equivalent
growth rate (C. Johannsen, Q. R. Rogers, J. G. Morris , unpublished results) .
In the rat, citrulline synthesis occurs primarily in the intestine (26 1); citrulline
released from the intestine reaches the kidney where it is converted to arginine
for use by other tissues (76, 203) . Since citrulline is made from ornithine, a lack
of glutamic acid reductase in cat intestine would preclude citrulline synthesis
from glutamate. The cat may have additional metabolic defects, such as a lack
of ornithine transcarbamylase in the intestine (see Figure 2). These metabolic
defects would also explain why the level of citrulline in cat plasma is normally
quite low (207).
Proline is dispensable for the cat (206), as it is for the rat. In neither the rat
(95) nor the cat (c. A . Buffington, Q. R . Rogers, J . G. Morris, unpublished
results) does proline ameliorate hyperammonemia. Although it might be ex
pected that proline would be converted to ornithine in the liver or kidney, the
kinetic characteristics of OAT in these tissues and the substantial activity of
pyrroline-5-carboxylate dehydrogenase would prevent the synthesis of
ornithine and favor the conversion of pyrroline-5-carboxylate to glutamate if
proline and glutamate were present at physiological levels. The difference

between the cat and the rat is that proline spares at least one half of the dietary
arginine requirement of the rat (204, 205); it does not spare the arginine
requirement of the cat. It seems likely that in the cat, OAT is a constitutive
enzyme like the urea-cycle enzymes (209) , so ornithine degradation would be

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538

MacDONALD, ROGERS & MORRIS

obligatory in the cat and thus would provide a precursor for proline synthesis
whether proline were in the diet or not. In contrast, OAT is adaptive in the rat,
and ornithine catabolism is reduced when rats are fed a low-protein diet
compared to when they are fed a high protein diet (220).
What is the physiological meaning of the differences in arginine metabolism
in the cat? From a teleological standpoint, it is attractive to postulate that as a
strict carnivore , the cat has never had a diet limiting in protein and therefore in
arginine or ornithine but has always had an excess of amino acids, much of
which is needed for gluconeogenesis because animal tissues are low in car
bohydrate. Thus, the metabolic need is not to make ornithine when nitrogen
intake is high, because arginine from dietary protein would provide the
ornithine needed anaplerotically in the urea cycle as well as providing arginine
for protein synthesis; rather, the need is to deplete ornithine during the post
absorptive state so that urea synthesis can be markedly reduced to prevent
excessive catabolism of amino acids to urea. This phenomenon also occurs in
rats , but to a lesser extent. Because the rat is an omnivore , there are times when
it ingests a low-protein diet and adapts by conserving nitrogen, in part via
metabolic adaptations (220); these adaptations , i.e. changes in enzyme activi
ties as a result of dietary compositional changes , appear to be much more
limited in the cat (209) . Work done with the mink ( 1 44) and the ferret (66)
indicates that the eat's arginine metabolism is not unique but is representative
of that of strict carnivores .
HISTIDINE , . LEUCINE, ISOLEUCINE, VALINE, LYSINE, PHENYLALANINE &

TRYOSINE

Nothing unique has been reported about histidine deficiency in the

cat; the usual depletion of hemoglobin has been found, and after long-term
histidine deficiency , cataracts have been found (D. Quam, J. G. Morris, Q. R .
Rogers, unpublished results). Isoleucine and valine requirements are similar in
the cat and rat, but the leucine requirement is somewhat higher for the cat (D.
M. Hargrove, Q. R. Rogers , 1. G. Morris, submitted for publication) . These
workers (unpublished results) recently found that little or no branched-chain
amino acid antagonism occurs in the kitten . That is, 1 0% of any one of the three
branched chain amino acids did not decrease the growth rate of kittens fed a
low-protein diet that was somewhat limiting in each of the branched-chain
amino acids .
The cat and the rat have similar lysine requirements , but as a percentage of
the protein, the requirement for lysine is considerably less for the cat than the
rat because the cat has a higher protein requirement. Lysine is limiting only
when a cereal protein such as wheat gluten is the major dietary protein ( 1 22 ,
207).
The total phenylalanine-plus-tyrosine requirement of the kitten is about
0 . 8-0.9% of the diet. Approximately 60% of that requirement can be met with
tyrosine (Table 2) , which has been shown to be a dispensable amino acid (206).

FELINE NUTRITION

539

The tryptophan requirement of the cat is quantitatively similar to those of

several other species (99). However, there is negligible flow of tryptophan
through the quinolinic acid pathway, and the cat therefore does not synthesize a
significant quantity of niacin (see section on Water-Soluble Vitamins).
There are several unique aspects of sulphur amino
acid nutrition and metabolism in the cat. First, the dietary requirement is
considerably higher for the cat than for most other mammals (Table 2). Second,
the cat excretes a unique, branched-chain sulphur amino acid (felinine) in the
urine. Third, the cat requires a dietary supply of taurine , a l3-amino sulphonic
acid, to prevent central retinal degeneration (CRD).
The reason for the cat ' s high requirement for sulphur amino acids is not
readily apparent, but it has been suggested that it is related to the cat's thick hair
and its need to synthesize felinine. This high sulphur amino acid requirement
results in these amino acids being the most limiting amino acids in most cat
diets. About 19% animal protein is needed in the diet to meet the sulphur amino
acid requirement of the growing kitten. This requirement would just barely be
met in a meat diet containing enough protein to meet the nitrogen requirement
(208). There is not an inordinate quantity of methionine converted to cysteine.
Cystine spares about one half of the methionine requirement in the cat, as in
other species (237, 245). Therefore, part of the higher sulphur amino acid
requirement appears to be for cystine and part of it for methionine per se.
Cysteine is used for felinine synthesis and for the synthesis of hair, and this may
account for part of the increased requirement. Since the cat normally eats a
high-fat diet, perhaps the increased need for phospholipids for absorption and
transport of fat has resulted in an increase in the need for S-adenosyl methionine
for methylation reactions. A high constitutive level of methionine transaminase
would also result in an increased need for dietary methionine. An examination
of the activities of the enzymes in the various pathways should help clarify the
reason for this anomaly.

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SULPHUR AMINO ACIDS

Felinine

The structure of felinine is shown below:

CH3

NH3 +

HO - CH2 - CH2 - C- S - CH2 - CH - COO-

I.

CH3
This branched-chain sulphur amino acid was first reported by Datta & Harris in
1 95 1 (62) and was isolated and characterized by Westall et al in 1 953 (255) .
Because felinine i s not available commercially, very little work has been done
on the effect of diet on the biosynthesis and excretion of felinine . RC1berts

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540

MacDONALD, ROGERS & MORRIS

(20 1 ) , however, examined several aspects of felinine metabolism and reported

that felinine levels were highest in adult male cat urine , quite low in female cat
urine, and undetectable in kittens of either sex. He found an approximately
fourfold variation in felinine excretion among a group of 19 male cats. He also
showed that giving an adult female cat testosterone for one week resulted in an
increase in felinine excretion to normal adult male levels and that the adminis
tration of estradiol to an adult male cat for two weeks had no effect on felinine
excretion. Roberts (20 1 ) and Avizonis & Wriston ( 1 7) both used isotopic
incorporation methods in vivo and found that leucine was a better precursor for
felinine biosynthesis than was mevalonic acid. Using similar techniques,
Roberts failed to get any 35 S incorporated in felinine from either
[35S]methionine or [35 S]cysteine . The site of felinine synthesis is uncertain
because Roberts (20 1 ) found some felinine in both liver and kidney and a
smaller amount in both skin and blood. Wang (25 1 ) also attempted to determine
the source and precursors of felinine. He too was largely unsuccessful in
showing felinine biosynthesis in vitro, but he did find [2- 14C]acetate incor
poration into feline in vivo.
The metabolic role of felinine is a matter for speculation. It may be a urinary
component for territorial marking or perhaps is somhow involved in the
regulation of sterol metabolism (230). It is interesting to note the similarity of
felinine (Equation I , above) and isovalthine:
COO-

NH) +

CH3 - CHrC- S - CH2-CH - COO-

2.

CH3
Isovalthine has been found i n cat urine (83) and i n the urine of hypercholester
olemic patients ( 1 8 1 ) . Little work has been done the past 20 years in this
interesting area of felinine synthesis and function.
The total quantity of dietary sulphur amino acids required to provide for the
synthesis of felinine that is excreted in the urine of a male cat should not exceed
0 .05% of the diet (50-75 mg). Therefore, regardless of the interesting aspects
that are still to be learned about felinine synthesis and function , it is doubtful
that it alone is the reason for the high sulphur amino acid requirement of the cat,
especially the kitten.
Taurine Taurine deficiency in the cat has been shown to cause central retinal
degeneration ( 1 04, lOS) . Taurine is a -amino sulfonic acid (2-amino ethane
sulfonic acid) and as such is not present in protein . It is normally made from
cysteine in the liver and some other tissues, e. g. , brain of mammals. Except

FELINE NUTRITION

54 1

for its conjugation to bile acids (1 00, 250) and its presence in a few peptides
such as the hormone glutarine (gamma-L-glutamyl-taurine) (77 , 84) , taurine
is essentially metabolically inert, i.e. taurine from either endogenous synthe
sis or from dietary intake is not further metabolized and is eventually excreted
as such in the urine. CRD had been reported in cats a number of times (28 ,

29, 1 69, 2 1 5 , 2 1 6, 227) before Hayes and coworkers ( 104, 105) discovered
the nutritional cause of the disease. The discovery of taurine deficiency
as the cause of CRD led Hayes and coworkers (106, 243) to examine its syn
thesis and metabolism in the cat. The effects of feline CRD and the func

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tion of taurine in general have been reviewed several times (20, 103 , 106 ,

243), but there are no published experiments that clearly define the taurine
requirement. Several laboratories have reproduced CRD under laboratory
conditions ( 1 74), so it is clear that the cat needs some taurine in the diet, but
the time required to produce CRD varies from 23 to 52 weeks or longer, and

the incidence of CRD in cats fed taurine-free diets varies from 1 2 to 1 00%
(8, 2 1 , 104) .
Part of the uncertainty about the requirement is caused by unknown dietary
or environmental factors that affect the requirement. For example , CRD has
been found in kittens fed commercial cat foods that contained between 200 and

300 mg of taurine/kg dry weight of diet ( 1 74) , but some laboratories have been
unable to produce lesions in weanling kittens after feeding purified diets
containing no taurine for one year. Q. R. Rogers and J. G. Morris (unpublished
results) examined the importance of type of dietary fat, level of dietary protein,
presence of dietary fiber, and level of dietary sulphur amino acids on the
incidence and severity of CRD in cats. After examining all these factors they
have concluded that only the level of sulphur amino acids affects the outcome
of CRD. When weanling kittens were fed a diet with no taurine and with a level
of sulphur amino acids near the requirement (8; Q. R. Rogers, and J. G. Morris,
unpublished results), all the kittens developed CRD within 5-6 months; when
twice the sulphur amino acid requirement was fed, no CRD was found in 1 2
months. Therefore, i t appears that the reason that kittens fed commercial cat
food containing 200--300 mg of taurine/kg diet have developed CRD is that the
total available sulphur amino acids were near the requirement, although even
when kittens are fed a high level of sulphur amino acids with no dietary taurine,
a low percentage of kittens develop CRD. Thus, the recommendation of the
National Research Council committee (174) that the taurine requirement (when
the sulphur amino acid requirement is just met) is between 250 mg and 1000
mg/kg of dry diet still appears valid. An interpolation of existing data might put
the minimal requirement at approximately 350 mg/kg diet. A more accurate
estimate of the requirement may not be available for some time, because studies
of the lower levels probably should be extended for three to five years before
they can be considered safe.

542

MacDONALD, ROGERS & MORRIS

Although Anderson et al ( 1 1 ) selected the threonine requirement

at 0 . 8% of the diet, a close examination of their results indicates that kittens
grew just as well on 0.7% threonine. Further, Titchenal et al (247) and Rogers
& Morris (206) found maximal weight gain with threonine at 0.7% of the diet
and somewhat less than maximal growth at a dietary level of 0.6% threonine, so
the minimal threonine requirement appears to be about 0.7% of the diet. Kittens
fed inadequate threonine developed neurological problems as early as the fifth
day, even though the kittens were growing (247). Signs included tremor,
ataxia, incoordination, dysequilibrium, and defective righting reflex . Neurolo
gical signs were progressive but completely reversible . All signs indicated
cerebellar dysfunction. In addition to the neurological signs, several kittens
developed thoracic and pelvic limb lameness associated with carpel deviation
and stiff movement of the hind limbs. These kittens seemed reluctant to walk or
run , but no visible pain or discomfort could be induced by vigorous palpation of
the affected limbs and joints . The problems were completely reversed by
feeding an excess of threonine.

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THREONINE

Amino Acid Intolerance

Little has been done to examine the possible effects of high dietary levels of
individual amino acids on cats. It is known that cats are less tolerant to an
excess of glutamic acid than are rats, chickens, and most other species (64).
Although the kitten appears to be able to tolerate 6% glutamic acid in the diet,
9% or 1 2% free glutamic acid results in increases in free glutamate in plasma to
three to ten times normal levels. These high levels of glutamic acid result in
. sporadic emesis and eventually cause classical thiamin deficiency in kittens fed
4.4 mg of thiaminikg diet, a level which is normally adequate ( 1 77). The nature
of the interaction between these two outrients.has oot been completely clar
ified, but it appears that high dietary glutamic acid somewhat increases the
fecal excretion of dietary thiamin (65). In relation to this , it is worth noting that
most animal proteins contain only about half the content of glutamic acid as that
in many plant proteins.
Fau et al (75) recently examined the effect of excess dietary methionine in
weanling kittens. They found a growth depression in kittens fed 2% additional
methionine . With 3% methionine, some cats completely rejected the diet. This
is in contrast to recent experiments in which feeding 10% of the diet as leucine,
isoleucine, or valine had no adverse effect (D. M. Hargrove , Q. R. Rogers, J.
G. Morris, unpublished results) . Thus, the cat appears to be less tolerant than
some other mammals to excesses of some amino acids, such as glutamic acid
and methionine, but more tolerant to excesses of other amino acids such as the
branched-chain amino acids .

FELINE NUTRITION

543

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MINERALS
There is a paucity of data on the cat's qualitative and minimal quantitative
requirements for minerals. Successful growth and reproduction have been
achieved with purified diets containing a mineral mixture similar to that
required by growing rats and pigs (e.g. 1 50, 1 52) . The cat's quantitative
requirements for essential minerals therefore do not greatly exceed those of
these species, and the cat does not have a requirement for any mineral that is not
essential for these species. However, these findings do not preclude the
possibilities of peculiarities in the transport, metabolism, or storage of minerals
by cats and of a lower quantitative requirement for a particular mineral.
When cats consume the whole bodies of their prey , they obtain all necessary
dietary minerals, but when the soft tissues are consumed without the skeleton,
the diet is deficient in calcium. A report of skeletal abnormalities in large felids
in the London Zoo was made by a surgeon of Middlesex Hospital as early as
1 888 (3 1 ) . He reported that "when cubs which early manifest signs of rickets
were promptly fed on bone dust and cod liver oil they made good recoveries . "
Presumably these lions were given an all-meat diet without bones. This
observation is of particular interest as it predates the demonstration by Sir
Edward Mellanby in 1 9 1 9 that rickets could be prevented by cod liver oil. It
took another 70 years before research and clinical reports appeared describing
the effects of all-meat diets on the induction of the disease now referred to as
nutritional secondary hyperparathyroidism (NSHP) in both wild captive and
domestic carnivores (46, 78, 1 07, 1 39, 192, 200, 226) .
The metabolism of calcium and phosphorus in the cat does not appear to
differ markedly from that in other mammals. The frequency of occurrence of
NSHP in cats appears to be the result of the combination of the low calcium
content of animal soft tissues , which are highly palatable to the cat, and the fact
that owners frequently feed animal tissues as the sole diet.
The quantitative requirements of the cat for magnesium have not been
defined, but excessive dietary intakes of magnesium have been shown to
predispose male cats to the formation of urinary calculi composed of struvite
(magnesium ammonium phosphate), which cause subsequent urethral obstruc
tion. Thus it has been suggested that high intakes of magnesium are an
etiological factor in producing FUS (70, 1 27).
The potassium requirement of growing kittens has been shown to be influ
enced by the protein level of the diet ( I l l ). The estimated potassium require
ment of kittens consuming a purified diet based on 33% soy protein was 0.3%,
and for 68% soy protein, 0. 5%. Potassium deficiency was evidenced by
hypokalemia, anorexia, retarded growth , emaciation, lethargy, locomotive
disorders, and unkempt fur.

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MacDONALD, ROGERS & MORRIS

Cats undoubtedly require dietary sources of sodium and chlorine , but quan
titative requirements of these elements have not been experimentally defined.
Salt (sodium chloride) has been used to increase water consumption and hence
urinary output to aid in preventing FUS ( 1 3 , 36, 97) .
The quantitative dietary requirements of the cat for iron have not been
studied, although Spray & Widdowson (239) measured the amount of iron in
the cat at various stages of development. The requirement for copper appears to
be approximately 5 mg/kg diet (69), which is similar to that of other mammals .
Copper deficiency induced i n post-weanling kittens resulted i n a decrease i n the
concentration of copper and Cu-Zn-superoxide dismutase (SOD) in plasma. No
changes were observed in Mn-SOD, packed cell volume, or coat color or
condition in these copper-deficient kittens . However, when the deficiency was
induced by giving pregnant queens a deficient diet (less than 1 mg copper/kg
diet) , histochemical changes in the aortas of neonatal kittens were observed that
indicated connective tissue defects . The latter changes occurred without de
pressions in tissue copper levels. This is in contrast to observations of weanling
kittens given the copper-deficient diet; changes in tissue copper levels were
apparent in this group. It also appears that the hematopoietic system of the adult
cat, in contrast to those of other mammalian species, is resistant to changes
induced by a low copper status.
There have been two reports (4, 1 30) of experimentally induced zinc de
ficiency in the cat. The clinical signs of the deficiency are similar to those
described in other mammals (249); however, while the dermal lesions appear to
be less severe in cats than in species like the pig, a mild deficiency of zinc,
which caused no apparent growth retardation and allowed reproduction in a
female, caused defective spermatogenesis in male cats ( 1 30) . There is no
information on the availability to cats of zinc in natural products or in commer
cial cat foods, but some studies suggest that it may have low availability (4; Q.
R. Rogers, J. G . Morris, unpublished results).
Iodine deficiency has been reported in zoo felines (78, 1 87) and in domestic
cats (94). Clinical signs include hypertrophy of the thyroid, alopecia, abnormal
calcium metabolism, and fetal resorption. An interaction has been reported
between calcium metabolism and iodine (200, 222, 226). Iodine supplementa
tion reduced clinical signs of the deficiency in cats given all-meat or low
calcium diets. It has been stated that euthyroid cats can tolerate relatively high
doses of iodine (223), but over a period of 42 months , one clinic has found
hyperthyroidism in 1 3 1 cats between 6 and 20 years of age ( 1 84). Clinical signs
of hyperthyroidism included polyphagia, increased actiVity, polydipsia,
polyuria, vomiting , and increased base circulating levels of thyroxine and
triiodothyronine. It is not known whether the concentration of iodine in com
mercial cat foods is an etiological factor in producing this disease.

FELINE NUTRITION

545

There are no published studies on the requirements of the cat for manganese,
selenium, chromium, nickel, silicon, vanadium, molybdenum, fluorine, or tin.
These elements have been shown to be essential in other species ( 1 78).

VITAMINS

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Fat-Soluble Vitamins
VITAMIN A
The most unusual aspect of fat-soluble vitamin nutrition in cats is
that preformed vitamin A is a dietary essential . The conversion of carotenes to
retinol, which occurs in the intestinal mucosa in other species including the dog
(9 1 , 1 80) , is negligible in the cat (3, 86) . As a result, neither dietary nor
intravenously administered -carotene can prevent the development of vitamin
A deficiency (86), Because preformed vitamin A is not present in plant lipids ,
the cat requires a source of animal fat (in particular, organ meats) to satisfy its
vitamin A requirement. Coombes has reported that the fox, another carnivore,
may also be unable to utilize carotenoids as a source of vitamin A (52).
There is some information regarding tissue levels of vitamin A in cats . The
kidneys of cats contain approximately ten times as much vitamin A as do the
kidneys of other animals ( 148, 1 58); however, liver stores of vitamin A are
more closely related to dietary status ( 1 58, 224) . The high levels of vitamin A
in cat kidney are not found in other Felidae ( 1 1 0) .
The quantitative requirement of the cat for vitamin A has not been precisely
defined. Scott & Scott (228) concluded that approximately 2000 IV/day were
necessary for normal reproduction. However, other workers (J. G. Morris, Q .
R. Rogers, unpublished results) found that 6000 IV/kg diet met the requirement
for normal reproduction in female cats . Vitamin A toxicity occurs frequently in
cats fed diets consisting largely of raw liver (229) and can be induced in kittens
given supplements of 1 00,000 IV daily for four weeks (44).

Vitamin E deficiency in cats was first observed by Cordy &

Stillinger (54) in kittens fed a canned, fish-based diet. Deficient cats develop
steatitis, in which the depot fat becomes firm and yellow-orange in color. This
painful deposition of ceroid pigment is irreversible and leads to death if not
treated. Cordy (53) showed that the deficiency could be prevented by 20 or 40
mg/day or D,L-a-tocopherol . Almost all naturally occurring cases of vitamin E
deficiency have been in cats fed diets high in fish (especially red tuna) , which
contains large amounts of highly unsaturated fatty acids (47, 1 73). Today, all
cat foods composed of red tuna meat are fortified with vitamin E .
VITAMIN E

Although vitamin D is essental for preventing rickets in kittens

(89), the requirement is probably quite low . When kittens were fed vitamin
VITAMIN D

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546

MacDONALD. ROGERS & MORRIS

D-deficient diets that contained 1 % calcium and 1% phosphorous, only one cat
out of seven was still alive after 21 months (89). When the diet contained 2%
calcium and 0.65% phosphorous, six out of nine cats survived. Rickets de
veloped in vitamin D-deficient cats after 4-5 months, but in those cats that
survived the first 12 months of the study , there were spontaneous remissions. In
these studies, cholecalciferol (250 IU twice a week) prevented rickets. Scott
(224) reported that clinical cases of rickets occur rarely and only in kittens kept
in the dark. Rivers et al ( 197) reported that levels of vitamin D3 in plasma of
vitamin D-deficient kittens shielded from ultraviolet light declined initially but
then tended to increase with age. They reported no signs of bone disease after 9
months. Excess vitamin D3 (2.5 mg/kg diet) caused calcification of soft tissues
( 1 97) , which indicates that large doses of vitamin D are toxic for cats, as they
are for other mammals .
VITAMIN K
The essentiality of vitamin K for cats has not been established.
Reber & Malhotra ( 1 88) observed that an irradiated beef diet, which caused
hemorrhage in weanling rats, did not have adverse effects on cats . The level of
vitamin K was calculated to be 60 jJ.g/kg of solids .

Water-Soluble Vitamins
In omnivores, the requirement for niacin can be met by dietary tryptophan. The
pathway of tryptophan metabolism in liver has a branch point at a-amino-f3carboxymuconic-E-semialdehyde , and this intermediate can be converted
either to quinolinic acid, which is then metabolized to niacin, or to picolinic
acid. In most mammals, the activity of picolinate carboxylase is quite high, so
most tryptophan is diverted away from the niacin-synthesizing pathway. The
activity of picolinate carboxylase in cats is 30-50 times higher than in rats, so
there is almost no synthesis of niacin ( 1 20, 244) . Cats or kittens fed a diet
lacking niacin develop signs of deficiency that cannot be reversed by the
administration of additional tryptophan (61). DaSilva et al (6 1 ) found that when
tryptophan was administered orally or subcutaneously in doses of up to 600
mg/day , there was no significant increase in urinary N-methylnicotinamide
excretion. Leklem et al ( 143) gave higher doses of tryptophan ( 1 g/kg body
weight/day) or kynurenine (0.25 g/kg body weight/day) and found a slight
increase in N-methylnicotinamide excretion, but the increase was only approx
imately 3% of that seen in rats. These authors also showed that less than I % of a
dose of L-[14C]tryptophan could be recovered as niacin metabolites in cat urine
(142). There appear to be other peculiarities in tryptophan metabolism in cats,
in that 80% of the radioactivity in urine of cats given labelled tryptophan could
not be identified as any of the known tryptophan metabolites.
The efficiency of conversion of tryptophan to niacin varies widely among
species: it is greatest in rats, less so in humans , and negligible in cats . Poston

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FELINE NUTRITION

547

& Combs ( 1 86) reported that picolinate carboxylase activity is even higher in
trout and salmon than in cats. Despite the fact that cats do not convert
tryptophan to niacin, their requirement for niacin does not appear to exceed that
of other species; however, the cat depends on animal tissues as a source of
niacin, because nicotinarnides are present in lower quantities in plant tissues.
The cat requires thiamin (73), riboflavin ( 14 1 ) , pantothenic acid (88) ,
pyridoxine (87), biotin (39), folacin (60), and vitamin B 1 2 ( 1 35), Ascorbic acid
is synthesized in adequate amounts and is not a dietary essential (59). Vitamin
B 12 is low in diets of vegetable origin, and an all-vegetable diet would
necessitate supplementation with this vitamin ( 1 35). Deficiencies of some
vitamins occur with relative frequency: thiamin deficiency is easily produced
by feeding fish products (especially carp and herring) in which the thiaminase
has not been destroyed (238).
Choline is required by kittens when the level of dietary methionine is just
enough to meet the methionine requirement (21 8) . There is evidence that the
choline requirement of the kitten, as of other species, can be met in part by
excess dietary methionine ( 1 2) , but it is not known whether dietary choline is
completely dispensable. There are reports that inositol is required by cats
(224), but this has not been investigated thoroughly.

OTHER FOOD CONSTITUENTS

Benzoic acid, a food preservative, is extremely toxic to cats. Bedford & Clarke
(26) showed that doses of benzoic acid in excess of 0.45 g/kg body weight led to
hyperesthesia, muscular tremors, depression, and often, death. In many spe
cies, benzoic acid is detoxified with glycine to form hippuric acid and with
glucuronic acid (258). Cats are able to form glycine conjugates but they have
low levels of glucuronyl transferase in liver (7 1 ) . This may also explain the
toxicity and slow metabolism of many drugs by cats (33 , 253). Cats excrete
unusual conjugates in which quinoline-2-carboxylic acid, a typical aromatic
acid, is combined with glycyltaurine or glycylglycine ( 1 25 , 1 26) . The signifi
cance of these reactions is not known.
ESSENTIAL. FAITY ACIDS

Metabolism
LACK OF 6 DESATURATION
The essential fatty acid (EFA) requirements of
most mammals can be met entirely by linoleate. In the liver, linoleate is
converted to arachidonate by alternating desaturation and elongation (Figure
3). The first indication that this scheme might be different in cats came in 1975,
when Rivers, Sinclair & Crawford (199) reported that cats fed purified diets
containing linoleate but lacking arachidonate had extremely low levels of

548

MacDONALD, ROGERS & MORRIS

n6 FATTY AC I DS

Figure 3

1 8 : 2 - 1 8 : 3 - 20 : 3 - 20 : 4 - 2 2 : 4 - 2 2 : 5
L I N OLEATE
ARACH 1 DONATE

5
20 : 2 - 5 , 1 1 , 1 4 - 20 : 3

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Pathways of linoleate metabolism in mammals. In the liver of the cat there is almost no
A6-desaturase activity, so arachidonate is a dietary essential. E= elongation, A= desaturation.

arachidonate in plasma lipids. The authors suggested that cats were unable to
synthesize arachidonate from linoleate. They also predicted that the cat would
require arachidonate in the diet.
Hassam et al (101) showed that the enzyme defect was at the Ll6-desaturase,
the fITst step in the conversion. In cats given injections of [1- 14C]linoleate, very
little radioactivity was incorporated into arachidonate. Sinclair et al (231)
confrrmed these results and showed that less than 0 . 5% of the radioactivity
from e4C]linoleate recovered from liver lipids was associated with fatty acids
having four double bonds.
Most of the information about EFA metabolism in cats has been obtained by
studying the effects of different diets on the fatty acid compositions of blood
and tissue lipids. When cats are fed purified diets containing safflower seed oil
as the only source of fat, the level of arachidonate in blood lipids decreases with
time (80). At the same time, linoleate comprises nearly 50% of the fatty acids in
plasma lipids (150, 199, 231).
In cats fed a diet low in linoleate, the level of linoleate in plasma and
erythrocytes decreases with time and levels of n7 and n9 fatty acids (16: In7 ,
18:1n9, 20 :1n9 , and 20:3n9) increase (150). These fatty acids are synthesized
de novo in liver, and an increase in their concentration is a sign of EFA
deficiency ( 1 14). Although the amount of 20:3n9 synthesized in linoleate
deficient cats is very small compared to rats , for example, the synthesis of
20:3n9 from 18:1n9 suggested that the cat might be able to synthesize some
arachidonate from linoleate, because the same enzymes are responsible for both
conversions. Therefore, Sinclair et al (232) suggested that dietary linoleate
could provide arachidonate in cats, whereas Rivers & Frankel (196) concluded
that the amount of arachidonate that could be synthesized would be insignifi
cant.
If linoleate were converted to arachidonate, the inclusion of a source of
linoleate in an otherwise EFA-deficient diet would result in increased levels of
arachidonate in cat tissues. However, examination of the fatty acid composi
tions of plasma, erythrocyte and liver lipids of cats fed diets with or without
safflower seed oil showed that there was no net increase in arachidonate when
safflower seed oil was included in the diet (150). Thus, it appears that the

FELINE NUTRITION

549

activity of the a6-desaturase is so low as to be nearly saturated with substrate

even in linoleate deficiency, so there is negligible synthesis of arachidonate in
cat liver.
This conversion, however, may occur in cat testes. Levels of arachido
nate and longer-chain n-6 fatty acids are higher in testes lipids of cats fed a
diet containing linoleate than in those fed a linoleate-deficient diet ( 152). How
ever, the arachidonate in testes is apparently not released into the blood
stream .
Sinclair and coworkers (23 1 ) showed that a A5desaturase is present in cat liver. They injected cats with 20:3n6 labelled with
14C in the 2-position and found radioactivity in liver arachidonate. This indi
cated that 20:3n6 could be converted to arachidonate.
The presence of a A5-desaturase results in the appearance of 5, 1 1 , 14--2 0:3 in
the tissues of cats fed diets containing linoleate (23 1 ; see Figure 3). Levels of
20:2n6 and 5 , 1 1 , 14--20:3 in blood increase as the level of linoleate increases
( 149, 1 50) . Although other mammals can also synthesize 5, 1 1 , 14--20:3 (248) ,
this fatty acid usually is not detectable in animal tissues. In human erythrocyte
lipids, the level is only 0. 1 % of total fatty acids (M. L . MacDonald, unpub
lished results); in cat erythrocyte lipids, the level is almost 3% ( 1 50). The
synthesis of relatively high amounts of 5 , 1 1, 14--20:3 by cats probably results
from the extremely low activity of the A6-desaturase, which allows linoleate to
accumulate and to be shunted toward 5 , 1 1 , 14--20:3.
Sinclair (23 1 , 232) suggested that the cat might be able to synthesize
arachidonate by A8-desaturation of 20:2n6 ( 1 1 , 14-20:2) to form 20:3n6 (8,
1 1 , 14--20:3), but since there is negligible synthesis of arachidonate by any
route, both the A8- and A6-desaturases apparently have extremely low activi
ties in cat liver.
The presence of a functional elongase and A5-desaturase (23 1) means that
1 8:3n6 should be a useful precursor of arachidonate. Frankel & Rivers (81)
used evening primrose oil, which contains 18:3n6, to supplement cats that had
previously been fed a diet containing 25% safflower seed oil as the only source
offat. After five days, there were increases in the levels of 18: 3n6 and 20: 3n6 in
plasma phosphatidylcholine, but levels of 20:4n6 were unchanged. At that
time, the authors concluded that cats lack a A5-desaturase and were unable to
convert 20:3n6 to 20:4n6. However, later studies by Frankel (80) showed that
the level of arachidonate in plasma lipids increased only after evening primrose
oil was fed for 10 weeks or more. Sinclair et al (23 1) showed that when the
methyl ester of 18:3n6 was fed to cats, the levels of 20:3n6 and 20:4n6 in
erythrocyte lipids increased, which is consistent with the A5-desaturation of
20:3n6.

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.15-DESATURATION

550

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EFA

MacDONALD, ROGERS & MORRIS

Deficiency in Cats

ARACHIDONATE DEFICIENCY
Rivers and coworkers ( 193, 194, 1 95 , 1 99)
reported signs of EFA deficiency in cats fed a diet high in linoleate but lacking
in arachidonate. The deficiency signs included poor growth, "staring" fur, skin
lesions around the mouth and on the hocks, slow wound healing, fatty liver,
increased susceptibility to infections, poor reproductive performance, underde
veloped testes , and cleft palates and other defects in kittens born to deficient
dams. Later, Frankel (80) showed that growth was not abnormal as long as
respiratory infections were prevented.
These early studies were done without the benefit of more recent knowledge
of the nutritional requirements of cats. The diets used by Rivers et al ( 1 99)
lacked taurine and a-tocopherol. Stephan & Hayes (240) suggested that the
deficiency signs could have resulted from vitamin E deficiency. The deficien
cies of taurine and vitamin E were corrected in later studies ( 1 95), but levels of
other nutrients may have been marginal. Examination of the diets they used
( 195), showed that level of zinc in the mineral mix was only 25% of the NRC
requirement ( 1 77); the diets also lacked several other trace elements . Since
many signs of zinc deficiency are similar to those described above e.g. poor
wound healing, perioral skin lesions, reproductive failure, and cleft palate
( 1 30; E. Kane, Q. R. Rogers, 1 . G. Morris , unpublished results), it was
difficult to determine which signs were attributable to arachidonate deficiency
alone. Although supplementation with evening primrose oil resulted in arachi
donate synthesis and caused female cats to come into estrus (81), reproductive
performance was not improved (80), which suggests that there may have been a
deficiency of another nutrient.
MacDonald et al ( 1 5 1 , 1 52) also found that cats fed diets containing linoleate
(5% safflower seed oil) but lacking arachidonate become arachidonate
deficient. Platelet aggregation was impaired in arachidonate-deficient cats, and
there was occasional thrombocytopenia ( 1 5 1 ) . Female cats had few litters;
kittens were born dead and underdeveloped ( 1 52), but there were no apparent
birth defects. When the same cats were supplemented orally with ethyl arachi
donate, reproductive performance improved greatly; kitten survival increased
from 0 to 75% . In cats fed a purified diet with animal fat added to provide
arachidonate at 0.04% of dietary kilocalories, reproduction was essentially
normal. When other diets containing as little as 0 . 0 1 % of kilocalories as
arachidonate were used, reproductive performance was not always completely
normal but was better than it was when arachidonate was absent. Reproductive
failure in females is therefore an extremely sensitive index of arachidonate
deficiency, and the arachidonate requirement for normal reproduction appears
to be very low ( 1 52).

FELINE NUTRITION

55 1

Because there is negligible synthesis of arachidon

ate from linoleate in cat liver, the cat is a useful model for studying the specific
physiological roles of these two fatty acids . Levels of linoleate can be altered
without changing levels of arachidonate in tissues. The results of studies by
Frankel & Rivers (8 1 ) led them to conclude that "18:2n6 Iacks EFA activity in
the cat, and that the syndrome encountered was a dietary deficiency in some or
all of the derived EFA." They noticed that the condition of the skin and coat was
worse in cats fed diets containing hydrogenated coconut oil (lacking linoleate)
than in those fed diets containing safflower seed oil (high in linoleate); howev
er, they attributed this to accentuation of arachidonate deficiency by the
saturated fatty acids in the coconut oil ( 1 94) .
Sinclair et al (232) reported that cats fed a diet containing saturated beef fat
developed signs of EFA deficiency i. e. lethargy, slow growth , dry , scaly skin,
and skin lesions. They also reported that safflower seed oil reversed the
deficiency signs ( 153), but their data have not been published.
MacDonald et al ( 1 50) found that cats fed a diet low in linoleate (0 .3% of
total kilocalories) had low feed efficiencies , scaly skin , hair loss, enlarged fatty
livers, and markedly increased rates of water loss through the skin. Necropsies
revealed degeneration of the kidneys, testes, and adrenals and hyperkeratosis of
the skin ( 149, 1 52). These problems were prevented by dietary linoleate (5%
safflower seed oil), which demonstrated that linoleate is an EFA for the cat.

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LINOLEATE DEFICIENCY

EFA Requirements
The EFA requirements of cats have not yet been precisely determined .
Although linoleate at 6.7% of kilocalories is more than adequate for growth and
normal skin condition ( 1 50), the minimum requirement is probably less than
this. Calculations of the double-bond index of liver lipids (149) based on
comparison to data from rats ( 1 1 5 , 157) indicate that the linoleate requirement
of the cat may be near 2.5% of dietary energy in the absence of dietary
arachidonate.
The discussion of quantitative requirements is complicated by two factors:
(a) Arachidonate alone will probably meet the total EFA requirement ofthe cat ,
as it does in the rat 0 15 , 157), so the linoleate requirement of the cat will be
negligible if there are high levels of arachidonate in the diet. (b) With linoleate
at 4.8% of dietary energy and arachidonate at 0.04%, reproductive perfor
mance is essentially normal ( 1 52), which indicates that 0 .04% of kilocalories is
near the minimum requirement for arachidonate . However, low levels of
dietary linoleate would be expected to increase the arachidonate requirement.
The reason for this is that both linoleate and arachidonate are active in main
taining membrane integrity ( 1 1 7) . Therefore, although a source of arachi
donate is indispensable for the cat, linoleate might spare or reduce the

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552

MacDONALD, ROGERS & MORRIS

arachidonate requirement. Further studies are needed to quantitate the linoleate

and arachidonate requirements when both are present in the diet.
An observation that deserves further study is that although linoleate prevents
liver enlargement due to fatty infiltration, the neutral fat content of liver
remains higher than normal ( 149) . Because levels of linoleate in tissues are near
maximal with diets containing 5% safflower seed oil, higher levels of dietary
linoleate would not be expected to have further beneficial effects . This raises
the question of whether a source of fatty acid that is more polyunsaturated than
linoleate is needed to minimize the accumulation of neutral fat in liver. In rats ,
liver fatty acid synthesis is regulated in part by levels of polyunsaturated fatty
acids (22 1 ) , and arachidonate may be more effective than linoleate (45).
Dietary arachidonate or other polyunsaturated fatty acids may be required by
the cat for normal liver fat metabolism. Before a minimum arachidonate
requirement can be assessed, a study is needed of the amount of neutral fat in
the livers of cats fed different dietary levels and combinations of linoleate and
arachidonate .
The lack of d6-desaturation, which prevents the synthesis of arachidonate,
would also prevent the conversion of 18:3n3 (linolenate) to longer-chain
n3-fatty acids . Rivers et al ( 1 99) suggested that these fatty acids may also be
required by cats. Because n3-fatty acids can be converted to eicosanoids that
can have various pharmacological effects, the cat would be useful in the study
of the physiological roles of these fatty acids.
The domestic cat is not the only carnivore that lacks the ability to desaturate
fatty acids at the d6 position. The lion ( 1 98), the turbot (a carnivorous fish)
( 1 82); and even an insect carnivore, the mosquito (58), have similar inabilities
to synthesize arachidonate . This metabolic peculiarity appears to be correlated
with species that are strict carnivores regardless of their position on the
phylogenetic tree.
SUMMARY
From the foregoing discussion of the nutritional requirements and some of the
metabolic anomalies of the cat, it is clear that the cat is adapted to eating a
carnivorous diet. It may, however, have less capability than omnivores and
herbivores to adapt to wide ranges in dietary composition. For example, the
lack of ability to synthesize sufficient vitamin A from carotene, ornithine from
glutamic acid, arachidonate from linoleate, and taurine from cysteine results
from a complete deletion or severe limitation of the enzyme or pathway that
makes each nutrient. Other nutrient requirements , such as the absolute require
ment for niacin and the high protein requirement, appear to result from the high
activity of one or more enzymes and the fact that these enzymes are not adaptive
in the cat. For example, the cat cannot decrease picolinic carboxylase in order

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FELINE NUTRITION

553

to force tryptophan toward the niacin-synthetic pathway (244) nor can it

decrease the urea cycle enzymes when dietary protein is decreased in the diet in
order to conserve nitrogen (209) .
Indeed, the cat appears to have less capability to adapt to most changes in
dietary composition because it cannot change the quantities of enzymes in
volved in the metabolic pathways (209) . This evolutionary development has
resulted in more stringent nutritional requirements for cats than for omnivores
such as the rat, dog , and man. What little evidence exists for other carnivore
species leads us to suggest that this pattern may well be common among other
strict carnivores.
The metabolic differe,ces between the cat and omnivores provide the re
searcher with a useful animal model for studying the biochemical basis of some
nutrient requirements . For example, because there is no significant conversion
of linoleate to arachidonate in cat liver ( 101 , 1 50, 23 1 ) , the physiological
functions of linoleate can be determined independent of it having a role as a
precursor of arachidonate ( 1 50) . This has not been possible with other species.
It is anticipated that further studies of the nutrition of the cat will increase our
understanding of metabolic adaptation and nutrient functions .
ACKNOWLEDGEMENT

The authors wish to express their appreciation to Ms. Karen Green for her
invaluable assistance in the preparation of this review.
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