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Therapeutic diets in clinical and pet nutrition

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  • ICAR-National Institute of Animal Nutrition and Physiology

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dog has fresh and clean
rblication, Association of
trol Officials Inc., Atlanta,
': Its Behavior, Nutrition,
owa: Iowa State University
29th World Congress of
I Animal Veterinary
ier
6-9, 2004, Rhodes,
al Science. Albany, New
hers, Inc.
it. (1985). Nutrient
igs. Washington, D.C.:
ress.
.. 2006. In: Proc. National
Practice and 3rd Annual
Society for Advancement
February 10-12, 2006,
5-193.
In:
Significance of
Livestock Health and
., Garg, AX., Pattanaik,
:hra, U.R. (Eds). Centre
; in Animal Nutrition,
:arch Institute, Izatnagar,
'cent Trends in Rumen
technology. Chaudhary,
unra, D.N. and Mehra,
f
Advanced Studies in
an Veterinary Research
dia, pp. 83-88.
ClinicalNutrition of Livestock and Pets:
An Advanced Short Course
CAS in Animal Nutrition, IVRI, lzatangar
November 3-23, 2006
Therapeutic Diets in Clinical Pet Nutrition
A. Sahoo and R.K. Singh
Environmental (climate, micorbes,
fauna, parasites, toxicants, and injury) stimulus
that initiates an adaptive change or stress
response, in the animal alters its normal
physiological metabolism and hence the system
is in need of therapeutic support, viz. therapeutic
treatment and supportive diets. While assessing
the nutritional requirement of such clinically ill
pet animals, it involves assessment of the
nutritional requirements for various life stages
and operational tasks, and formulations of
balanced and complete diets and/or therapeutic
diets for different patho- or pathophysiological
conditions. It involves nutrition of clinically ill
animals, supportive nutrition for the
convalescent animals, and preventive nutrition
to fight against the occurrence of clinical illness
(Sahoo, 2002). Therapeutic nutrition thus plays
a fundamental role in determining the health and
performance of any animals, and also, a correctly
balanced diet is essential to avoid disease
associated with a deficiency or toxicity of a
particular nutrient. Furthermore, disease and
nutrition are closely interlinked and dietary
modification forms an important part of the
veterinary management of the case and thus the
concept is coined in the name of 'therapeutic
diets'.
Infection and dietetics
Nutritional deficiency apparently
increases the severity of infection by viral,
bacterial, fungal or paratsitic pathogens. Studies
indicate that most nutrition may affect
pathogenesis either synergistically or
antagonistically (Scrimshow
et al.,
1968) and
also has significant impact on cell mediated
immunity (Latshaw, 1991). Infection induced
immune stimulation decreases appetite and
muscle protein aceretion, increases metabolic
rate, body temperature and oxidative damage to
cells (Swick, 1995). Increased incidence and
severity of infections secondary to
immunological impairement as a result of
generalized malnourishment as well as selective
nutrient deficiencies may result in vaccination
failure, increased condemnation and mortality,
poor feed conversion, and increased morbidity
and medication costs.
Nutritional support replenishes tissue
stores, improves immune function and wound
healing and prevents death from cachexia. In
persistent clinical illness nutritional status can
be severely compromised by the combined
effects of reduced feed intake and increased
metabolic demands secondary to fever and
tissue catabolism. The clinically ill animals are
usually less active and while calculating energy
requirements, it is best to use the estimated
requirement for animals confined to stalls and
multiply these basal energy requirement by a
"fudge factor" that reflects the severity of the
disease and stress (Ralston, 1985). Oral
supplementation is preferred first, and extra-oral
or parenteral nutrition are alternatives to feeding
animals that do not respond to managerial or
chemical stimulants of appetite.
The specificity of therapeutic diets with
respect to its composition, special/essential
supplements and/or additives, feeding and
management for different disease conditions are
briefed under specific disease conditions.
Cardiovascular disease
The conditions are congestive heart
failure, hypertension, ascites and edema. The
diet should be highly digestible and easily
metabolized with low sodium and saturated fat
and extra potassium, B-complex vitamins and
taurine.
93
SAHOO AND SINGH _
Respiratory disorder
The commonly associated disease
conditions are bronchitis, pharyngitis and
pneumonia. The ill pets should be provided with
a highly palatable balanced diet with readily
metabolizable carbohydrate, added antioxidant
vitamins (C, A and E) and expectorants
(glycerine, honey).
Nephrotic disorder
Renal failure is commonly associated
with early stages of congestive heart failure,
hepatic disease associated with encephalopathy
and hypertension. The therapeutic diet should
be balanced with caloric requirement from non-
protein sources and it should have low protein,
low P and Na, added K, water soluble vitamins
and sources of 003 and
ro6
FA. Renal calculi
(urolithiasis) are a systemic disease and in
majority cases it occurs because of disturbances
in one way or the other in the uptake, metabolism
or excretion of urolith constituents (struvite:
magnesium ammonium phosphate, calcium
oxalate, urate, purines and cystine) (Senior et
al., 1996). Cats are observed to be at higher risk
than dogs. Typical diet for treatment of
urolithiasis in dog should contain 8%CP, 0.3%
Ca, 0.12% P, 0.02% Mg and 1.2% Na in the DM
(Lewis, 1989). The factors that predispose cats
and dogs to urolithiasis include inadequate
liquid intake, sudden change to a dry diet with
excess total minerals (P, Mg or Na), alkaline diets
or diets supplying inadequate K (Wolter, 1990).
Acidifying diets, often termed as 'struvite' diets
contain acidifiers like ammonium chloride with
low base (Na or Ca carbonates), DL-methionine
and should be used judiciously. The diet should
have low mineral content (Ca, Mg, and P) and
oxalates and may be enriched with alkalizing
ingredients. Urate uroliths can be treated by
feeding low protein diets with low purine food
type and xanthine oxidase inhibitors and cystine
uroliths by low protein and low sodium diets.
Liver disorder
Various {Oxicmetabolites of food origin
or from infections impaired liver function
resulting in disease conditions like hepatitis,
cirrhosis, hepatic encephalopathy, etc. The pets
should have a maintenance balanced diet with
low fat, low protein with high biological value
(low purine containing foods), highly digestible
starch and sugar, supplemental deficient
digestive enzymes and B-complex vitamins with
lipotropic factors.
Toxicity and oxidative stress
Dietary components playa crucial role
in the health of companion animals, especially
those exposed to elevated levels of toxins and
free radicals. Investigation into animals' hepatic
antioxidant and metabolite conjugation systems,
and the metabolic processes that influence them,
provides some understanding regarding the
relationship of diet to disease prevention and
treatment. The results of recent in vivo
assessments, clinical trials, and observational
studies show oral supplementation with vitamin
E, selenium, glutathione, and taurine to be
beneficial for both maintaining natural
antioxidant systems and protecting against a
number of degenerative diseases associated
with free radical damage and toxin exposure
(Scanlan, 2001). In many instances, it has been
observed that the introduction of specific
nutrients positively influences the health status,
symptomatic presentation, and life span of
animals whose natural detoxification systems are
compromised.
Gastro-intestinal diseases
Different disease conditions are
enteritis, gastritis and diarrhea, inflamatory bowel
disease, malabsorption and maldigestion,
exocrine pancreatic insufficiency,
lymphangiectasia, pancreatitis, hepatic disease
not associated with encephalopathy,
hyperlipidemia. The diet should be complete and
balanced for growth of puppies and maintenance
of adults that contains highly digestible
carbohydrate and protein of high bilogical value,
low fiber and gluten free, low lactose,
hypoallergenic food proteins, low long chain
triglycerides (LCT) , source of medium chain
94 _
triglycerides (MeT,:
and w6 fatty acids, pI
care should be n
electrolytes and wat
and diarrhea.
Diarrhoea
Diet plays
1
of all aspects of d
Inappropriate diet,
primary cause, bu
duration of diarrhc
cause is not diet-n
consideration of die
some cases is an ess
(Simpson, 1988). )
water is reabsorbed
j
small decrease in
secretion) can readi
water content and (
Oral rehydration
therapy is importan
excessive loss offlt
depletion and acic
1989). Fluids and e
orally in mild dise
severe cases. Oral
the lower sodium
appropriate for the
in the dog, in whicl
an important aet
solutions with big
provide additional
hypertonic and rna:
(Leiper, 1986; M
increase luminal O!
osmotic diarrho
potentially, dam
(Kameda et al, 19~
solutions should
cases with reduce
villus atrophy or (
where the possib
increased (Simrm
appears that hyp
glucose polymers
isotonic or hypertc
iditions like hepatitis,
lalopathy, etc. The pets
nee
balanced diet with
1
high biological value
lOds),highly digestible
plemental deficient
complex vitamins with
ress
ents playa crucial role
onanimals, especially
d levels of toxins and
Il
into animals' hepatic
econjugation systems,
esthat influence them,
mding regarding the
sease prevention and
, of recent in vivo
Is, and observational
ientation with vitamin
e, and taurine to be
iaintaining natural
protecting against a
diseases associated
: and toxin exposure
instances, it has been
duction of specific
Ices the health status,
In, and life span of
xification systems are
se conditions are
ea,inflamatory bowel
and maldigestion,
insufficiency,
titis, hepatic disease
encephalopathy,
ouldbe complete and
liesand maintenance
highly digestible
high bilogical value,
ree, low lactose,
ins, low long chain
e of medium chain
••
__________________________ Therapeutlc Diets in Pet Nutrition
,
triglycerides (MCT, 22-34% of fat), source ofw3
and w6 fatty acids, probiotics(yogurt). However,
care should be taken to infuse parental
electrolytes and water replacement in vomiting
and diarrhea.
Diarrhoea
Diet plays a key role in the management
of all aspects of diarrhoea (Zimmer, 1986).
Inappropriate diet, for example, may be the
primary cause, but it may also prolong the
duration of diarrhoea even if the underlying
cause is not diet-related. Conversely, careful
consideration of diet can speed recovery and in
some cases is an essential component of therapy
(Simpson, 1988). Approximately 95% of this
water is reabsorbed from the colon, so a relatively
small decrease in absorption (or increase in
secretion) can readily result in increased colonic
water content and diarrhoea.
Oral rehydration therapy: Appropriate fluid
therapy is important in acute diarrhoea to check
excessive loss of fluids, dehydration, electrolyte
depletion and acidosis (Zenger and Willard,
1989). Fluids and electrolytes may be provided
orally in mild disease or parenterally in more
severe cases. Oral rehydration solutions with
the lower sodium concentration may be most
appropriate for the treatment of acute diarrhoea
in the dog, in which viral infection appears to be
an important aetiological factor. Further,
solutions with high concentrations of glucose
provide additional energy, but are considered
hypertonic and may reduce net water absorption
(Leiper, 1986; Maughan and Leiper, 1990),
increase luminal osmolality thus contributing to
osmotic diarrhoea (Farthing, 1988) and,
potentially, damage the intestinal mucosa
(Kameda et al, 1986). Use of highly hypertonic
solutions should be avoided, particularly in
cases with reduced absorptive capacity due to
villus atrophy or damage (rotavirus infection),
where the possibility of glucose overload is
increased (Simmons and Bywater, 1991). It
appears that hypotonic solutions containing
glucose polymers may be more beneficial than
isotonic or hypertonic solutions (Farthing, 1990;
Maughan and Leiper, 1990). Some dogs with
acute diarrhoea, concurrent with substantial
stool losses of potassium, may develop
hyperkalaemia. A potassium concentration in
the range of 20-30mmol/L is normally adequate
to replace existing losses (Farthing, 1988).
Substantial stool losses of chloride are known
to occur during acute diarrhoeal episodes
(Hirschhorn and Greenough, 1991). Chloride is
normally included in oral rehydration solution
as the anion of the sodium and, occasionally,
potassium salts. Citrate and other base
precursors (bicarbonate and acetate) have been
shown to promote sodium and water absorption
in normal mammalian intestine (Farthing, 1988).
Inclusion of glycine in oral rehydration solutions
may be of benefit since additional absorption of
this amino acid may enhance sodium and water
absorption and thereby reduce stool output.
(Hirschhorn and Greenough, 1991).
'Bland' diets: A bland diet can be defined as a
high quality, highly digestible, non-spicy diet
containing components that pose a low risk of
adverse reactions, such as a protein source that
is novel to the animal. Following an acute bout
of diarrhoea, this type of diet helps to ensure
that the enterocytes are presented with minimal
digestive challenge, and the acquired food
allergies or intolerance is minimised.
Elimination diet and/or hypoallergenic diet:
Acquired sensitivities may develop as a result
of increased permeability of the inflamed gut,
which facilitates the uptake of dietary antigens
that can then initiate a hypersensitivity response.
Potentially, hypersensitivity could develop to
one or more protein sources that are fed during
this critical period. Although the response is
normally short lived, it may be sustained
following repeated presentation of these
allergens resulting in chronic diarrhoea. To
reduce the risk of possible complications, a
minimal number of. protein sources should be
fed during, and following, a period of acute
diarrhoea. Preferably, the protein source should
be novel to the animal and should not form part
of the maintenance diet that will be used
_____________________________ 95
SAHOOAND SINGH _
following recovery. It should have no additives
or supplements and be fed to the exclusion of all
other foods for at least 4 weeks before
considering an alternate diet. Components of
the original diet may be introduced one at a time
once the patient has responded to the elimination
diet (Patterson, 1995). The introduction of a
second 'novel' protein diet after a minimum
period of 4 weeks is usually made in the long-
term management of the patient. It is important
that the diet is nutritionally complete and
balanced and that the actual level of protein is
not compromised, since this· may hinder
enterocyte repair. High digestibility of the protein
will help to reduce the amount ofluminal antigen
available for absorption and, hence, the risk of
sensitization.
Small intestinal disease (SID)
Specific causes of small intestinal
diarrhoea include exocrine pancreatic
insufficiency (EPI), dietary sensitivity, neoplasia,
bile acid deficiency and short bowel syndrome.
Small intestinal bacterial overgrowth (SmO) is a
common problem that may occur asa
complication in up to 50% of dogs with chronic
diarrhoea. Idiopathic disorders include
inflammatory bowel disease (mD), which is
characterised most commonly by infiltration with
lymphocytes and plasmacytes, or occasionally
by eosinophils. Lymphangiectasia is a chronic
condition characterised by insufficiency and
marked dilation of the intestinal lymphatics, which
may result in protein losing enteropathy and fat
malabsorption with diarrhoea (and steatorrhoea).
Diet plays an important role in the
management of many small intestinal diseases,
generally in conjunction with appropriate
pharmacological therapy. High fibre diets are
contraindicated for the management of small
intestinal disease. Restriction of dietary fat (low
fat: 12-20% of ME; moderate fat: 20-30% of ME)
reduces the challenge to an already compromised
gastrointestinal tract and is recommended in a
range of small intestinal diseases. In some cases,
medium chain triglycerides (MCTs) may form a
useful supplemental source of energy, since
some MCTs can be absorbed intact from the
gastrointestinal tract and can reach the
circulation via portal rather than lymphatic
channels, which suffers damage in many SID
and are hydrolysed by gastric lipase more
readily than long chain fatty acids. Moderate to
high quantities of good quality protein are
recommended, since protein deficiency may
further compromise a diseased intestinal tract
through impairment of immune function and the
luminal barrier, arid through decreased formation
of brush border enzymes. Highly digestible
sources of carbohydrate, such as rice, are
recommended. Mono-and disaccharides,
particularly lactose, should be avoided because
they provide an osmotic load in the gut.
Although dietary fibre is commonly used in the
non-specific therapy of acute diarrhoeas, it is
generally contraindicated in chronic diseases
because of its interference in digestion and
absorption thereby further compromising an
impaired gastrointestinal tract. Specifically,
soluble fibre is contraindicated in exocrine
pancreatic insufficiency (EPI) since this may
interfere with pancreatic enzyme activity and
aggravate fat malabsorption. Several small
intestinal diseases can result in deficiencies of
water soluble B-complex vitamins. Patients with
EPI are particularly susceptible to cobalamin
(vitamin B12)deficiency due to binding of the
vitamin by bacteria; decreased pancreatic
intrinsic factor, which is essential for cobalamin
absorption in the ileum; and decreased
production of pancreatic proteases to release
cobalamin fromR-proteins (Simpsonetal, 1989).
Diets for small intestinal disease are, therefore,
supplemented with B-complex vitamins, although
additional parenteral administration of cobalamin
may be necessary in cases of EPI.
Nutritional management of exocrine pancreatic
insufficiency
In EPI, there is impaired digestion and
absorption of fat and, toa lesser extent,
carbohydrate and protein, resulting in weight
loss, despite a ravenous appetite, and diarrhoea
with steatorrhoea. Management of the condition
therefore involves:
96 _
Feed a highlj
amounts. base
weight
Divide food a
day
Prescribe thea
replacer.Dnc
gradually inc
enzyme replac
If diarrhoea re
food, or if the
too quickly, fal
gradually rein
Use only the :
of stabilisatio
For long term
or moderate
j
dietary chang
and only afte
sometime.
Any diet char
in dose of the
Large intestinal
I
Specific
diarrhoea includ
bacterial infectio
Escherichia coli
e
large intestinal di~
supplementation v
responsive' whet
as functional dian
bowel syndrome'
part in the mana.
intestinal origin.
I1
dietary proteins :
aetiology of a
nui
conditions, inclur
which may be mo
highly digestibl
number of novel]
source providinj
forms may be b
treatment of sorm
helps to normalis
content (Lieb, 19
rbed intact from the
md can reach the
her than lymphatic
amage in many SID
~astric lipase more
y acids. Moderate to
quality protein are
ein deficiency may
.ased intestinal tract
tune
function and the
.decreased formation
. Highly digestible
, such as rice, are
nd disaccharides,
be avoided because
c load in the gut.
unmonly used in the
ute diarrhoeas, it is
in chronic diseases
:e in digestion and
r compromising an
tract. Specificaliy,
icated in exocrine
iPI) since this may
nzyme activity and
on. Several small
It in deficiencies of
amins. Patients with
xible to cobalamin
e to binding of the
reased pancreatic
entialfor cobalamin
I;
and decreased
roteases to release
iimpsonetal,1989).
leaseare, therefore,
xvitamins, although
trationof cobalamin
fEP!.
~ocrine pancreatic
aired digestion and
i.a lesser extent,
esulting in weight
etite,and diarrhoea
entof the condition
___________________ .•...•• Therapeutic Diets in Pet Nutrition
Feed a highly digestible, low fat diet in
amounts. based on the dog's current body
weight
Divide food allowance into two meals per
day
Prescribe the appropriate amount of enzyme
replacer. Once faecal character is restored,
gradually increase food allowance and
enzyme replacer to allow body weight gain
If diarrhoea recurs because of access to other
food, or if the food allowance is increased
too quickly, fast the animal for 24 hours before
gradually reintroducing the regimen
Use only the low fat diet during the period
of stabilisation
For long term maintenance, alternative (low
or moderate fat) diets may be tried but all
dietary changes should be made gradually
and only after the dog has been stable for
sometime.
Any diet changes may necessitate a change
in dose of the enzyme supplement.
Large intestinal disease
Specific causes of large intestinal
diarrhoea include parasitism, neoplasia and
bacterial infections (Clostridium perfringens,
Escherichia coli etc.). Some idiopathic cases of
large intestinal diarrhoea may respond to dietary
supplementation with fibre and are termed 'fibre-
responsive' whereas others may be classified
as functional diarrhoea, often known as 'irritable
bowel syndrome'. Dietary fibre plays a major
part in the management of diarrhoea of large
intestinal origin. However, sensitisation to certain
dietary proteins appears to have a role in the
aetiology of a number of chronic inflammatory
conditions, including idiopathic chronic colitis,
which may be more effectively managed using a
highly digestible diet based on a restricted
number of novel protein sources. Adding afibre
source providing both insoluble and soluble
forms may be beneficial in the symptomatic
treatment of SOmelarge bowel diseases, as fibre
helps to normalise transit time and faecal water
content (Lieb, 1991). Infective diarrhea can also
be managed with feeding of probiotics-
Lactobacillus acidophilus (Pasupathyetal.,
200 1) or plant bioactive components like essential
oil (Singh, 2(05).
Irritablebowel syndrome: It is thought to be
associated with stressful situations that lead to
altered intestinal motility. Dietary fibre
supplementation may be beneficial in some cases
through its physical properties, which help to
normalise colonic contractility. Although acute
cases resolve spontaneously and chronic cases
generally respond to antibiotic therapy, dietary
fibre supplementation may be of benefit in
intermittent cases which require long term
therapy. This may be due to the effects of soluble
dietary fibre on microbial population and the
production of an acidic environment from short
chain fatty acids.
Idiopathic chronic colitis (ICC): It is one of the
most common causes of chronic diarrhoea in
the dog (Bush, 1985). Diet plays an important
role in the pathogenesis of this condition and it
seems that both digestibility and the allergen
component of the diet are key factors in
successful dietary management (Leib, 1991;
Nelson et al, 1988). Studies involving dogs with
confirmed lymphocytic plasmacytic colitis have
shown that the condition could be successfully
managed using a commercial low residue,
'hypoallergenic' diet, in which the protein
sources were limited to chicken and rice (Nelson,
1988; Simpsonetal, 1998). The rationale behind
the use of a highly digestible, 'hypoallergenic'
diet can be based on three criteria: high
digestibility of macro-nutrients reduces the
digestive challenge to the terminal gut. Low
antigen content reduces the chance of an
immunological reaction and high digestibility;
further limit the dietary antigens entering the
colon. The rationale for using high fibre diets in
colitis is primarily related to the fact that bacterial
fermentation of dietary fibre results in changes
in colonic flora and production short chain fatty
acids (SCF A), and epithelial energy deficit may
be partly responsible for progression of colitis
(Kripke et al., 1987; Roediger, 1982; Settle, 1988).
97
administration of certain hormones and drugs
(glucocorticoids, progesterone-like drugs).
A
juvenile form of diabetes mellitus sometimes
occurs in dogs of less than one year of age to
an extent of 1.5% of canine diabetes with a
definite breed predisposition. Factors
precipitatingthe development of diabetes
mellitusare estrus, pregnancy, pancreatitis,
genetic, pharmaceutical .• (glucocorticoids,
magestrol acetate), hormonal, immunologic,
infectious (viral), stress, illness and obesity.
Until the establishment of oral hypoglycemic
agents, insulin will remain the primary therapy
for canine diabetes mellitus. However, long-
term diabetic management involves weight
control and dietary management. Dietary
components may directly influence insulin
sensitivity and insulin output, and hence
contribute to hyper-insulinaemic, insulin-
resistant state independent of obesity.
Dietary therapy should therefore be
designed to enhance insulin therapy and
improve glycemic regulation of the diabetic dog.
Commonly recommended guidelines for feeding
diabetic dogs are as follows:
Daily caloric intake should maintain the dog
at its ideal body weight. If the diabetic dog
is obese, a weight reduction program
should be initiated.
The daily caloric requirement should be
between 40 and 50 kcallkg of ideal body
weight depending on age and activity. If
the dog is obese, the calculated daily caloric
requirement should be reduced to an
additional 40% to promote weight loss.
An ideal initial daily feeding schedule
consists of three meals, fed at 6 hr intervals,
beginning at the time of the insulin injection.
Subsequent adjustments in the time of
feeding should be based on results of serum
blood glucose determinations.
Soft-moist foods should not be fed to
diabetic dogs; dry. and canned foods are
more acceptable diets as the former mostly
contains readily absorbable mono- and di-
saccharides.
r
SAHOOANDSINGH •.•..•. ...•....__
In dogs, however, high fibre diets have proven
much less efficacious than 'hypoallergenic' diets
in the management of ICCand there are
suggestions for supplementing various fiber.
sources inhypoallergenic diets to obtain the best
response (Guilford, 1996; Simpson, 1998).
Appropriate ratios of
(CIHi):
(co-
3)polyunsaturated
fatty acids help in regulating the severity and
chronicity of colitis (Simpson, 1998).
Diabetes
Diabetes mellitus is characterized by an
absolute or relative lack of the pancreatic
hormone, insulin,' resulting in glucose
intolerance. It results from impaired or deficient
insulin secretion or impaired action of insulin in
peripheral tissues. Insufficiency
of
insulin has
consequences on carbohydrate, lipid and
protein metabolism with secondary disturbances
of water and electrolytes. Based on the causative
factors diabetes is of three main types, viz.
insulin-dependent diabetes mellitus (IODM) -
Type 1, noninsulin-dependent diabetes mellitus
(NIODM) - Type 2 and secondary diabetes
mellitus. Type I is most common in the dog and
is characterized by hypoinsulinaemia and
impaired insulin secretion even after a glucose
challenge with a necessity for insulin injection
and a tendency to develop keto-acidosis. It
usually occurs between 5 and 12 years of age
and affects females twice as frequently as males
and is seen commonly in small dogs. Type 2 is a
form of insulin resistant one, which is usually
diagnosed in older overweight ones. The
increased amount of adipose tissue is believed
to inhibit the interaction of circulating insulin
with fat cell-associated insulin receptors.
Therapy for Type 2 diabetes mellitus includes
dietary management and use of oral
hypoglycaemic agents to stimulate insulin
secretion or increase peripheral tissue sensitivity
to the action of circulating insulin. Due to
degeneration of pancreatic beta cells, Type 2
may progress to Type I. The third type occur
secondary to conditions like, pancreatitis,
acromegaly (growth hormone overproduction),
Cushing's syndrome, and prolonged
98
Based on re
with
diabetes
60% comple:
and<25%fa
of fibre.
Although, in
fibre intake
0
has not beet
diabetic dog,
some of the
I
Dietary then
depending 01
disorders, me
Obesity
Obesity
i
energy, stored
imbalances betwe
energy. The incide
males (Mason, 19~
to play and intend
effects (hypotl
corticodism, diabe
approaches inch
restriction by redu
normal diet or
concentration of tl
a-meal practice or
with the dog recei'
mineral suppleme
there are
neuro-mi
leptin treatment fo
1996). Chromiun
increase lean 1
percentage body
humans
(Andersoi
Geriatrics
Dogs
am
age-related chan]
twelve years old.
result in health is
of skin and coat,
frequent intestinal
dental problems, ,
off infection. ~
unavoidable and '
,
,
___________ ••••• ••••• T,herapeutic Diets in Pet Nutrition
.hormones and drugs
erone-like drugs). A
• mellitus sometimes
in one year of age to
nine diabetes with a
iposition. Factors
opment
of diabetes
nancy, pancreatitis,
I••
(glucocorticoids,
tonal,
immunologic,
illness and obesity.
f oral hypoglycemic
I
the primary therapy
tus. However, long-
mt involves weight
nagement. Dietary
y influence insulin
output, and hence
rlinaemic, insulin-
It of obesity.
should therefore be
.sulin therapy and
,nof the diabetic dog.
midelines for feeding
s:
midmaintain the dog
t. If the diabetic dog
'eduction program
-Based on recommendations for humans
with diabetes, the. diet should contain 55-
60% complex carbohydrates, 20% protein
and
<
25% fat and reasonably good amount
of fibre.
- Although, influence of increased dietary
fibre intake on improving glycemic control
has not been completely established in
diabetic dog, it proved to be beneficial in
some of the patients.
- Dietary therapy may need modification
depending on the presence of concurrent
disorders, most notably pancreatitis.
Obesity
Obesity is the accumulation of excess
energy, stored as fat in the body due to
imbalances between intake and expenditure of
energy. The incidence was higher in females than
males (Mason, 1970). Drugs usually have no role
to play and intended at treating the progressive
effects (hypothyroidism, hyperadreno-
corticodism, diabetes mellitus, etc.). The dietary
approaches include partial or total calorie
restriction by reducing the quantity of the dog's
normal diet or by diluting the calorie
concentration of the diet or by starvation or skip-
a-meal practice or by prolonged hospitalization
with the dog receiving only water and a vitamin!
mineral supplement (Markwell, 1990). Besides,
there are neuro-molecular approaches involving
leptin treatment for the control of obesity (Wood,
1996). Chromium has also been reported to
increase lean body mass and decrease
percentage body fat leading to weight loss in
humans (Anderson, 1998).
Geriatrics
Dogs and cats begin to show visible
age-related changes when they are seven to
twelve years. old. Changes in body tissues may
result in health issues, including deterioration
of skin and coat, loss of muscle mass, more
frequent intestinal problems,arthritis, obesity,
dental problems; and decreased ability to fight
off infection. Some of the changes are
unavoidable and others can be managed with
uirement should be
:al/kg of ideal body
age and activity. If
lculateddaily caloric
be reduced to an
aoteweight loss.
r
feeding schedule
fed at 6 hr intervals,
theinsulin injection.
nts in the time of
I on results of serum
nations.
iuld
not be fed to
I canned foods are
s the former mostly
able mono- and di-
diet. Nutritionaladjustment should begin early,
but the exact age in dogs is not as simple as it is
in cats. Cats should start eating a senior diet at
about 7 years of age. The age for dogs depends
upon its size. Since smaller dogs live longer and
don't experience the age-related changes as
early as bigger dogs and thus size is used to
determine the time to change diets.
The main objectives in the feeding of
geriatric dogs. and cats should be to maintain
health and optimum body weight, slow or
prevent the development of chronic disease and
minimize or improve clinical signs of diseases
that may already be present. Older dogs and
cats have been shown to progressively put on
body fat in spite of consuming fewer calories.
This change in body composition is inevitable
and may be aggravated by either reduced energy
expenditure or a change in metabolic rate. Either
way, it is important to feed a diet with a lower
caloric density to avoid weight gain from fat and
with a normal protein level to help maintain muscle
mass. Studies have shown that the protein
requirement for older dogs does not decrease
with age and that protein levels do not contribute
to the development or progression of renal
failure. It is important to feed older dogs diets
that contain optimum levels of highly digestible
protein to help maintain good muscle mass.
Avoid "senior"diets that have reduced levels
of protein. Other special nutrients with beneficial
role in older animals are:
Vitamin E for senior cats can increase their
antibody level back to levels seen in younger
cats.
Gamma-linolenic acid (GLA), an ~6 fatty acid
that acts like an
0>-3
plays a role in the
maintenance of a healthy skin and coat. It is
normally produced in the dog's liver, but at old
age its levels may be diminished and therefore,
needs supplementation.
Fiber and fructooligosaccharides (FOS) in
senior diets promote the growth of beneficial
bacteria at the expense of detrimental ones since
older dogs often have changes in the intestinal
99
SAHOOAND SINGH _
bacterial population which can result in clinical
signs of gastrointestinal disease (e.g. diarrhea)
(Simpson, 1998; Pasupathy et al., 2002). Inulin
and Fructo-oligosaccharides (POS) are the newly
discovered members of the carbohydrate family
thatact asprebiotics and their beneficial role is
summarized in Table 1.
Skeletal abnormalities
The major osteopathic conditions are
rickets and osteomalacia, osteoporosis, arthritis
and abnormal bone growth. The diet of diseased
animals should be balanced for growing pups
(extra protein for growth) and adult maintenance
with meat and bone based supplement. It should
(Zn, Fe, Ca, P,
I
(lysine, methion
Further Readin
Abdulla, M.,
Ande
Svensson,
86-92.
Anderson; RA. 11
Bush, B.M. (1985:
and Raw,
Farthing, MJ.G.lI
Guilford, W.G. 19'
'TX, pp. 5
Hirschhorn, N. al
Parenteral
Kameda, H., Abe
Physiol., ;
Kripke, S.A, Fox,
Surgery F<
Latshaw, D.L. 19!
30: tn-r:
Leib, M.S. (1991).
Philadelph
Leiper, J.B. (1986)
Lewis, L.D. 1989.
165: 665.
Markwell, PJ., val
and Shant
Anim. Pra
Table 1. Beneficial role of inulin and fructo-oligosaccharides
Benefits Purpose
Promotes the growth of beneficial bacteria
in the intestine
Enhances mineral absorption, especially
Ca for healthy bones
Lowers triglycerides, LDL and total cholesterol
Controls blood glucose
Reduces calorie intake
Delays gastric emptying time
Antioxidant such as vitamin E and beta-carotene
help eliminate the free radical particles, which
accumulate and can damage body tissues and
contribute to the signs of aging. Antioxidants
can also increase the effectiveness of the immune
system in senior cats and dogs.
Routine care for geriatric pets should
involve adherence to a consistent daily routine,
regular attention to normal health care
procedures and periodic veterinary examinations
for assessment of the presence or progression
of chronic disease. Stressful situations and
abrupt changes in daily routines should be
avoided and if at all a drastic change must be
made, attempts should be made to minimize
stress and to accomplish the change in a gradual
manner.
.
..
Formation of soft stools, supportive therapy in
animals exposed to strong antimibioticslhigh
stress levels. and in constipation (supports good
bowel movement)
Maintenance of adults, supports during
osteoporosis, osteomalacia, arthritis
Supports to hypereholesterolemic/dyslipidemic
adults
Supports to diabetic patients
Weight management in obese/overweight adults
Early satiety- supports to diabetic, obese/
overweight pets
have added Ca and P at proper ratio (1.3:1) and
adequate vitamin A and D. In conditions like
arthritis and joint pain, the protein content
should be low to support minimum maintenance
and should have prebiotics like. inulin and
oligofructans and nutraceuticals (glucosamine,
chondroitin sulfate).
Surgical operations
Various surgical conditions are
gastrectomy and intestinal surgery, wounds or
burns, surgery of joints or bones, etc. The
patients should have provision for complete and
balanced diet with emphasis on pre and
postoperative nutrition, viz. liquid preparations,
high protein and calorie based diet, nutrient
dense low volume diet, enzyme preparations,
added vitamins (A, C and E), added minerals
Mason, E. 1970. V
Maughan, R.J. a
Therapeutii
Nelson, R.W., Stoc
Vet. Intern
Pasupathy, K., Sal
N.N.2002
364.
Pasupathy,
K,
Saho
Anim. Nut!
100. _
_______ ...••. Therapeutic
Diets in Pet Nutrition
teopathic conditions are
ia,osteoporosis, arthritis
wth.The diet of diseased
anced for growing pups
It}and adult maintenance
ed supplement. It should
(Zn, Fe, Ca, P, etc.),supplemental amino acids
(lysine, methionine, arginine).
Further Readings
Abdulla, M., Anderson, B., Evander, A., Lundquist, I,
Svensson, S. and Ihse,I. 1978. Digestion, 18:
86-92.
Anderson"R.A. 1998. Nutr. Rev., 56: 266-270.
Bush, B.M. (1985). In: Grunsell, C.S.G, Hill, F.W.G.
and Raw, M.E. (Eds). pp 189.-194.
Farthing,
M.I.G.1988.
Drug, 36 (Supplement4):80-90.
Guilford, W.G. 1996. In: Proc.:ACVIM, San Antonio,
'TX, pp. 50-51..
Hirschhorn, N. and OreenoughIII, W.B. 1991.
I.
Parenteral Enteral Nutr., 12: 104S.
Kameda, H., Abei, T. and Iber, F.L. 1986. Am.
I.
PhysioI., 214: 1090-1095.
Kripke, S.A, Fox, A.D., Berman, I.M.
et
al. (1987)
Surgery Forum, 38: 47-49.
Latshaw, D.L. 1991. Vet. Immunol. ImmunopathoI.,
30: 111-120.
Leib, M.S. (1991).
Canine and Feline Gastroenterology.
Philadelphia: WB Saunders pp 221-256.
Leiper, J.B. (1986), Proc, Nutrition Society, 45: 78A.
Lewis, L.D. 1989. Recueil-de-Medicine-veterenaire,
165: 665.
Markwell,
P.I.,
vanErk, W., Parkin, G.D., Sloth, C.J.
and Shantz-Christienson, T. 1990.
J.
Small
Anim. Pract., 31: 533-537.
Mason, E. 1970. Vet. Rec., 86: 612-616.
Maughan,
R.I.
and Leiper,
I.B.
1990. Clinical
Therapeutics, 12 (Supplement A): 63-72.
Nelson, RW., Stookey,
L.I.
and Kazacos, E. 1988.
I.
Vet. Intern. Med., 2: 133-137.
Pasupathy, K., Sahoo,
A.,
Kamra, D.N. and Pathak,
N.N. 2002. Indian
I
Anim. Nutr., 19: 359-
364.
Pasupathy, K., Sahoo, A. and Pathak, N.N. 2001. Arch.
Anim. Nutr., 55: 243-253.
..
supportive therapy in
\ antimibiotics/high
tipation (supports good
ipports during
a, arthritis
:rolemicldyslipidemic
nts
lese/overweight adults
diabetic, obese/
iroper ratio (1.3:1) and
D. In conditions like
, the protein content
minimum maintenance
otics like inulin and
euticals (glucosamine,
cal conditions are
u
surgery, wounds or
s or bones, etc. The
ision for complete and
iphasis on pre and
z. liquid preparations,
:based diet, nutrient
enzyme preparations,
d E), added minerals
Paterson, S. 1995.
I.
Small Anim. Pract., 36: 529-534.
Ralston, S.L. 1985.
I.
Equine Vet. Sci., 5: 336.
Roediger, W.E.W. (1982). In:
Colon and Nutrition.
Goebbel,H. and Kaspar,
H.
(Eds), MTP Press,
Lancaster. pp 1l-26.
Sahoo, A. 2002. Compendium, IVth Biennial
, Conference
&
Exhibition, WBUAFS, Kolkata,
pp 69-83.
Scanlan N. 2001. Altern Med Rev.,
6
(Suppl):
S24-
37.
Scrimshow, N.S., Taylor, C.E.'and Hordan,
I.E. 1968.
Interactions of Nutrition and Infection. WHO,
Geneva.
Senior, D.F., Kelly, N.C. and Wills,
I.M.
1996. In:
Manual of Companion Animal Nutrition and
Feeding.
N.C. Kelles (Ed.). pp. 188-197.
Settle, R.G. (1988). Scientific Am., 264: 16-22.
Simmons, R.D. and Bywater,
R.I.
(1991). Cont. Ed.,
13: 131-134.
Simpson,
I.W.
(1988). Vet. Pract.,
20: 5.
Simpson,I.W. 1998.
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Nutr., 128: 2717 S- 2722 S.
Simpson, K.W., Morton, D.B. and Batt, RM. (1989).
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50:
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Singh, R.K. 2005. Nutrient utilization and growth
performance of pups fed on essential oil
supplemented diet. M.V.Sc. Thesis, Indian
Veterinary Research Institute, Izatnagar, India
Swick, R.A. 1995. Zootrech. International, 18: 40-45.
Weibel E. W., Taylor C. R, Weber
I.,
Vock R., Roberts
T.
I.,
Hoppeler H. 1996.
I.
Exp. BioI., 199:
1699-1709.
Wolter, R 1990. Practique-Medicale and Chirurgicale-
de-I Animal-de-Compagnie, 25: 255.
Wood, P.D. 1996. Nutr. Rev., 54: Sl3I-Sl35.
Zenger, E. and Willard, M.D. (1989). Compo Anim.
Pract., 19: 6-11.
Zimmer,
I.F.
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R.W. Kirk (Ed.), IX W.B. Saunders,
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____________________________ 101
ResearchGate has not been able to resolve any citations for this publication.
Article
Chromium is an essential nutrient involved in the regulation of carbohydrate and lipid metabolism. Normal dietary intake of chromium in humans and farm animals is often suboptimal. In addition to its effects on glucose, insulin, and lipid metabolism, chromium has been reported to increase lean body mass and decrease percentage body fat, which may lead to weight loss in humans. The effects of chromium on body composition are controversial but are supported by animal studies, which increase their validity. A subject's response to chromium depends on his or her chromium status, diet consumed, type and amount of supplemental chromium, and study duration. There have been no confirmed negative effects of chromium in nutritional studies. Chromium is only a small part of the puzzle in the control of weight loss and body composition, and its effects, if present, will be small compared with those of exercise and a well-balanced diet.
Article
Serum and liver concentrations of zinc and copper were studied in the rat after ligation of the pancreatic duct. Ligation of the bile duct was done close to the duodenum and high up in the hilum of the liver. The bile flow was by-passed into the intestine via a plastic catheter. The surgical method used was found suitable for a study of moderate exocrine pancreatic insufficiency since significant--although markedly reduced--concentrations of amylase and trypsin were estimated in intestinal contents at sacrifice 19 weeks after the operation. The serum zinc level was unaffected by duct ligation except for a slight decrease after 2 weeks. Similarly zinc in whole blood was unaffected. The copper concentration in serum was, however, significantly enhanced during in first 10 weeks. The copper zinc ration was markedly increased in duct ligated rats during the whole period. Zinc and copper concentrations in liver tissue were significantly decreased after 19 weeks. The findings suggest that a decrease function of exocrine pancreas might induce a disturbed balance of zinc and copper in the rat.
  • M I G Farthing
Farthing, M.I.G.1988. Drug, 36 (Supplement4):80-90.
  • N Hirschhorn
  • W B Oreenoughiii
Hirschhorn, N. and OreenoughIII, W.B. 1991. I. Parenteral Enteral Nutr., 12: 104S.
  • H Kameda
  • T Abei
  • F L Iber
Kameda, H., Abei, T. and Iber, F.L. 1986. Am. I. PhysioI., 214: 1090-1095.
  • S A Kripke
  • A D Fox
  • I M Berman
Kripke, S.A, Fox, A.D., Berman, I.M. et al. (1987) Surgery Forum, 38: 47-49.
  • D L Latshaw
Latshaw, D.L. 1991. Vet. Immunol. ImmunopathoI., 30: 111-120.