Vol. 21, No.
8 August 1999
CE Refereed Peer Review
FOCAL POINT
★ Managing canine diabetes
mellitus requires a consistent
feeding plan and food that
minimizes postprandial
fluctuations in blood glucose
concentrations.
KEY FACTS
■ Dietary modification, in
conjunction with insulin therapy,
is an effective adjunct in the
control of diabetes mellitus in
dogs.
■ The single most effective dietary
change is to include moderate
amounts of insoluble and/or
soluble dietary fiber.
■ For most dogs, feeding at the
daily energy requirement for ideal
body weight in conjunction with
adequate pharmacologic control
of diabetes mellitus will maintain
a desired body weight.
■ For obese animals, a conservative
weight-loss protocol should be
instituted after primary medical
problems have been stabilized.
20TH ANNIVERSARY
Nutritional
Management of
Diabetic Dogs
Angell Memorial Animal Hospital, Boston, Massachusetts
Rebecca L. Remillard, PhD, DVM
ABSTRACT: The goals of nutritional therapy in the management of diabetes mellitus are to ap-
proach physiologic blood glucose levels, match postprandial glucose absorption with insulin
therapy, attain and maintain optimal body weight, reduce the likelihood of diabetic complica-
tions, and address other concurrent disease conditions amenable to dietary therapy. Managing
diabetes mellitus requires a consistent feeding plan and food that minimizes postprandial fluc-
tuations in blood glucose concentrations. Because fiber modulates blood glucose levels and
favors optimum body weight maintenance, the single most effective dietary tool in the medical
management of diabetic dogs is feeding a diet containing insoluble or soluble fiber at 8% to
18% on a dry-matter basis.
D
iabetes mellitus (DM) in dogs is a complex disorder caused by a multi-
tude of factors; it is characterized by an insulin deficiency or dysfunc-
tion that results in hyperglycemia and abnormal lipid and protein metab-
olism. In 1985, a revised classification system divided diabetes in humans into
four categories: insulin-dependent diabetes mellitus (IDDM or type 1), non–
insulin-dependent diabetes mellitus (NIDDM or type 2), gestational diabetes,
and secondary diabetes.1 DM in dogs is broadly classified as IDDM or NIDDM
based on the need for insulin.1 –3
When approximately 75% of pancreatic beta cells have been destroyed in pa-
tients, the ability to maintain normal blood glucose level is decreased.4 IDDM is
characterized by low blood insulin levels, and therefore the patient is dependent
on an exogenous insulin source. Immune-mediated insulitis may play a role in
development of IDDM in dogs because beta-cell–specific antibodies have been
identified in approximately 50% of diabetic dogs studied.5
Non–insulin-dependent DM is classically characterized by insulin resistance
in peripheral tissues and/or dysfunctional beta cells.6 NIDDM is less common
in dogs than in cats and not well described but still accounts for approximately
one in five cases of diabetes.7,8 NIDDM has been referred to as a relative insulin
deficiency because blood insulin levels may be increased, decreased, or normal.
Patients with NIDDM are not completely dependent on administration of ex-
ogenous insulin to maintain glucose homeostasis. The number and intrinsic ac-
tivity of glucose transporters are decreased in humans and rats with NIDDM.9 The
pathophysiologic defect in NIDDM more likely involves depletion of glucose
Small Animal/Exotics 20TH ANNIVERSARY
transporters and/or a dysfunctional receptor/post-
receptor intracellular signaling event resulting from trans-
lational suppression of the transporter genes.10–12 In
dogs, NIDDM appears to be associated with obesity
and possibly a subsequent down-regulation of peripher-
al insulin receptors similar to that noted in humans.13
Some authors consider the pathogenesis and clinical
picture of IDDM and NIDDM to be different,1 where-
as others report that patients may initially appear to
have one type but either progress to the other type or
alternate between the two through the course of the
disease.3 The cause is probably multifactorial; genetics,
immune-mediated disease, obesity, inflammatory/infec-
tious conditions, exogenous drugs, concurrent disease,
and pancreatic beta-cell degeneration have been sug-
gested. Regardless of pathophysiology, most diabetic
dogs should be considered to have IDDM and treated
with insulin and dietary management unless there is a
strong indication that the diabetes is secondary.3
Dietary recommendations cannot be made based on
research alone because of the paucity of well-designed
studies using diabetic dogs. Therefore the state of the
art in making dietary recommendations is based on re-
search in normal and diabetic dogs, extrapolations from
other species, and simple clinical experience.
PATIENT ASSESSMENT
Dogs diagnosed with DM may be of any age and sex
but are more commonly 4 to 14 years of age; females
are affected twice as often as are males. Breeds appar-
ently at higher risk include the keeshond, puli, cairn
terrier, miniature pinscher, and poodle.14 Obese dogs
have been shown to be glucose intolerant and hyperin-
sulinemic.15 Regardless of the etiology, therapy must be
directed at eliminating the clinical signs of hyper-
glycemia and preventing the development of chronic
secondary complications.
Dogs with DM are usually presented for examination
because of polyuria, polydipsia, polyphagia, weight loss,
and diminished activity and thus have fasting hyper-
glycemia and glycosuria.3 Weight loss in the face of
polyphagia, the hallmark of DM, occurs as the disease
progresses. Weight loss is not always synonymous with
being underweight; an obese dog could have a history
of losing weight but still be overweight at the time of
presentation, which is true for most diabetic dogs. Ad-
ditional physical findings may include lethargy, hep-
atomegaly, cataracts, and dehydration.16 Other disease
conditions (e.g., infection, hypokalemia, hypomagne-
semia, renal failure, pancreatitis) or concurrent use of
drugs that decrease insulin secretion or cause insulin re-
sistance may precipitate a diabetic ketoacidotic state.17
The clinical expression of DM may not be apparent to
AT-RISK BREEDS ■ PRESENTING SIGNS ■ BODY CONDITION SCORES ■ OBESITY
Compendium August 1999
an owner until the patient becomes ketoacidotic.
Body condition scores (BCSs) for diabetic dogs range
from emaciated (BCS = 1) to obese (BCS = 9) depend-
ing on the severity and duration of disease; most dia-
betic dogs, however, have a BCS greater than 5.18 BCSs
provide estimates of total body fat composition (r2 =
.90a) via the palpation of subcutaneous fat stores at spe-
cific anatomic sites; thus this method is still useful
when patients have diseases associated with muscle
wasting.19 Many diabetic dogs are obese, and therefore
attainment of an ideal weight (BCS = 5) is an early
goal. Studies in obese dogs suggest that obesity causes
insulin resistance that may be resolved with weight
loss.15,20,21 As a dog loses weight, insulin requirements
may decrease.22
A small number of diabetic patients with a history of
maintaining optimal weight or being overweight will
have lost weight as the disease progressed and could be
underweight at the time of diagnosis. Underweight dia-
betic dogs may regain weight with insulin therapy as
cells, once again in the presence of insulin, metabolize
serum glucose and fat (through improved lipoprotein li-
pase activity). The feeding plan for underweight dogs
should include increased caloric intake in the form of fat
as well as increased fiber. Adding vegetable oil or cooked
animal fatb to the diet and feeding meals frequently may
improve body weight (BW) in addition to providing
better glycemic control. In clinical experience at Angell
Memorial Animal Hospital, however, most of these un-
derweight dogs do not attain normal weight; continue
to be difficult to control; and have some other compli-
cation, usually one that includes the pancreas (exocrine
insufficiency and/or cancer).
KEY NUTRITIONAL FACTORS
Key nutritional factors emphasize food-related issues
that markedly affect the management of a disease. The
consequences of an absolute or relative insulin deficien-
cy are a constant catabolic state with increased hepatic
glucose output; decreased tissue utilization of glucose;
and concurrent increases in glycogenolysis, lipolysis,
and proteolysis. Therefore key nutritional factors for
managing diabetic pets include specific dietary nutri-
ents (nutrients of concern), food type and digestibility,
and a feeding schedule (see Current Feeding Recom-
mendations and Diet Characteristics Helpful in Man-
aging Diabetic Dogs). These factors help to successfully
aThis
indicates that 90% of the variation in BCSs can be ex-
plained by differences in total body fat content.
bOne tablespoon of fat is approximately 150 kcal; feeding a
dog 1 tbsp of fat per 30 lb BW per day increases caloric intake
by approximately 15%. The added fat should be divided
among the meals fed.
Compendium August 1999
manage diabetic dogs when the
primary disease is controlled with
insulin or other pharmacologic
treatments. The goals of nutri-
tional therapy are to approach
physiologic blood glucose levels,
match postprandial glucose ab-
sorption with insulin therapy, at-
tain and maintain optimal BW,
reduce the likelihood of diabetic
complications, and address other
concurrent disease conditions
that are amenable to dietary ther-
apy. Caloric intake, nutrient
composition of the diet, form of
the food, feeding schedule, and
control of concurrent disease
must be considered in planning
the dietary management of dia-
betes.2 3
Nutrients of Concern
Nutrients of concern, in de-
creasing order of importance, are
water, carbohydrate (sugar, fiber),
energy, fat, protein, and micro-
nutrients (minerals and vitamins).
A diabetic dog’s current diet
should be evaluated in terms of
these nutrients and then com-
pared with recommendations for
diabetic dogs. If key nutrients in
the current food(s) do not match
the recommended levels, chang-
ing to a more appropriate food is
indicated.
Water
When glucose is present in the
urine, an osmotic diuresis occurs
and water loss via urination in-
creases. Ad libitum potable water
is recommended and is usually
accomplished by providing ad li-
bitum access to water (e.g., hav-
ing several water bowls in differ-
ent places available at all times).
Carbohydrate
Sugar. Commonly used sources
of carbohydrate in dog foods in-
clude barley, corn, rice, wheat,
oats, and sorghum. These ingre-
GOALS OF NUTRITIONAL THERAPY ■ OSMOTIC DIURESIS ■ DIETARY GUIDELINES
20TH ANNIVERSARY Small Animal/Exotics
Current Feeding Recommendations and
Diet Characteristics Helpful in Managing Diabetic Dogs
Nutrients of Concern
Water Available ad libitum
Carbohydrate Referred to as nitrogen-free extract; approximately 50%
(DMB)
Fiber 8%–18% crude fiber (DMB; insoluble and/or soluble fiber)
Energy intake A reasonable initial estimate of daily energy intake is 1.6 ×
RER for neutered dogs and 1.8 × RER for intact dogs; RER
is approximately 15 kcal per lb BW
Fat 6%–10% (DMB) when dog is at optimal weight or needs
to lose weight; fat contents of 10%–20% can be used if
weight gain is indicated; no recommendations can be
made at this time concerning omega-3 fatty acid content
Protein 18%–25% (DMB) with a protein digestibility >85%
Minerals Foods formulated as complete and balanced according to
AAFCO recommendations for adult maintenance provide
an adequate supply of macro- and microminerals
Vitamins Foods designed as complete and balanced according to
AAFCO recommendations for adult maintenance provide
an adequate supply of fat- and water-soluble vitamins;
antioxidant formulations of vitamin C, α-tocopherol, and
beta-carotene may be given
Food Type
Form A dry diet is preferred over a canned diet, and a canned
diet over soft–moist foods
Formulation Fixed; products designed to be sold through veterinarians
usually have fixed formulations (i.e., the ingredient
formulation does not vary from unit to unit)
Digestibility Diets containing dry-matter digestibility coefficients of
70%–80% are desirable; highly digestible (i.e., >90%)
and poorly digestible (i.e., <70%) diets should be avoided
unless warranted in dogs that have difficulty maintaining
optimal body weight
Feeding schedule Most owners can feed two equal-sized meals daily: one
at the time of insulin injection and the other 8–10 hr later
AAFCO = Association of American Feed Control Officials; BW = body weight; DMB = dry-
matter basis; RER = resting energy requirement.
Small Animal/Exotics 20TH ANNIVERSARY
dients are primarily composed of starch (more than
60% starch), although they differ in their nutrient anal-
ysis and availability of protein, fat, minerals, and vita-
mins. Glucose from dietary starch digestion is the most
potent secretagogue of insulin; diets that result in more
manageable postprandial blood glucose increases are
recommended for diabetics. In humans, glycemic index
and dietary carbohydrate concentrations explain almost
90% of blood glucose and insulin responses to a
meal.24,25
Glycemic index classifies foods based on their blood
glucose–raising potential; this valid and potentially use-
ful concept is also deceptively complex.2 6 There are a
number of unresolved problems and unanswered ques-
tions (particularly of a mixed-carbohydrate meal). Pre-
dicting glycemic response is no longer based on the dif-
ference between a simple versus a complex carbohydrate
but depends on a variety of such factors as the carbohy-
drate type, the matrix in which the carbohydrate is
found, type of processing the carbohydrate has under-
gone, and total amount of carbohydrate consumed.2 7
For example, extrusion is the process of cooking a grain
to gelatinize the starches, which increases digestibility.
In one study, dog foods containing 67% extruded corn,
rice, barley, or oats had small intestinal and total gas-
trointestinal tract starch digestibility coefficients above
98%.28 When these grains were fed whole to dogs, how-
ever, their dry-matter digestibilities were lower and dif-
fered according to the level of fiber in the grain (rice is
the most digestible, oats are the least).
The glycemic and insulin responses of normal dogs
to diets containing the same amount of different carbo-
hydrate types (corn, wheat, barley, rice, and sorghum)
have been investigated.29 Sorghum produced the lowest
postprandial glucose response; however, there was an
unexplained, disproportionate response between glu-
cose and insulin levels (i.e., sorghum produced the low-
est blood glucose levels but did not produce the lowest
insulin levels). Starches that resist intestinal hydrolysis,
called resistant starches, have resulted in significant re-
ductions in postprandial glycemia and insulinemia in
humans and may prove useful in diabetic pets.30,31 Di-
etary carbohydrate content is not commonly reported;
it is referred to as nitrogen-free extract and is a calculat-
ed, not a determined, value. The dog foods successfully
used in managing canine diabetes contain 45% to 55%
nitrogen-free extracton a dry-matter basis (DMB).
Fiber. The amount of crude fiber in the various types
of commercial dog food ranges from 0.4% to 25% on a
DMB; estimates of crude fiber in grocery-brand dog
foods (i.e., foods generally available in grocery or pet
stores as opposed to therapeutic diets) average 3.7% for
dry (range, 1.5% to 10.9%) and 1.5% for canned
GLYCEMIC INDEX ■ NITROGEN-FREE EXTRACT ■ SOLUBLE VS. INSOLUBLE FIBER
Compendium August 1999
(range, 0.1% to 4.2%) products. However, the analytic
crude fiber method required by the Association of
American Feed Control Officials (AAFCO)32 excludes
variable fractions of insoluble (hemicellulose, cellulose,
lignin) and soluble (pectins, gums, resistance starches)
fibers and therefore underestimates the fiber content.
Total dietary fiber as described for human foods is
probably a more meaningful estimate when comparing
different fiber levels across foods, but this information
is rarely available for pet foods.33
Fiber types are differentiated by their physiologic
characteristics and in vivo systemic effects. Soluble
fibers (pectins and gums) are soluble in water and in-
crease the viscosity of the intestinal contents, thereby
delaying gastric emptying and slowing intestinal transit
times. The increased viscosity is also thought to slow
glucose absorption.34 Viscosity markedly affects the ex-
tent of intraluminal mixing of digesta and digestive en-
zymes, which can shift absorption sites and subsequent-
ly the rate of nutrients entering the bloodstream.35
Soluble fibers are fermented in the colon to short-chain
fatty acids (SCFAs; acetic, propionic, and butyric acid).
Butyrate appears to be used by colonocytes, whereas pro-
pionic and acetic acid are absorbed. These properties re-
sult in an acidic colonic pH and increased colonic bacteri-
al numbers, colonic mucosal mass, fecal dry matter, and
water content.36 Soluble fiber incorporated into foods at
5%, 10%, or 13% DMB did decrease postprandial blood
glucose and insulin levels in normal dogs.37,38 The clinical
significance of feeding soluble fiber to diabetic patients
may be limited to a particular type because only some
gums—not all soluble fiber types—have been reported to
lower fasting and postprandial blood glucose levels.
Insoluble fiber is primarily composed of cellulose and
structural polysaccharides, which are relatively resistant
to digestion, ferment slowly, and increase intestinal
residue and transit times.39–41 Insoluble fibers reportedly
have less of an effect on gastric emptying, lowering of
blood glucose, or colonic microflora compared with
soluble fibers.34 However, there is evidence to support
the hypothesis that feeding foods with moderate
amounts of insoluble fiber substituted for starch has a
positive effect on glycemic control in dogs. Diabetic
dogs eating foods with more than 50% digestible car-
bohydrate and 10% to 15% DMB cellulose had signifi-
cantly better glycemic control than did dogs fed the
same food without the insoluble fiber.42,43
Fiber helps modulate postprandial blood glucose lev-
els by several plausible mechanisms: delaying gastric
emptying, slowing carbohydrate digestion and
monosaccharide absorption from the small bowel, alter-
ing gastrointestinal hormones (which in turn affects
nutrient metabolism), and producing SCFAs that may
Compendium August 1999 20TH ANNIVERSARY
directly affect hepatic glucose metabolism. 44–47 Al-
though the mechanism is not precisely known, long-
term consumption of guar gum has been shown to in-
crease plasma insulin levels and improve glucose
homeostasis in humans.48,49
In vitro, propionate has been shown to inhibit hepat-
ic glucose production and stimulate glucose utilization
via glycolysis.48 SCFAs administered parenterally to rats
(and possibly those absorbed from the large bowel) in-
crease the concentration of plasma proglucagon-derived
peptides (GLP-1).50,51 GLP-1 is a potent insulin secreta-
gogue and an inhibitor of glucagon secretion and gas-
tric acid secretion and emptying.52,53 Normal dogs fed a
highly fermentable fiber (8% DMB) for 14 days had
significantly lower blood glucose but greater GLP-1
and insulin concentrations compared with dogs fed the
same concentration of a less fermentable fiber source.54
An ideal fiber content and type have not yet been es-
tablished; based on a limited number of published ca-
nine studies and personal clinical experience, a moderate
amount (8% to 18% crude fiber DMB) of insoluble
fiber evidently improves glucose management in dia-
betic dogs. Results of some published studies in dogs
and other species indicate that the same level of soluble
fiber may be equally effective.54,55
Energy
Before making feeding recommendations to owners,
it is important to emphasize that a diabetic animal’s
clinical response to dietary manipulation depends on
the level of control achieved over the primary disease
process as well as the presence or absence of concurrent
disease.17 For example, ideal BW may not be achieved if
there is poor control of the diabetes or if such compli-
cations as hypothyroidism or hyperadrenocorticism are
present. Owner education and consistent reevaluations
are important tools in adjusting the food, dose, and
feeding plan.
Basal metabolic rate may actually be decreased in un-
regulated diabetic patients because of decreased tri-
iodothyronine (T3) levels. The thyroxine (T4)-deiodi-
nase system that converts T4 to T3 is directly responsive
to blood insulin levels (i.e., as blood insulin levels de-
crease, T3 levels decrease). Basal metabolic rate is direct-
ly responsive to T3 concentrations and therefore bal-
ances energy expenditure, presumably with energy
(glucose) intake. T4 levels may be decreased, and cau-
tion should be taken not to interpret a low T4 level at
this time as being diagnostic of hypothyroidism (euthy-
roid sick syndrome).
For most animals within the ideal BCS range (4 to
6), feeding at the daily maintenance energy require-
ment (DER) in conjunction with adequate control of
GLP-1 ■ BASAL METABOLIC RATE ■ LIPID DERANGEMENTS ■ OMEGA-3 FATTY ACIDS
Small Animal/Exotics
DM should effectively maintain a desired BW. It is best
to initially calculate DER as a multiple of resting ener-
gy requirement (RER) based on the standard formulas
for normal animals. A reasonable initial estimate of
DER is 1.6 × RER for neutered dogs and 1.8 × RER
for intact dogs (RER is 70 × [BW in kg]0.75, or 15
kcal/lb BW).56 Patients should be reevaluated monthly
and food amounts adjusted as indicated by body condi-
tion and weight.
After medical problems have been stabilized, a con-
servative weight-loss protocol may need to be instituted
for overweight animals. Frequent monitoring and read-
justment should be the norm rather than the exception
in weight-loss programs for animals with such concur-
rent diseases as DM. A weekly loss of 1% to 4% of
weight is considered safe, although it may take several
months to a year to achieve an ideal weight in severely
obese animals.57,58
Fat
In diabetic dogs, abnormalities in lipid metabolism
are manifested as increased serum concentrations of
triglycerides, cholesterol, lipoproteins, chylomicrons,
and free fatty acids. Lipid derangements can occur for
several reasons but appear to be related to decreased in-
sulin levels; most serum lipid values improve with in-
sulin and dietary therapy (decreased fat, increased
fiber).3 Cardiovascular disease accounts for the majority
of deaths in humans with diabetes; canine patients,
however, are more likely to suffer from pancreatitis as-
sociated with persistent hyperlipidemia.59–61 Although
diets high in fiber (10% to 25% DMB) have decreased
overall dry-matter digestibilities, fat digestibility re-
mains above 90% when the fiber source is powdered
cellulose.39,62 Therefore feeding a lower-fat (12% or less
DMB), high-fiber diet is recommended to minimize
the risk of pancreatitis, control some aspects of hyper-
lipidemia (chylomicrons), and reduce overall caloric in-
take to favor weight loss or maintenance.
Major initial benefits reported with omega-3 fatty
acid supplementation in humans with DM included
markedly lower serum triglycerides; moderately de-
creased levels of cholesterol; a general increase in high-
density lipoprotein concentrations; and reduced blood
pressure, viscosity, and platelet aggregation. In addition,
all of these benefits potentially reduce the risk of
atherosclerosis, coronary heart disease, and stroke.34
However, some diabetic patients that consume omega-3
fatty acids have increased levels of blood glucose, glyco-
hemoglobin, low-density lipoprotein, and cholesterol.63
Because there is little cardiovascular risk associated with
canine diabetes, the use of omega-3 fatty acids may not
be warranted given the potential loss of glycemic control.
Small Animal/Exotics 20TH ANNIVERSARY Compendium August 1999

Protein TABLE I
When insulin levels are low or ineffective, the body Balanced Generic Homemade Diet (1000 kcal/day)
“assumes” that blood glucose is low and begins to ca- for a 40-lb Adult Dog with Diabetesa
tabolize heart and skeletal muscle to supply amino acids
As-Fed Formulation
to gluconeogenesis as a substrate for the production of Ingredient Amount (g/day)b
“new glucose.” As insulin levels fall, serum glucagon in-
creases. Glucagon decreases protein synthesis and in- Rice (long-grain, white, cooked) 332
creases amino acid membrane transport, protein Chicken (dark meat, cooked) 202
catabolism, and amino acid conversion into glucose via Fiber (Fiber One Cereal®, General
gluconeogenesis. Studies completed in humans, rats, Mills, Inc, Minneapolis, MN)c 53
and dogs demonstrate that the catabolism of skeletal Vitamin/mineral supplement d
16 (1.5 tablets)
muscle is directly proportional to serum levels of amino Bonemeal 16
acids, insulin, and glucagon. It is therefore important ®
to provide protein of a quality and in a quantity that Salt (Morton’s Light Salt, 6
Morton International, a subsidiary
will meet the amino acid requirements of the diabetic of Rohm and Haas, Philadelphia, PA)
animal, which may have increased skeletal catabolism
and urinary losses of amino acids during periods of low Fat (corn oil) 5
insulin/high glucagon blood levels. Daily total 630
Protein quality is the quantity and ratio of the essen-
tial and nonessential amino acids and digestibility and Dry-Matter Analysis Compared
with AAFCO Allowances for Adult Dogs
metabolizability of dietary protein. Food for diabetic Nutrient AAFCO Homemade diet
dogs should contain approximately 18% to 25% pro-
tein DMB, preferably from an animal source and with Dry matter (%) ≥12 43
a true protein digestibility above 85%. Dietary protein Energy (kcal/100 g) 350 366
has been implicated in the pathogenesis of canine dia- Protein (%) 18 25
betic renal disease, and restricting protein has been rec- Fat (%) 5 10
ommended to retard the progression of the nephropa-
thy; however, there is currently very little scientific data Fiber (%) None 10
upon which to modify protein recommendations for Calcium (%) 0.60–2.5 1.6
human or canine diabetics.64 Phosphorus (%) 0.50–1.6 1.1
aFormulated using Mixit-Win, version 2.34, 1999, Agricul-
Micronutrients tural Software Consultants, Inc., San Diego, CA, and Food
Although high-fiber (approximately 10% DMB) diets Processor® Plus, Diet Analysis Software, version 5.03, 1990,
do decrease overall diet dry-matter digestibility and have ESHA Research, Inc., Salem, OR.
bApproximate conversions between grams and dry volumes: 1
been reported to inhibit the absorption of some ingested
tsp = 5 g, 1 tbsp = 15 g, 1 cup = 250 g. Owners should be en-
minerals, instances of clinically important deficiencies of couraged to use a dietary gram scale to weigh these foods con-
vitamins or minerals induced by dietary fiber have not sistently. All items should be mixed together in a blender to
been found in humans or dogs. In general, when a com- prevent dogs from picking out single food items. When a
plete and balanced diet is consumed in quantities suffi- homemade diet is fed, the patient should be examined by a
cient to maintain optimum BW, there is no need for ad- veterinarian regularly. Vitamin/mineral supplements should
not be cooked, heated, or stored with the food; instead, they
ditional vitamin or mineral supplementation. However, should be kept separate from the food and administered just
patients with uncontrolled diabetes, on weight-loss pro- before, during, or after a meal to ensure proper dosing. Over-
grams, or with other concurrent diseases are at greater all digestibility and availability of the vitamin and mineral
risk of developing a micronutrient imbalance when con- supplements are improved when using a United States Phar-
suming home-cooked foods (hamburger and rice) or macopoeia (USP)–labeled product and when the product is in
the small intestine along with a meal composed of proteins,
single-item diets (e.g., eating just baby food or just fats, and carbohydrates.
chicken). Patients with poor appetites should be fed a c To increase fiber content, Post® 100% Bran™ (Kraft Foods

specifically formulated homemade recipe using ingredi-
ents that dogs will consistently consume and be given a
vitamin–mineral supplement known to be in proper
balance with the recipe (Table I).
Macrominerals. Increased urine output associated
with DM may increase obligatory loss of such elec-
Inc, Northfield, IL) can be used; to decrease fiber content,
Kellogg’s® All Bran® (Kellogg Company, Battle Creek, MI)
can be used.
d Theragran M ® (Mead Johnson and Co., Evansville, IN)
adult vitamin/mineral tablet.
AAFCO = Association of American Feed Control Officials.

GLUCONEOGENESIS ■ AMINO ACIDS ■ PROTEIN QUALITY AND DIGESTIBILITY

Compendium August 1999 20TH ANNIVERSARY
trolytes as sodium, potassium, chloride, calcium, and
phosphorus. A ketoacidotic diabetic may have whole-
body potassium and/or phosphorus deficits despite
normal or near-normal serum concentrations. The ke-
toacidotic state hastens the urinary loss of cations and
moves intracellular potassium into extracellular spaces.
Correction of acidosis with fluid, glucose, and insulin
can cause a precipitous decline in serum potassium.65
When serum calcium, potassium, or phosphate con-
centrations are difficult to maintain, measuring serum
magnesium and/or giving a loading dose of magnesium
and then providing supplemental magnesium should be
considered.66,67 Body magnesium stores are depleted via
an osmotic diuresis when hyperglycemia is poorly con-
trolled.68,69 In a magnesium-deficient patient, insulin
sensitivity may improve with supplementation but the
clinical signs of diabetes are not expected to resolve
with dietary repletion of magnesium alone. In general,
treatment of DM that results in glycemic control will
also correct macromineral deficiencies if the patient is
fed an adult maintenance food; however, excess dietary
phosphorus should be avoided in dogs with renal im-
pairment. Foods that meet AAFCO recommendations
for adult maintenance should supply adequate amounts
of macrominerals to compensate for the increased on-
going losses in controlled diabetic dogs.
Microminerals. Changes in micromineral nutrition
status associated with DM have been evaluated in
many species. Zinc plays a clear role in the synthesis,
storage, and secretion of insulin as well as the confor-
mational integrity of insulin. Whole-body stores of
zinc are usually low in diabetic humans and rats,
which affects the ability of islet cells to produce and se-
crete insulin and compounds the problem.70,71Diabetic
complications in humans are postulated to be related
to increased intracellular oxidants and free radical pro-
duction associated with decreases in intracellular zinc
and zinc-dependent antioxidant enzymes.72 The rela-
tionship among diabetes, insulin, and zinc is complex
with no clear cause and effect. The exact mechanisms
underlying altered zinc metabolism in diabetes have
not been adequately identified to make specific recom-
mendations.
Chromium (Cr) is an essential nutrient involved in
normal carbohydrate and lipid metabolism; require-
ments are postulated to increase with increased glucose
intolerance and diabetes. Cr supplementation improves
the glucose–insulin system in humans with hypo-
glycemia, hyperglycemia, diabetes, and hyperlipemia.73
Cr improves insulin binding, insulin receptor numbers,
insulin internalization, beta-cell sensitivity, and insulin
receptor enzymes with overall increases in insulin sensi-
tivity.74 Cr has no known enzymatic cofactor function,
KETOACIDOSIS ■ MAGNESIUM ■ ZINC ■ CHROMIUM
Small Animal/Exotics
but it may exist as a complex with nicotinic acid and
amino acids to form a “glucose tolerance factor” that
may aid insulin action. Chinese subjects with NIDDM
receiving 500 µg of Cr twice daily for 2 and 4 months
had improved fasting and 2-hour insulin values.75 How-
ever, these beneficial effects were associated with Cr in-
takes higher than the upper limit regarded as safe and
adequate in the United States.76 Because investigations
evaluating Cr supplementation in canine diabetics have
not been done, Cr supplementation is at best intriguing
based on information from other species and from nor-
mal dogs.
Substantiation of micromineral benefits in diabetics
has been confounding in most species.77 Improvement
may occur in malnourished patients receiving supple-
mentation, but no micromineral has been implicated in
the pathogenesis of DM. For example, manganese defi-
ciency has also been associated with alterations in in-
sulin secretion, carbohydrate and lipid metabolism, and
impaired glucose utilization; repletion of manganese in
deficient animals restores normal glucose tolerance and
improves insulin secretion, yet treatment of diabetic
subjects with manganese supplements had no impact
on glycemic control.78 Iron overload can cause glucose
intolerance due to pancreatic damage secondary to
hemochromatosis; however, iron status does not seem
to play a role in the pathogenesis of DM.79 Selenium
deficiency has also been associated with changes in glu-
cose tolerance or insulinlike activity but does not ap-
pear to play a role in the development or manifestation
of DM.68
In general, until proven otherwise, providing a food
with microminerals supplied according to AAFCO rec-
ommendations for an adult maintenance diet should
suffice for most patients with DM. For clients interest-
ed in antioxidant supplementation, an over-the-counter
human antioxidant formulationc (1 tablet/dog/day)
containing zinc, selenium, copper, and manganese is
well within the AAFCO allowances.
Vitamins. DM may increase or decrease vitamin bal-
ance, and, conversely, vitamin status may affect the de-
velopment and manifestations of DM. Much of the in-
vestigative work in this area is controversial and needs
clarification but probably involves protecting diabetics
cAntioxidant vitamin and mineral supplement containing
5000 IU vitamin A (as beta-carotene), 250 mg vitamin C,
200 IU vitamin E (as α-tocopherol), 7.5 mg zinc, 15 µg sele-
nium, 1 mg copper, and 1.5 mg manganese per tablet and
that carries a United States Pharmacopoeia (USP) label
(Spring Valey Antioxidant Vitamins, Pharmavite Corp., Mis-
sion Hill, CA). When recommending supplements, it is advis-
able to use products that carry the USP label, which indicates
a standardized formulation and ensures product disintegra-
tion, weight, purity, and potency.
Small Animal/Exotics 20TH ANNIVERSARY
from oxidative and free radical damage.80–82 Supplemen-
tation of vitamins C and E in humans at a rate of two
to 10 times the recommended daily allowance has been
suggested based on reported benefits in a few small tri-
als and because these supplements are generally regard-
ed as safe and affordable.83 For clients interested in an-
tioxidant supplementation, an over-the-counter human
antioxidant formulationc (1 tablet/dog/day) containing
beta-carotene, vitamin C, and α-tocopherol is well
within the AAFCO allowances.
In diabetic patients requiring intravenous fluid thera-
py to correct polyuria/polydipsia, water-soluble B-vita-
min supplements should be administered until hyper-
glycemia is controlled. Based on the daily vitamin
recommendations for adult dogs and the vitamin con-
centrations available in most solutions,d a recommend-
ed dose of 1 ml of B vitamins per 100 kcal DER will
meet, and in some cases exceed, a dog’s daily B-vitamin
(except for B12) requirements by severalfold. Most for-
merly healthy pets and humans, however, have hepatic
stores of B12 that are sufficient for 3 to 5 years.
Food Type and Digestibility
Soft–moist canine foods contain increased amounts
of humectants (e.g., corn syrup, sucrose, dextrose, cane
molasses, propylene glycol) to control water activity or
microbial growth and thus tend to have a hyper-
glycemic effect compared with canned or dry foods.84,85
Fructose in the form of sucrose (or high-fructose corn
syrup) may also be used as a humectant in commercial
semimoist foods. The potential effects of fructose in
foods for dogs with DM have not been evaluated.
Soft–moist foods also have the highest digestible energy
content because highly digestible carbohydrate sources
are used. Canned and dry foods tend to have lower dry-
matter and energy digestibilities and thus are preferred
for diabetic pets. Dry foods may have a slight advantage
over canned foods in controlling postprandial blood
glucose levels because dry foods empty from the stom-
ach more slowly than do canned foods; this is because
stomach contents must have a high water content be-
fore passing into the duodenum.
A fixed-, as opposed to an open-, formula diet is also
important in the overall successful management of dia-
betic dogs (Table II). “Open-formula diets” are typical of
those purchased from the grocery or pet store; the exact
ingredient formulation varies with market prices. Hence
glycemic index and postprandial glucose response will
vary as the formulation varies over time (e.g., unit to
dProduct containing 50 mg thiamin, 2 mg riboflavin, 100 mg
niacin, 2 mg pyridoxine, 10 mg pantothenic acid, and 0.4 µg
vitamin B12 per ml (B-Vitamin Complex, Butler Co., Colum-
bus, OH).
B-VITAMIN SUPPLEMENTS ■ HUMECTANTS ■ POSTPRANDIAL HYPERGLYCEMIA
Compendium August 1999
unit). A consistent “fixed” dietary formula eliminates this
source of variables and need not be examined when
glycemic control is poor or weight begins to change.
Highly digestible foods (i.e., those for which more
than 90% of dry matter is digested) make it more diffi-
cult to control serum glucose and should be avoided.
Diets containing 8% to 18% crude fiber (DMB) typi-
cally have dry-matter digestibility coefficients between
70% and 80%. Diets with less than 70% dry-matter
digestibility and low fat concentrations may not ade-
quately maintain optimal BW.
Dogs with difficult appetites that are fed homemade di-
ets, table food, vegetarian diets, or single-food items are at
greater risk of developing subclinical nutritional imbal-
ances. Foods designed, formulated, or prepared by owners
are rarely nutritionally complete, balanced, or consistent.
These patients may not only have protein–calorie malnu-
trition but are more likely to have several vitamin and
mineral imbalances concurrently (e.g., calcium and trace-
mineral deficiencies if no supplements are used and/or
subclinical vitamin A and D toxicities if liver is fed). A
well-formulated homemade diet (Table I) composed of a
meat and carbohydrate source readily consumed by the
patient is preferable to unpredictable consumption of var-
ious pet foods or single food items. Once a homemade
recipe is determined to be successful (i.e., consistently
made by the owner and consumed by the dog), insulin
dosage can be determined and adjusted.
Feeding Schedule
Because insulin is usually administered in conjunc-
tion with meals, feeding methods must complement
pharmacologic protocols. Feeding must be coordinated
with administration of exogenous insulin. The goal is
to have glucose slowly absorbed when insulin levels are
adequate, thereby minimizing postprandial hyper-
glycemia. Ideally, small meals fed at the time of insulin
administration and at regular intervals throughout the
day result in minimal hyperglycemia.24,86 Most owners
can feed two equal-sized meals daily: one at the time of
insulin injection and the other 8 to 10 hours later.22 For
animals with poor glycemic control, feeding should be
divided into three or more smaller meals to help main-
tain serum glucose concentrations within an acceptable
range.1,24,87 For example, patients receiving two insulin
injections daily and fed four equal small meals are fed a
meal with each insulin injection; the other two meals
are spaced equally throughout the day.
REASSESSMENT
Diabetes mellitus can be frustrating to manage. The
long-term side effects of poor glycemic control seen in
humans are uncommon in dogs.88 Clinical signs of im-
Small Animal/Exotics 20TH ANNIVERSARY Compendium August 1999

TABLE II
Approximate Nutrient Profiles of Foods Marketed for Canine Diabetics versus Average Grocery or Pet Store Brands
Crude
Diet Calories a Fat Protein) NFE b Fiber Fiber
Product Name Type (kcal) (DMB) (DMB) (DMB) (DMB) Type
Hill’s Prescription Dry 223 6.9 16.7 55.2 16.8 Insoluble
Diet® Canine w/d® Canned 347 12.0 16.5 53.9 13.5 Insoluble
(Hill’s Pet Nutrition,
Topeka, KS)

Eukanuba Veterinary Dry 253 8.0 29 48.3 2.9 Soluble

Diets® Nutritional
Weight Maintenance
Formula™ Glucose-
Control™ (The IAMS
Company, Dayton, OH)

CNM OM-Formula® Dry 276 6.0 22.8 48.6 15.2 Mixedc

Canine Diet (Pro-Visions, Canned 204 8.4 44.1 21.7 19.2 Mixedc
Pet Specialty Enterprises,
a division of Ralston
Purina Company,
St. Louis, MO)

IVD™ Select Care™ Dry 278 9.8 23.7 43.9 15.8 Mixedc
Canine Hifactor Formula Canned 282 7.9 24.7 47.6 15.9 Mixedc
(Innovative Veterinary
Diets, Newport, KY)

Waltham® Veterinary Dry 223 7.5 20.0 48.8 4.5 Mixedc

Diet Canine High
Fiber (Waltham Company,
Vernon, CA)

Grocery or pet Dry 350 11.8 23.6 52.8 3.7 Mixedc

store brands (n = 33) Canned 450 27.4 41.9 18.4 1.5 Mixedc
aCalories per 8 oz of dry food or 14 oz of canned food.
bNFE as a measure of carbohydrates.
cA mixture of soluble and insoluble types. Proper ratio for diabetics is unknown.

DMB = dry-matter basis; NFE = nitrogen-free extract.

provement are indicated by decreased water intake, uri-
nation, and food intake; achievement of weight goals;
and a generalized increased thriftiness. Conversely, per-
sistent polyuria, polydipsia, polyphagia, urinary tract
infections, and inability to achieve weight goals indi-
cate poor glycemic control. Response to treatment can
be assessed through careful questioning of the owner,
by performing a 12- to 24-hour blood glucose curve,
and by measuring glycosylated hemoglobin.89 Exercise
should be consistent from day to day because large vari-
ations in activity level may affect glycemic control.
Dietary changes (e.g., increasing or decreasing fiber
levels) or weight changes (intentional or unintentional)
may require adjustments in the insulin dosage to main-
tain glycemic control. It is also important to monitor
and control concurrent disease processes commonly as-
sociated with diabetes. Reassessment may take place ev-
ery 3 to 4 months if the animal is stable and reportedly
doing well; if the patient should become symptomatic,
however, reassessment may be necessary every 1 to 2
weeks until control has been reestablished. Regardless
of how frequent the recheck visits occur, the owner
should always be asked to describe the diet being con-
sumed by the dog and the feeding schedule.

EVALUATING TREATMENT RESPONSES ■ REASSESSMENT SCHEDULES

Compendium August 1999 20TH ANNIVERSARY
REFERENCES
1. Hoenig M: Pathophysiology of canine diabetes. Vet Clin
North Am Small Anim Pract 25(3):553–561, 1995.
2. Stogdale L: Definition of diabetes mellitus. Cornell Vet
76:156–174, 1986.
3. Feldman EC, Nelson RW: Diabetes mellitus, in Canine and
Feline Endocrinology and Reproduction, ed 2. Philadelphia,
WB Saunders Co, 1996, pp 339–391.
4. Porte D Jr: β-cells in type II diabetes mellitus. Diabetes
40:166–180, 1991.
5. Hoenig M, Dawe DL: A qualitative assay for beta cell anti-
bodies. Preliminary results in dogs with diabetes mellitus.
Vet Immunol Immunopathol 32:195–203, 1992.
6. Hales CN: The pathogenesis of NIDDM. Diabetologia
37(Suppl 2):S162–S168, 1994.
7. Robertson KA, Feldman EC, Polonsky K: Spontaneous dia-
betes mellitus in 24 dogs: Incidence of type I versus type II
disease (Abstr). Proc 7th ACVIM Forum:1036, 1989.
8. Feldman EC, Nelson RW: Diabetic ketoacidosis, in Canine
and Feline Endocrinology and Reproduction, ed 2. Philadel-
phia, WB Saunders Co, 1996, pp 392–421.
9. Garvey WT, Huecksteadt TP, Matthaei S, Olefsky JM: Role
of glucose transporters in the cellular insulin resistance of
type II non–insulin dependent diabetes mellitus. J Clin In-
vest 81:1528–1536, 1988.
10. Garvey WT, Maianu L, Huecksteadt TP, et al: Pretransla-
tional suppression of GLUT4 transports causes insulin resis-
tance in type II diabetes. J Clin Invest 87:1072–1081, 1991.
11. Eriksson J, Koranyi L, Bourey R, et al: Insulin resistance in
type 2 (non–insulin-dependent) diabetic patients and their
relatives is not associated with a defect in the expression of
the insulin-responsive glucose transporter (GLUT4) gene in
human skeletal muscle. Diabetologia 35:143–147, 1992.
12. DeFronzo RA: The triumvirate: Beta cell, muscle, liver. A
collusion responsible for NIDDM. Diabetes 37:667–687,
1988.
13. Hoenig KA: Pathophysiology of canine diabetes. Vet Clin
North Am Small Anim Pract 25:553–561, 1995.
14. Marmor M, Willeberg P, Glickman LT, et al: Epizootiologic
patterns of diabetes mellitus in dogs. Am J Vet Res 43(3):
465–470, 1982.
15. Mattheeuws D, Rottiers R, Baeyens D, Vermeulen A: Glu-
cose tolerance and insulin response in obese dogs. JAAHA
20:287–293, 1984.
16. Plotnick AN, Greco DS: Diagnosis of diabetes mellitus in
dogs and cats. Vet Clin North Am Small Anim Pract
25:563–570, 1995.
17. Kirk CA, Ford RB, Zicker SC, Nelson RW: Endocrine and
lipid disorders, in Hand MS, Thatcher CD, Remillard RL,
Roudebush P (eds): Small Animal Clinical Nutrition IV.
Topeka, KS, Mark Morris Institute, 1999 (in press).
18. Laflamme DP: Development and validation of a body con-
dition score system for dogs. Canine Pract 22(4):10–15,
1997.
19. Laflamme DP, Kealy RD, Schmidt DA: Estimation of body
fat by body condition score (Abstr). J Vet Intern Med 8:154,
1994.
20. Mattheeuws D, Rottiers MD, Kaneko JJ, Vermeulen A: Di-
abetes mellitus in dogs: Relationship of obesity to glucose
tolerance and insulin response. Am J Vet Res 45:98–103,
1984.
21. Wolfshiemer KJ, Kombert M, Jeansonne L: The effects of
caloric restriction on IV glucose tolerance tests in obese and
Small Animal/Exotics
non-obese beagle dogs (Abstr). J Vet Intern Med 7:113,
1993.
22. Armstrong PJ, Ihle SL: Nutritional management of hepatic
and endocrine diseases, in Ettinger SJ, Feldman EC (eds):
Textbook of Veterinary Medicine, ed 4. Philadelphia, WB
Saunders Co, 1995, pp 228–233.
23. Ihle SL: Nutritional therapy for diabetes mellitus. Vet Clin
North Am Small Anim Pract 25(3):585–597, 1995.
24. Jenkins DJA, Wolever TMS, Taylor RH, et al: Glycemic in-
dex of foods: A physiological basis for carbohydrate ex-
change. Am J Clin Nutr 34:362–366, 1981.
25. Wolever TMS, Bolognesi C: Prediction of glucose and in-
sulin responses of normal subjects after consuming mixed
meals varying in energy, protein, fat, carbohydrate and
glycemic index. J Nutr 126:2807–2812, 1996.
26. Wolever TMS: The glycemic index: Flogging a dead horse?
Diabetes Care 20(3):452– 456, 1997.
27. Wolever TMS, Miller JB: Sugars and blood glucose control.
Am J Clin Nutr 62:212s–227s, 1995.
28. Walker JA, Harmon DL, Gross KL: Evaluation of nutrient
utilization in the canine using the ileal cannulation tech-
nique. J Nutr 124:2672s–2676s, 1994.
29. Sunvold GD, Bouchard GF: The glycemic response to di-
etary starch, in Reinhart GA, Carey DP (eds): Recent Ad-
vances in Canine and Feline Nutrition, vol 2. Wilmington,
OH, Orange Frazer Press, 1998, pp 123–131.
30. Franz MJ, Horton ES, Bantle JP, et al: Nutrition principles
for the management of diabetes and related complications.
Diabetes Care 17:490–518, 1994.
31. Raben A, Tagliabue A, Christensen NJ, et al: Resistant
starch: The effect on postprandial glycemia, hormonal re-
sponse, and satiety. Am J Clin Nutr 60:544–551, 1994.
32. Association of American Feed Control Officials Publication. At-
lanta, AAFCO, 1999.
33. Harmon DL, Walker JA, Silvio JM, et al: Nutrient di-
gestibility in dogs fed fiber-containing diets. J Vet Clin Nutr
6(1):6–10, 1999.
34. Anderson JW, Geil PB: Nutritional management of diabetes
mellitus, in Shils ME, Olson JA, Shike M (eds): Modern Nu-
trition in Health and Disease, ed 8. Philadelphia, Lea &
Febiger, 1994, pp 1259–1286.
35. Gurr MI, Asp NG: Dietary Fibre. ILSI Europe Concise
Monograph Series. Brussels, International Life Science Insti-
tute Press, 1994, p 15.
36. Hallman JE, Moxley RA, Reinhart GA, et al. Cellulose, beet
pulp and pectin/gum arabic effects on canine colonic mi-
crostructure and histopathology. J Vet Clin Nutr 2(4):137–
142, 1995.
37. Diez M, Hornick JL, Baldwin P, Istasse L: Influence of a
blend of fructo-oligosaccharides and sugar beet fiber on nu-
trient digestibility and plasma metabolite concentrations in
healthy beagles. Am J Vet Res 58(11):1238–1242, 1997.
38. Diez M, Hornick JL, Baldwin P, et al: The influence of sug-
ar beet fibre, guar gum and inulin on nutrient digestibility,
water consumption and plasma metabolites in healthy beagle
dogs. Res Vet Sci 64(2):91–96, 1998.
39. Burrows CF, Kronfeld DS, Banta CA, Merritt AM: Effects
of fiber on digestibility and transit time in dogs. J Nutr
112:1726–1732, 1982.
40. Harvey RF, Pomare EW, Heaton KW: Effects of increased
dietary fiber on intestinal transit. Lancet 1:1278–1280,
1973.
41. Payler PK, Pomare EW, Heaton KW, Harvey RF: The effect
of wheat bran on intestinal transit. Gut 16:209–213, 1975.
Small Animal/Exotics 20TH ANNIVERSARY
42. Nelson RW, Duesberg CA, Ford SL, et al: Effect of dietary
insoluble fiber on control of glycemia in dogs with naturally
developing diabetes mellitus. JAVMA 212(3):380–386,
1998.
43. Graham PA, Maskell IE, Nash AS: Canned high fiber and
postprandial glycemia in dogs with naturally occurring dia-
betes mellitus. J Nutr 124:2712s–2715s, 1994.
44. Nuttall FQ: Dietary fiber in the management of diabetes.
Diabetes 42:503–508, 1993.
45. Morgan LM, Goulder TJ, Tsiolakis D, et al: The effect of
unabsorbable carbohydrate on gut hormones: Modification
of post-prandial GIP secretion by guar. Diabetologia 17:85–
89, 1979.
46. Anderson JW, Ziegler JA, Deakins DA, et al: Metabolic ef-
fects of high carbohydrate, high fiber diets for insulin depen-
dent diabetic individuals. Am J Clin Nutr 54:936–943,
1991.
47. Anderson JW, Bridges SR: Short chain fatty acid fermenta-
tion products of plant fiber affect glucose metabolism of iso-
lated rat hepatocytes. Proc Soc Exp Biol Med 177:372–376,
1984.
48. Aro A, Uusitupa M, Voutilainen E, et al: Improved diabetic
control and hypocholesterolaemia effect induced by long-
term dietary supplementation with guar gum in type 2 dia-
betes. Diabetologia 21:29–33, 1981.
49. Groop PH, Aro A, Stenman S, Goop L: Long-term effects of
guar gum in subjects with non–insulin-dependent diabetes
mellitus. Am J Clin Nutr 58:513–518, 1998.
50. Gee JM, Lee-Finglas W, Wortley GW, Johnson IT: Fer-
mentable carbohydrates elevate plasma enteroglucagon but
high viscosity is also necessary to stimulate small bowel mu-
cosal proliferation in rats. J Nutr 126:373–379, 1996.
51. Reimer RA, McBurney MI: Dietary fiber modulates intesti-
nal proglucagon mRNA and postprandial secretion of GLP-
1 and insulin in rats. Endocrinology 137:3948–3956, 1996.
52. Wettergran A, Schjoldager B, Mortensen PE, et al: Truncat-
ed GLP-1 inhibits gastric and pancreatic functions in man.
Dig Dis Sci 38:665–673, 1993.
53. Ahern B, Larsson H, Holst JJ: Effects of glucagon-like pep-
tide-1 on islet function and insulin sensitivity in non in-
sulin-dependent diabetes mellitus. J Clin Endocrin Metab
82:473–478, 1997.
54. McBurney MI, Massimino SP, Field CJ, et al: Modulation
of intestinal function and glucose homeostasis in dogs by the
ingestion of fermentable dietary fibers, in Reinhart GA,
Carey DP (eds): Recent Advances in Canine and Feline Nutri-
tion, vol 2. Wilmington, OH, Orange Frazer Press, 1998, pp
113–122.
55. Nelson RW, Ihle SL, Lewis LD, et al: Effects of dietary fiber
supplementation on glycemic control in dogs with alloxan
induced diabetes mellitus. Am J Vet Res 52(12):2060–2066,
1991.
56. Thatcher CD, Hand MS, Remillard RL: Small animal clini-
cal nutrition: An iterative process, in Hand MS, Thatcher
CD, Remillard RL, Roudebush P (eds): Small Animal Clini-
cal Nutrition IV. Topeka, KS, Mark Morris Institute, 1999
(in press).
57. Laflamme DP, Kuhlman G, Lawler DF: Evaluation of
weight loss protocols for dogs. JAAHA 33(3):253–259,
1997.
58. Laflamme DP, Kuhlman G, Lawler DF, et al: Obesity man-
agement in dogs. J Vet Clin Nutr 1(2):59–65, 1994.
59. Ford RB: Clinical management of lipemic patients. Com-
pend Contin Educ Pract Vet 18(10):1053–1065, 1996.
Compendium August 1999
60. Hall JA, Macy DW, Husted PW: Acute canine pancreatitis.
Compend Contin Educ Pract Vet 10(4):403–416, 1988.
61. Nair S, Pitchumoni CS: Diabetic ketoacidosis, hyperlipi-
demia, and acute pancreatitis: The enigmatic triangle. Am J
Gastroenterol 92(9):1560–1561, 1997.
62. Muir HE, Murray SM, Fahey GC, et al: Nutrient digestion
by ileal cannulated dogs as affected by dietary fiber with vari-
ous fermentation characteristics. J Anim Sci 74:1641–1648,
1996.
63. Nettleton JA: Omega-3 fatty acids in other diseases: Dia-
betes, in Omega-3 Fatty Acids and Health. New York, Chapman
& Hall, 1995, pp 287–298.
64. Chiarelli F, Verrotti A, Basciani F, et al: Controversies on
the prevention of diabetic nephropathy. J Pediat Endocrinol
Metab 11(Suppl 2):365–369, 1998.
65. MacIntire DK: Emergency therapy of diabetic crises: Insulin
overdose, diabetic ketoacidosis, and hyperosmolar coma. Vet
Clin North Am Small Anim Pract 25(3):639–650, 1995.
66. Khanna C, Lund EM, Raffe M, Armstrong PJ: Hypomagne-
semia in 188 dogs: A hospital population-based prevalence
study. J Vet Intern Med 12(4):304–309, 1998.
67. Dhupa N, Proulx J: Hypocalcemia and hypomagnesemia.
Vet Clin North Am Small Anim Pract 28(3):587–608, 1998.
68. Mooradian AD, Morley JE: Micronutrient status in diabetes
mellitus. Am J Clin Nutr 45:877–895, 1987.
69. Shils ME: Magnesium, in Ziegler EE, Filer LJ (eds): Present
Knowledge in Nutrition, ed 7. Washington, DC, Internation-
al Life Science Institute Press, 1996, pp 256–264.
70. Terres-Martos C, Navarro-Alarcon M, Martin-Lagos F, et al:
Serum zinc and copper concentrations and Cu/Zn ratios in
patients with hepatopathies or diabetes. J Trace Elements
Med Biol 12(1):44–49, 1998.
71. Aguilar MV, Laborda JM, Martinez-Para MC, et al: Effect
of diabetes on the tissue Zn/Cu ratio. J Trace Elements Med
Biol 12(3):155–158, 1998.
72. Chausmer AB: Zinc, insulin and diabetes. J Am Coll Nutr
17(2):109–115, 1998.
73. Mertz W: Chromium in human nutrition: A review. J Nutr
123(4):626–633, 1993.
74. Anderson RA: Chromium, glucose intolerance and diabetes.
J Am Coll Nutr 17(6):548–555, 1998.
75. Anderson RA: Nutritional factors influencing the glucose/in-
sulin system: Chromium. J Am Coll Nutr 16(5):404–410,
1997.
76. Anderson RA, Cheng N, Bryden NA, et al: Elevated intakes
of supplemental chromium improve glucose and insulin varia-
bles in individuals with type 2 diabetes. Diabetes 46(11):
1786–1791, 1997.
77. Mooradian AD, Morley JE: Micronutrient status in diabetes
mellitus. Am J Clin Nutr 45:877, 1987.
78. Keen CL, Zidenberg-Cherr S: Manganese, in Ziegler EE,
Filer LJ (eds): Present Knowledge in Nutrition, ed 7. Wash-
ington, DC, International Life Science Institute Press, 1996,
pp 334–343.
79. Barton JC, McDonnell SM, Adams PC, et al: Management
of hemochromatosis. Ann Intern Med 129(11):932–939,
1998.
80. Ford ES, Will JC, Bowman BA, Narayan KM: Diabetes
mellitus and serum carotenoids: Findings from the third na-
tional health and nutrition examination survey. Am J Epi-
demiol 149(20):168–176, 1999.
81. Bloomgarden ZT: Antioxidants and diabetes. Diabetes Care
20(4):670–673, 1997.
Small Animal/Exotics 20TH ANNIVERSARY
82. McDonagh M, Ali L, Kahn A, et al: Antioxidant status, ox-
idative stress and DNA damage in the etiology of malnutri-
tion related diabetes mellitus. Biochem Soc Trans 25(1):146s,
1997.
83. Cunningham JJ: Micronutrients as nutriceutical interven-
tions in diabetes mellitus. J Am Coll Nutr 17(1):7–10, 1998.
84. Cowell CS, Stout NP, Brinkmann MF, et al: Making com-
mercial pet foods, in Hand MS, Thatcher CD, Remillard
RL, Roudebush P (eds): Small Animal Clinical Nutrition IV.
Topeka, KS, Mark Morris Institute, 1999 (in press).
85. Holste LC, Nelson RW, Feldman EC, Bottoms GD: Effect
of dry, soft moist, and canned dog foods on postprandial
blood glucose and insulin concentrations in healthy dogs.
Am J Vet Res 50:984–989, 1989.
86. Nelson RW: Dietary therapy for diabetes mellitus. Compend
Contin Educ Pract Vet 10(12):1387–1392, 1988.
87. Bertelsen J, Christiansen C, Thomsen C, et al: Effect of meal
frequency on blood glucose, insulin, and free fatty acids in
Compendium August 1999
NIDDM subjects. Diabetes Care 16(1):4–7, 1993.
88. Wallace MS, Kirk CA: The diagnosis and treatment of in-
sulin-dependent and non–insulin dependent diabetes melli-
tus in the dog and cat. Probl Vet Med 2(4):573–590, 1990.
89. Elliott DA, Nelson RW, Feldman EC, Neal LA: Glycosylat-
ed hemoglobin concentrations in the blood of healthy dogs
and dogs with naturally developing diabetes mellitus, pan-
creatic beta-cell neoplasia, hyperadrenocorticism, and ane-
mia. JAVMA 211(6):723–727, 1997.
About the Author
Dr. Remillard is the staff nutritionist at the Angell Memorial
Animal Hospital, Boston, Massachusetts. She is a Diplo-
mate of the American College of Veterinary Nutrition.