Consultant on Call ENDOCRINOLOGY

Peer Reviewed
Alice Huang, VMD, DACVIM
Purdue University

Feline
Diabetes
Mellitus

PROFILE Signalment
● Burmese cats are overrepresented in Australia,
Definition New Zealand, and the UK.1,2
● Diabetes mellitus (DM), classified as type I or ● Most cats are diagnosed ≥7 years of age.3,4
type II, is a treatable condition caused by ● Males are more frequently affected.4
complete or relative insulin deficiency.
● Most diabetic cats have type II, characterized Causes
by b-cell dysfunction and peripheral insulin ● Multiple causes of peripheral insulin resistance
resistance. have been identified (see Causes of Insulin
◗ Type I diabetes, uncommon in cats, results Resistance in Cats, next page):
from immunologic destruction of b cells, ◗ Obesity.
leading to complete insulin insufficiency. ◗ Concurrent disease.
● Reversion to noninsulin-dependent diabetic ◗ Diet.
mellitus (NIDDM) state is more likely with ◗ Drugs.
type II diabetes, as some causes of peripheral ● Direct b-cell loss can be secondary to chronic
insulin resistance are reversible and islet cell amyloid deposition or pancreatitis but does
dysfunction is variable in these cases. not cause DM; instead, conditions that lead to
b-cell loss may increase susceptibility to DM
Systems when faced with peripheral insulin resistance.
● In uncomplicated DM, urinary and immune
systems are most commonly affected. Risk Factors
● Long-standing, uncontrolled DM can lead to ● Risk factors for DM include obesity, male
complications (eg, polyneuropathy, hepatic gender, advanced age, and renal transplanta-
disease [hepatic lipidosis], bacterial infec- tion.3-5
tions).

Prevalence CONTINUES
● Up to 1% of cats in the United States and
Australia are affected.

DM = diabetes mellitus, NIDDM = noninsulin-dependent diabetes mellitus

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 Consultant on Call CONTINUED

Pathophysiology fructosamine measurement.

● Insulin deficiency results in hyperglycemia by ■ Normal serum fructosamine is 200–360

causing uninhibited hepatic glucose produc- µmol/L.

tion, impaired glucose tissue entry, and accel- ■ Diabetic levels are frequently >400

erated protein and lipid catabolism. µmol/L.

● Persistent hyperglycemia results in glycosuria ● For evaluation of persistent glycosuria, owners
when the renal tubular threshold for glucose may collect urine for glucose strip testing or
excretion exceeds 200–300 mg/dL in cats. use Glucotest (glucotest.com) flakes in litter
● Ultimately, endothelial damage, immunosup- box.
pression, and glucose toxicity (ie, negative
effects of chronic hyperglycemia) occur. Differential Diagnosis
● Glucose toxicity initially suppresses insulin ● Hyperthyroidism, chronic kidney disease, and
secretion (reversible), but eventually can cause exocrine pancreatic insufficiency can result in
permanent b-cell loss, thereby perpetuating classic complaints (eg, polyuria, polydipsia,
CAUSES OF INSULIN diabetic disease. polyphagia, weight loss).
RESISTANCE IN ● Increased proteolysis can lead to muscle wast- ● Stress hyperglycemia must be considered in a
CATS ing and poor wound healing. hyperglycemic cat.
● As accelerated lipid catabolism persists, hepatic ● Concurrent diseases (eg, pancreatitis, renal fail-
● Obesity
lipidosis develops; ketoacidosis can occur sec- ure, infection) may complicate the diagnosis.
● Chronic pancreatitis
ondary to enhanced ketone body production.
● Bacterial infection
Laboratory Findings
● Kidney disease
Signs ● Mild anemia.
● Hyperthyroidism
History ● Hypercholesterolemia.
● Heart disease
● Patients with DM may have a history of ● Hypertriglyceridemia.
● Neoplasia
polyuria, polydipsia, polyphagia, weight loss, ● Mild increases in serum alanine transaminase
● Hyperadrenocorticism
lethargy, lack of grooming, and/or plantigrade (ALT) and alkaline phosphatase (ALP).
● Acromegaly
posture. ● Less common findings:
● Glucocorticoid or
◗ Trace to small amounts of ketones in urine.
progestogen
Physical Examination ◗ Evidence of urinary tract disease (pyuria,
administration
● Lackluster coat. hematuria, bacteriuria) on urinalysis.
● Obese despite history of weight loss. ◗ Nonspecific hepatic changes seen via
● Hepatomegaly. abdominal imaging.
● Signs of polyneuropathy (eg, plantigrade
posture, pelvic limb weakness). Postmortem Findings
● Findings related to concurrent disease or ● Hepatic lipidosis.
diabetic ketoacidosis (DKA). ● Pancreatic amyloid deposits.
● Concurrent disease.

DIAGNOSIS
TREATMENT
Definitive Diagnosis
● Based on clinical signs, history, and documen- Inpatient or Outpatient
tation of persistent hyperglycemia and glyco- ● Healthy diabetics ± minimal ketonuria can be
suria. managed on outpatient basis.
◗ Stress hyperglycemia can complicate diag- ● Hospitalization may be required with DKA or
nosis, suggesting consideration of serum concurrent disease.

ALP = alkaline phosphatase, ALT = alanine transaminase, DKA = diabetic ketoacidosis, DM = diabetes mellitus, NIDDM = noninsulin-
dependent diabetes mellitus

22 .................................................................................................................................................................NAVC Clinician’s Brief / October 2012 / Consultant on Call

Nutritional Aspects Client Education
● Dietary therapy may minimize postprandial ● Treatment is lifelong; owners should be pre-
blood glucose fluctuations. pared for complications or remissions.
● Diets should be palatable to ensure predictable ● At-home insulin therapy, dietary manage-
consumption. ment, and careful monitoring are cornerstones
● A consistent feeding schedule is more impor- of successful management.
tant than timing between insulin administra- ◗ Insulin administration.
tion. ◗ Insulin storage. A consistent
◗ Owners may feed q12h, at time of insulin ◗ Syringe sizes and use (U-40 vs U-100). feeding schedule
administration, or small amounts through- ● Weight reduction (if necessary) and consistent is more important
out the day. diet and feeding schedule facilitate glycemic
than timing
● The ideal dietary composition is debatable, as control.
low-carbohydrate/high-protein and high- between insulin
fiber/low-fat (and occasionally adult-mainte- administration.
nance) diets can result in good glycemic MEDICATIONS
control when used with insulin.6
◗ Low-carbohydrate diets result in higher Drugs/Fluids
remission rates.7,8 ● Short-acting insulin (eg, regular insulin) is
◗ Both diets can induce remission. primarily used in the hospital for clinically ill
● Dietary glycemic control is not different in diabetics or DKA cases, as increased potency
insulin-dependent cats. increases risk for hypoglycemia.
● Overweight cats require a weight-reduction ● Long-acting insulin, the mainstay of therapy,
program, as obesity is a reversible cause of should be administered immediately after
insulin resistance. diagnosis.
● Compared with dry foods, canned foods are ● Common insulin choices for cats are human
generally preferred, as they typically have a recombinant types:
lower carbohydrate content. ◗ Protamine zinc insulin (PZI) (ProZinc,
prozinc.us).11
Alternative Therapy ■ Only insulin FDA approved for cats.

● Few insulin alternatives are available. ■ U-40 syringe.

● Although most diabetic cats are insulin- ◗ Insulin glargine (Lantus, lantus.com).12
dependent, there is higher NIDDM incidence ■ In conjunction with a low-

in cats than dogs. carbohydrate/high-protein diet, may

● Oral hypoglycemic agents may be considered comparatively increase likelihood for dia-
for diabetic cats; however, studies evaluating betic remission.12
their efficacy are sparse. ■ U-100 syringe.

◗ Neutral protamine Hagedorn (NPH)

Clinical Remission insulin (duration short in cats).
● Up to 60% of cats enter diabetic remission ■ U-100 syringe.

with insulin and dietary therapy. ◗ Lente insulin (Vetsulin, vetsulin.com) is

◗ Remission may not be permanent (median, currently unavailable.
11 months).9 ● PZI and glargine result in similar glycemic
◗ Approximately 30% of cats in remission will control and can induce remission.10
revert to a diabetic state and require reinsti- ● Insulin should be administered q12h rather
tution of insulin therapy.9,10 than q24h, as duration of effect is often
◗ Remission rates increase in cases with good unpredictable and shorter than expected in cats.
glycemic control within 6 months of diag- ● Hypoglycemia can occur with insulin therapy.
nosis.9
CONTINUES

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Consultant on Call CONTINUED

FOLLOW-UP
Tx AT A GLANCE
Patient Monitoring
● Long-acting insulin should be admin- Two Dietary Options
● Clients should monitor for changes:
istered immediately after diagnosis. ● Low-carbohydrate/high-protein diet.
◗ Polyuria.
● Insulin should be administered q12h ● High-fiber/low-fat diet.
◗ Polydipsia.
rather than q24h.
◗ Appetite. Two Medical Options
● Concurrent dietary and medical
◗ Weight. ● PZI (0.25 Units/kg SC q12h after a
therapy is often best.
◗ Hypoglycemia (eg, disorientation, meal).
wobbliness, tremors, seizures). ● Insulin glargine (0.25 Units/kg SC
◗ Signs of concurrent disease (eg, q12h after a meal).
pollakiuria, stranguria, hematuria,
anorexia, vomiting, skin infections,
weakness). stress hyperglycemia than clinic- Prognosis
generated curves.13,14 ● Fair with diligent care and monitor-
Complications ◗ Advantage of at-home glucose ing.
● Iatrogenic hypoglycemia. monitoring includes the ability to ● Can be stabilized with appropriate
● DKA and severe electrolyte abnor- frequently monitor cats that are treatment, although diabetic remis-
malities (uncontrolled diabetics). difficult to regulate. sion may result in a waxing/waning
◗ Can be fatal, particularly in pres- ● Once well-controlled, BGCs and/or course of disease.
ence of severe pancreatitis. fructosamine may be performed q3– ● Dependent on owner commitment,
● Polyneuropathy (from chronic hyper- 6mo or more, based on owner obser- ease of glycemic control, and possible
glycemia) frequently resolves with vations (eg, changes in polyuria, concurrent diseases.
good glycemic control. polydipsia, appetite, weight). ● Many cats can do well for months to
● Urine cultures should be performed years with diligent care.
Future Follow-up regularly (eg, q3–6mo) regardless of
● Twelve-hour blood glucose curves whether the urinalysis suggests infec- Prevention
(BGCs) should be performed q10– tion.15 ● Minimizing circumstances for insulin
14days from each insulin dose adjust- resistance (eg, obesity, inactivity).
ment until patient appears healthy ◗ Not all obese cats become diabetic,
and blood glucose is relatively con- IN GENERAL and many diabetic cats are of nor-
trolled. mal size.
◗ BGC measurements should be Relative Cost
100–300 mg/dL. ● Diagnostic workup for uncomplicated Future Considerations
● Fructosamine measurements: DM: $$ ● More studies to evaluate the impact
◗ For cats experiencing stress hyper- ● Treatment and follow-up care for of diet on diabetic control are neces-
glycemia. uncomplicated DM: $$–$$$ monthly sary.
◗ For cats with good glucose control ● Diagnostic workup for complicated ● Remission studies directly comparing
based on the initial BGC. DM: $$$$–$$$$$ insulin types would be valuable.
◗ For fractious cats in which BGCs ● Treatment and follow-up care for ● Given the changing insulin market,
are difficult to perform. complicated DM: $$$–$$$$$ continued investigation into alterna-
● Owners can be taught to perform tive insulin types for diabetic cats is
at-home BGCs (AlphaTrak, important.
Cost Key
alphatrakmeter.com).
◗ May minimize stress hyperglycemia. $ = up to $100 $$$$ = $501–$1000 See Aids & Resources, back page, for
■ However, at-home BGCs may $$ = $101–$250 $$$$$ = more than references & suggested reading.
not represent significantly lower $$$ = $251–$500 $1000

BGC = blood glucose curve, DKA = diabetic ketoacidosis, DM = diabetes mellitus, NIDDM = noninsulin-dependent diabetes mellitus, NPH = neutral protamine Hagedorn,
PZI = protamine zinc insulin

24 .................................................................................................................................................................NAVC Clinician’s Brief / October 2012 / Consultant on Call