Underlying causes of diabetes mellitus, a common endocrinopathy in dogs and cats, include chronic pancreatic inflammation,
pancreatic atrophy, and immune-mediated destruction of the insulin-producing beta cells. Chronic insulin resistance with subsequent
beta cell exhaustion and pancreatic amyloidosis are primarily described in cats.1 In dogs, diabetes mellitus is generally a permanent condition, although transient diabetes may occur in pregnant and diestrus
females. In cats, diabetes may go into remission, but recurrence is likely.2
A range of insulin choices and management strategies are available for our veterinary patients. Recently, a new type of insulin,
glargine, has become available, and many owners are now able to monitor blood glucose concentrations at home. This article
reviews these options and provides guidelines for starting therapy in stable, nonketotic dogs and cats.
Persistent fasting hyperglycemia is the hallmark of diabetes mellitus. In dogs, you can confidently diagnose diabetes mellitus
if a patient has a fasting serum glucose concentration > 200 mg/dl. As the threshold for glucose resorption from the glomerular
filtrate is 180 to 220 mg/dl, concurrent glycosuria will be present.1
Cats can become transiently hyperglycemic (serum glucose concentration > 300 mg/dl) when stressed, so a single elevated serum
glucose concentration, even with concurrent glycosuria, is not enough to diagnose diabetes mellitus. Supportive clinical signs
such as weight loss, polyuria, and polydipsia must be documented. In equivocal cases, measuring the serum fructosamine concentration
(which reflects serum glucose levels for the previous three weeks) may be necessary. Alternatively, diagnostic litter additives
(e.g. Glucotest—Nestlé Purina) can be used to document persistent glycosuria in the home environment. Unless a cat is ketoacidotic,
insulin therapy should not be started without clear evidence of persistent hyperglycemia.
Once diabetes mellitus has been confirmed, certain tests are indicated to direct appropriate therapy and to check for concurrent
disease. Many patients are presented to their veterinarian after many weeks of hyperglycemia, and it is often an acute complication,
such as pancreatitis or a urinary tract infection, that prompts the owner to seek help. Failure to recognize concurrent problems
will affect the patient's response to therapy and may ultimately affect the outcome.
It is essential to determine whether a new diabetic is ketotic. A routine urine dipstick test will readily identify acetone
and acetoacetate; the urine must be mixed with hydrogen peroxide to facilitate detection of beta-hydroxybutyrate, which is
often the most prevalent ketone body. In early ketosis, renal and respiratory compensation prevent substantial acidosis, but
these systems soon become overwhelmed, and dehydration and compromised tissue perfusion then exacerbate the situation. Once
diabetic ketoacidosis is established, aggressive in-hospital care becomes necessary, but this is beyond the scope of this
Because glucose is a nutrient source for microorganisms, many diabetic patients present for evaluation of bacterial urinary
tract infections. It is important to remember that severe polyuria may make it difficult to identify bacteria and white blood
cells on a urine sediment examination. A urine culture with antimicrobial sensitivity testing is always indicated, but start
appropriate antibiotics immediately if infection is suspected.
Serum chemistry profile
Concurrent problems, such as renal failure, pancreatitis, and hyperadrenocorticism, can profoundly affect a patient's response
to insulin. A serum chemistry profile is necessary to identify other diseases and to provide a baseline for future comparison.
Closely evaluate markers for dehydration, such as azotemia or hyperproteinemia, and provide fluid therapy if necessary. Serum
cholesterol and triglyceride concentrations may be elevated as a result of the diabetes but can also suggest concurrent thyroid
or adrenal dysfunction. The serum sodium concentration is often decreased in response to glucose-related hyperosmolality;
this hyponatremia does not need to be specifically addressed in an adequately hydrated patient. Total body stores of potassium
and phosphate are often low, despite normal serum concentrations. In dehydrated or anorectic patients, these parameters need
close monitoring, and supplementation is necessary to prevent precipitous decreases as insulin is introduced.
Complete blood count
A diabetic patient that seems otherwise healthy is expected to have normal complete blood count results. Anemia (which may
be masked by dehydration) or leukocytosis should prompt further investigation.