The Feline Diabetic

24 05 2011

The Feline Diabetic

Is your cat constantly at the water bowl?  Do you find yourself emptying out the litter box more than usual?  Has your can been eating well but is actually losing weight?  Then your cat may be suffering from diabetes mellitus.

A cat is traditionally throught to be a diabetic if they have a blood glucose level of over 171 mg/dL.  A single blood glucose above this level is not considered to be completely diagnostic since cats may exhibit stress induced hyperglycemia.  Simply put, this means that a cat may exhibit high glucose levels in the blood when stresses and what could be more stressful for a cat than visiting their local veterinarian and giving blood.  A study of the effects a bath had on blood glucose levels of cats found that the not so simple act of giving a bath to a cat elevated their individual blood glucose levels as much as 194 mg/dL.  These elevated blood glucose levels were seen for at least 90 minutes following the bath.

For cats that stress easily, persistent glucosuria may be used to demonstrate persistant levels of glucose in the urine.  Alternatively a Fructosamine level may be taken which is a reflection of the mean blood glucose levels over the preceding 1 to 3 weeks.  Low levels of blood protein (hypoproteinemia) and hyperthyroidism have been demonstrated to decrease the fructosamine levels reported.  Other biochemical abnormalities seen with diabetes mellitus include an increase in alanine aminotransferase and alkaline phosphatase and hypercholesterolemia (high cholesterole levels).

Variable levels of urine glucose are present in the diabetic cat.  The presence of ketones in the urine (Ketonuria) is important and may make it necessary to evaluate the pet for ketoacidosis.  The presence of protein in the urine (proteinuria) may be an indication of secondary bacterial infection in the bladder or kidneys or damage to the kidney as a consequence of the diabetes.  Pets with urinary tract infections, typically 13% of those diagnosed with diabetes, will also have red and/or white blood cells in the urine.  More than half of these cats with urinary tract infections do not exhibit clinical signs associated with such an infection.  The urine specific gravity is typically in the fixed specific gravity range of 1.010.  These levels may be confusing however since the presence of glucose in the urine may increase the urine specific gravity as measured by a refractometer.

Cats are an obligate carnivore (must eat meat), and are programmed in the wild to eat 10 to 20 small yet high-protein meals, e.g. mice throughout the day.

Cats cannot metabolize large glucose load, such as those obtained when eating carbohydrates.  Instead a constant supply of amino acids serve as the building blocks for gluroneogenesis.   Cats produce glucose continuously and therefore do not experience the post feeding (postprandial) surge glucose surge seen in most species.

Conversion to a low-carbohydrate and low fiber diet will reverse the glucoenemia in 68% of cases.  If a cat is stable with a blood glucose of less than 350 mg/dL, therapy may be started with diet alone.  Sometimes this can bring about remission without further medical treatment.

Weight loss will likely decrease the insulin requirements.  Typically a weight loss of 1 to 2% of the total body weight per week should be conducted.

Oral hypoglycemic agents, commonly used for type 2 diabetes in humans, are not effective for feline diabetics for several reasons including:  many cats are difficult to pill, adequate diabetic control cannot be achieved by their use alone, evidence that the use of some of these medications may worsen pancreatic amyloidosis in cats, side effects from the medications are common.

Despite the positive impact of dietary management most cats suffering from diabetes will require insulin either short or long-term.

References:

Rios, Lori and Cynthia Ward.  “Feline Diabetes Mellitus:  Diagnosis, Treatment, and Monitoring.  Compendium Continuing Education for Veterinarians.”  Vol. 30(12).  December 2008. Pp. 626-639.

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