Diabetes mellitus (DM) is one of the two most common endocrine disorders in cats. While we tend to think of diabetes as a
disease entity, we should remember that it really is a heterogeneous group of disorders in which insulin production is reduced
or in which tissue cells are resistant to the effects of insulin, resulting in impaired glucose homeostasis. Regardless of
the causes, from a clinical perspective, diabetes mellitus can be challenging to diagnose and treat in the cat because of
this species' stress- induced hyperglycemia.
Insulin is secreted after a meal, to facilitate "tissue uptake, utilization and storage of glucose, fat and amino acids in
three primary tissues: liver, muscle and fat. With mild insulin deficiency, decreased transfer of ingested nutrients into
tissues causes mild to moderate hyperglycemia. Severe insulin deficiency not only hampers tissue uptake of ingested fuels,
but also results in marked glucose overproduction and excessive mobilization of the body's protein and fat stores. Marked
insulin deficiency, coupled with a relative or absolute glucagon excess, results in an increased delivery of fatty acids to
the liver and their subsequent oxidation to ketone bodies (beta-hydroxybutyrate, acetoacetate, and acetone), culminating in
the clinical state of ketoacidosis." In short, there is no insulin available to deliver the glucose into the cells, resulting
in cell starvation; polyphagia results with concurrent weight loss. Hyperglycemia results in glucose spilling into the urine
and drawing water with it. This causes polyuria and compensatory polydypsia.
Classification and differentiation between type 1 and type 2 diabetes
In human diabetes, Type 1 refers to the condition seen in people who are generally lean, young and prone to ketogenesis.
Type 2 DM usually occurs in the older human, who is often obese but is less prone to the development of ketoacidosis. Type
1 DM patients require insulin therapy, while Type 2 may be controlled, at least initially, with weight loss, diet and oral
In cats, the categorization is not as clear. Generally, diabetes is a disorder of the older, often overweight cat, more similar
to the Type 2 human patient. However, often by the time the diagnosis of diabetes is made, these cats are insulin dependent
although most are not prone to ketogenesis. In addition to these differences, cats may also develop diabetes secondary to
primary pancreatic disease, endocrinopathies (acromegaly or hyperadrenocorticism), or drug therapy (glucocorticoids and progestins).
In Type 1 DM, there is beta cell depletion, resulting in absolute insulin deficiency. In Type 2 DM, the problem is one of
insulin receptor and post receptor defects, causing impaired insulin uptake by tissues. This insulin resistance and associated
hyperglycemia, causes the beta cells to produce more insulin, thus this state is one of a relative insulin deficiency. Obese
cats appear to have a defect in insulin secretion along with a lower tissue sensitivity to insulin. Weight loss results in
an imrovement in tissue sensitivity, thus weight loss, is not only helpful, but also imperative in treatment.
Another important feature about diabetes in cats is that pancreatic islet amyloid deposits are believed to interfere with
insulin secretion, and that oral hypoglycemics (such as the sulfonylureas, glucatrol) may actually increase islet amyloid polypeptide (IAPP) deposition. IAPP is co-secreted with insulin. Islet amyloidosis occurs in 90% of humans
with Type 2 DM.
Risk factors include body weight > 7 kg, older age (> 10 years), male gender, neutered. Unlike in humans, DM does not predispose
cats to hypertension.
In the stressed patient, epinephrine release cause hyperglycemia and glucosuria. It is essential to differentiate between
this stress response and diabetes. This can be done by either verifying that the hyperglycemia and glucosuria are persistent
or request a fructosamine level be run on the previously collected sample. Fructosamine measures the protein bound glucose levels over the preceding
10 - 20 days. It can be affected by protein metabolism as well, hence hyperthyroidism, with more rapid muscle turnover, may
result in artificially lower fructosamine values.