While sometimes thought of as a disease entity, diabetes mellitus is a heterogeneous group of disorders in which insulin production
is reduced or tissue cells are resistant to the effects of insulin, resulting in impaired glucose homeostasis.
Table 1. Absolute or relative insulin deficiency levels
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In people, type I diabetes mellitus refers to the condition seen in individuals who are generally lean, young, and prone to
ketogenesis. Type II diabetes mellitus usually occurs in older people who are often obese but less prone to the development
of ketoacidosis. Type I diabetic patients require insulin therapy, whereas type II diabetics may be controlled—at least initially—with
weight loss, diet, and oral hypoglycemic agents. This is because in type I diabetes, beta cell depletion results in a decreased
insulin production and an absolute insulin deficiency. In type II diabetes, insulin receptor and postreceptor defects cause
impaired insulin uptake by tissues. This insulin resistance and associated hyperglycemia cause the beta cells to produce more
insulin; thus, this state is one of a relative insulin deficiency at the tissue level. Various levels of absolute or relative
insulin deficiency exist (see Table 1).
In cats, the categorization of diabetes is not as clear. Generally, diabetes is a disorder of older, often overweight cats
that are not prone to ketogenesis, more similar in signalment to type II diabetes in people. However, obese cats appear to
have a defect in insulin secretion along with lower tissue sensitivity to insulin.1,2 Weight loss of even 10% to 15% results in improved tissue sensitivity, but, often by the time of diagnosis, these cats require
treatment with insulin. Cats may also develop diabetes secondary to primary pancreatic disease, endocrinopathies (e.g., acromegaly, hyperadrenocorticism), or drug therapy (e.g., glucocorticoids, progestins). Risk factors for feline diabetes include weighing greater than 7 kg (15.4 lbs), not being
physically active, or being over 9 years old, a neutered male, or a Burmese.1,3
Complications of unregulated diabetes mellitus
In short, diabetes mellitus results in cell starvation in the presence of hyperglycemia. While cell starvation results in
polyphagia with concurrent weight loss, hyperglycemia results in polyuria and compensatory polydipsia due to glucose spilling
into the urine and osmotically drawing water with it.
Table 2. Complications of unregulated diabetes mellitus
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Some diabetic cats are affected by a polyneuropathy that can result in functional, structural, and biochemical defects in
the peripheral motor and sensory nerves of the limbs. It generally affects the pelvic limbs more than the thoracic limbs.4 The pathology in nerve biopsies from 12 cats with spontaneously occurring diabetes included damage to Schwann cells, demyelination
of nerve fibers, thin myelin sheaths, and an overall decrease in myelinated fiber density.5 See Table 2 for a list of functional changes associated with unregulated feline diabetes. Different than in people, diabetes does not
predispose cats to hypertension, hypertensive retinopathy, or proteinuria.6
A recent study investigated associations among clinical signs, serum biochemical markers, and urinalysis results and found
that, "Many of the cats with urinary tract infections had no clinical signs of lower urinary tract disease or changes in their
laboratory values indicative of infection. Therefore, a urinalysis alone should not be used to exclude urinary tract infections
in these cats."7 I recommend a urine culture for this purpose. An interesting report of pulmonary changes (such as congestion, edema, pneumonia,
fibrosis, mineralization, and neoplasia) in diabetic cats without clinical signs of respiratory disease also shows the need
for greater vigilance in monitoring the respiratory system.8
