Diabetes mellitus (DM) is a treatable condition that requires a committed effort by veterinarian and client. Due to many factors that affect the diabetic state, a pet’s changing condition, and variable response to therapy, management of DM is often complicated. Success requires understanding of current scientific evidence and sound clinical judgment. Each patient requires an individualized treatment plan, frequent reassessment, and modification of that plan based on the patient’s response. This document provides current recommendations for the diagnosis, treatment, and management of DM in dogs and cats.

Diabetes mellitus is a syndrome associated with protracted hyperglycemia due to loss or dysfunction of insulin secretion by pancreatic beta cells, diminished insulin sensitivity in tissues, or both. In the dog, beta-cell loss tends to be rapid and progressive, and is usually due to immune-mediated destruction, vacuolar degeneration, or pancreatitis.² Intact female dogs may be transiently or permanently diabetic due to the insulin-resistant effects of the diestrus phase. In the cat, loss or dysfunction of beta cells is the result of insulin resistance, islet amyloidosis, or chronic lymphoplasmacytic pancreatitis.³Studies have shown that diabetic cats have remission rates that have been reported to be variable (15–100%). Because remission can occur, cat owners may be advised that remission is a possibility when treated with combination of diet and insulin.^4,5

Risk factors for developing DM for both dogs and cats include insulin resistance caused by obesity, certain diseases (e.g., acromegaly and kidney disease in cats; hyperadrenocorticism [HAC], hypertriglyceridemia, and hypothyroidism in dogs; dental disease, systemic infection, pancreatitis, and pregnancy/diestrus in both dogs and cats), or medications (e.g., steroids, progestins, cyclosporine). Genetics is a suspected risk factor, and certain breeds of dogs (Australian terriers, beagles, Samoyeds, keeshonden) and cats (Burmese, especially in Australia and Europe) are more susceptible.^6,7 Researchers continue to redefine and reclassify the different etiologies responsible for the development of DM in dogs and cats.⁸ As different etiologies become better understood, treatment can be more specifically tailored to the individual patient. Treatment that is more specific to the underlying etiology will presumably lead to better control of clinical signs of DM and possibly increase remission rates.

Regardless of the underlying etiology, classic clinical signs of polyuria (PU), polydipsia (PD), polyphagia (PP), and weight loss result from protracted hyperglycemia and glucosuria. Increased fat mobilization leads to hepatic lipidosis, hepatomegaly, hypercholesterolemia, hypertriglyceridemia, and increased catabolism. Eventually, if left untreated or inadequately controlled, ketonemia, ketonuria, and ketoacidosis develop and result in progressive compromise of the patient’s health.

It is important to differentiate patients with clinical DM from those with transient hyperglycemia or mildly increased blood glucose (BG). The subgroup of patients with mildly elevated BG but without concurrent clinical signs associated with higher levels of hyperglycemia may require additional diagnostic and therapeutic measures but not insulin therapy. At this time, there is not a standard definition for subclinical DM in veterinary medicine or any validated testing to determine which patients are at risk for developing DM. In lieu of “subclinical DM,” the Task Force has elected to use the more descriptive terminology “patients at risk of developing DM,” or simply “at-risk patients” throughout the guidelines. As potential new etiologies emerge for overt or subclinical DM, they will be discussed in future guidelines or consensus statements.