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Clinical Suite: Feline Diabetes Mellitus

Andrew Bugbee, DVM, DACVIM, University of Georgia

Tracy Dowdy, CVPM, MRG Consulting

September 2014|Peer Reviewed

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Clinical Suite: Feline Diabetes Mellitus

Overview

Andrew C. Bugbee, DVM, DACVIM, Purdue University

Diabetes mellitus (DM) is a disease of relative or absolute insulin deficiency. Insulin is produced by pancreatic beta cells within specialized endocrine areas known as “islets of Langerhans” and is best known for its facilitation of glucose uptake into cells (in particular, within muscular tissue) for energy production. Insulin is also critically involved in handling multiple nutrients (eg, fats, proteins) and electrolytes.

Diabetes develops when the pancreatic beta cells produce insufficient insulin (ie, absolute deficiency) or when cells are unresponsive to insulin (ie, resistance, relative deficiency). The lack of insulin action elevates blood glucose concentration and impairs the metabolism of other nutrients.

Diabetes develops when the pancreatic beta cells produce insufficient insulin (ie, absolute deficiency) or when cells are unresponsive to insulin (ie, resistance, relative deficiency). The lack of insulin action elevates blood glucose concentration and impairs the metabolism of other nutrients.

Most diabetic cats (70% to 75%) are clinically insulin-dependent at diagnosis,1 meaning that their pancreatic beta cells are permanently unable to secrete enough insulin. These patients will require lifelong insulin injections. 

The remaining 25% to 30% have a form of DM similar to type 2 DM in humans.1 These patients initially have functional beta cells that produce insulin; however, many factors (eg, obesity, high-carbohydrate diet, sedentary lifestyle) are hypothesized to contribute to the development of peripheral insulin resistance. Over time, beta cells are damaged through mechanisms associated with hyperglycemia (eg, glucose toxicity), abnormal fat metabolism (eg, lipotoxicity), and reactive oxidative injury from inflammation. If dietary and insulin therapy are not instituted in a timely manner, the remaining beta cells will become nonfunctional and permanently lose their insulin-secreting ability.

Insulin dependence is far more common than long-term diabetic remission.

Insulin therapy may eventually be discontinued in some patients whose glycemic control is rapidly corrected with insulin and dietary therapy before all functional beta cells are lost (ie, the patient is in diabetic remission). However, although remission rates of up to 75% have been reported,2 in the author’s experience, insulin dependence is far more common than long-term diabetic remission.

Noninsulin therapies (eg, maintenance of ideal body weight; exercise; low-carbohydrate, high-protein diet) should be continued indefinitely for patients that achieve remission to minimize the chance for relapse and future insulin dependence. Unfortunately, relapse is common in these patients, and clients should be vigilant of clinical signs suggestive of diabetic recurrence.

References and Author Information

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

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