Dietary treatment of diabetes mellitus in dogs and cats (Sponsored by Nestle Purina)

Part of the 2009 Nestlé Purina Veterinary Symposium publication
source-image
Jun 01, 2009

Dietary therapy is the key to proper management of the diabetic cat and dog. Cats develop type II diabetes mellitus; therefore, feeding a low-carbohydrate, high-protein diet is essential for optimizing and utilizing the gluconeogenic capacity and obligate carnivore aspect of this species. In fact, cats fed low-carbohydrate, high-protein diets are more than twice as likely to go into remission and discontinue insulin injections compared with cats fed low-glycemic index, high-fiber diets. On the other hand, dogs develop type I diabetes mellitus which requires continuous insulin therapy. Dogs are more omnivorous than cats, and feeding a low-glycemic index, high-fiber diet is the key to good diabetic regulation. Dogs are susceptible to exocrine pancreatic disorders, such as pancreatitis and pancreatic insufficiency, therefore, fat content of the diet is important as well.

Feline diabetes mellitus

Diabetes mellitus is one of the most common feline endocrine diseases, affecting one in every 200 to 300 cats, or roughly 240,000 diagnosed cases per year.1 Despite the increasing frequency of the disease in the cat population, treatment of diabetic cats is frustrating and often associated with serious complications.

While insulin therapy and high-fiber diets have been mainstays of diabetes treatment, many diabetic cats experience complications associated with this therapy, such as hypoglycemia and progressive neuropathy.2-7 In a recent study, 10 percent of diabetic cats had documented hypoglycemia caused by an insulin overdose.6 Obese cats (>6 kg) were more likely to become hypoglycemic and lack autonomic warning signs of hypoglycemia. 6 Because of the difficulty in achieving adequate glycemic control with insulin therapy in cats, diabetic neuropathy is a common finding in diabetic cats. In one study, all diabetic cats suffered from subclinical forms of diabetic neuropathy as evidenced by impaired motor and sensory peripheral nerve conduction.7 In summary, current dietary and insulin therapy is associated with increased risk of severe hypoglycemia and often results in poorly-controlled diabetes and progressive neuropathy in cats with type II diabetes.

The latest clinical and histologic evidence suggests that type II diabetes is the most frequently occurring form of diabetes in cats and people.2-4 Type II diabetes in cats is characterized by an impaired ability to secrete insulin following a glucose stimulus and is caused by both a defect in pancreatic beta cells and by peripheral insulin resistance.2-4 The etiology of type II diabetes is undoubtedly multifactorial; obesity, genetics, diet, and islet amyloidosis are involved in the development of this form of diabetes in humans and cats.2-4 It is now recognized that the classic metabolic abnormalities found in type II diabetes—decreased insulin secretion and peripheral insulin resistance—may be consequences of abnormal amyloid production by pancreatic cells.2-4 Despite the prevalence of type II diabetes in cats, the advanced nature of their disease (amyloid deposition, glucose toxicity) often requires that insulin therapy be instituted.2

Unique mammal

The cat is an obligate carnivore and, as such, is unique among mammals in its insulin response to dietary carbohydrates, protein, and fat. The feline liver exhibits normal hexokinase activity, but glucokinase activity is virtually absent.8 Glucokinase converts glucose to glycogen for storage in the liver and is important in decreasing postprandial glucose. Normal cats are similar to people in that glucokinase levels drop precipitously with persistent hyperglycemia in people with type II diabeties. Amino acids, rather than glucose, are the signal for insulin release in cats.9 In fact, a recent publication demonstrated more effective assessment of insulin reserve in cats using the arginine response test rather than a glucose tolerance test.10

Another unusual aspect of feline metabolism is the increase in hepatic gluconeogenesis seen after a meal. Normal cats maintain essential glucose requirements from gluconeogenic precursors (e.g., amino acids) rather than from dietary carbohydrates. As a result, cats can maintain normal blood glucose concentrations even when deprived of food for more than 72 hours.9 Furthermore, feeding has very little effect on blood glucose concentrations in normal cats.2,11 In summary, the cat is uniquely adapted to a carnivorous diet and is not metabolically adapted to ingestion of excess carbohydrates.