Diabetes mellitus is one of the common endocrine diseases in dogs. Many cases of the disease in dogs are similar to human type 1 diabetes mellitus (about 50% of diabetic dogs in populations in which female dogs are routinely castrated). Autoimmune destruction of β-cells (cells producing insulin) of the pancreatic islets is observed in this type of the disease (Fleeman and Rand 2013; Reusch et al. 2010). Moreover, dogs with this type of the diabetes mellitus may also have other endocrine disorders (e.g. hypothyroidism or hypoadrenocorticism) with potential immune-mediated destruction of the endocrine glands (Reusch et al. 2010). The remaining cases of canine diabetes mellitus are secondary to other diseases which cause destruction of β-cells (pancreatitis or pancreatic neoplasia) or tissue insulin resistance (acromegaly or hyperadrenocorticism). Moreover, glucose intolerance caused by tissue insulin resistance may reveal during the diestrus phase of the estrous cycle, pregnancy, and may also be caused by steroid drug administration such as with glucocorticoids and progestins (Hess 2010; Rucinsky et al. 2010; Reusch et al. 2010). In some breeds such as Beagles, Pugs, Australian Terriers, Fox Terriers, Cairn Terriers, Tibetan Terriers, Yorkshire Terriers, Border Terriers, West Highland White Terriers, Standard and Miniature Schnauzers, Bichon Frises, Spitzes (Swedish Elkhounds or Keeshonds), Miniature and Toy Poodles, Samoyeds and Swedish Lapphunds there is higher risk for the development of this disease. However, different breed predisposition have been observed in various countries. Moreover, obesity and female gender (especially intact females) are considered as risk factors for diabetes mellitus in dogs (Fleeman and Rand 2013; Hess 2010; Nelson 2004; Reusch et al. 2010; Rucinsky et al. 2010).

In most cases the disease reveals in dogs older then 4-5 years old. Polyuria (excessive urine production), polydipsia (increased thirst), polyphagia (increased appetite) and weight loss are the first clinical signs of canine diabetes mellitus. They develop slowly (from weeks to months) and may be unnoticed by the owner of the dog or considered as irrelevant (Fleeman and Rand 2013; Nelson 2004). The clinical signs such as polyuria, polydipsia and polyphagia are compensatory mechanisms of the dog that contribute to glycemic (blood glucose level) control (Reusch et al. 2010). In many cases of uncomplicated diabetes mellitus no clinical signs other than the four symptoms mentioned above are observed. In some dogs, however, cataracts leading to blindness, hyperkeratosis and scales, and dry, matt hair coat are also present (Nelson 2004). In diabetic dogs any concurrent disease causing anorexia or vomiting may lead to development of ketoacidosis (uninhibited synthesis of ketone bodies in the liver) because of total lack of glycemic control (Fleeman and Rand 2013). Lethargy, dehydration, polyuria, polydipsia, anorexia and vomiting are the main clinical signs of diabetic ketoacidosis in dogs. Hyperglycemic hyperosmolar syndrome (characterized by severe hyperglycemia, hyperosmolality and dehydration but without significant or detectable ketonemia or ketonuria) is another but rare complication of canine diabetes mellitus with clinical signs similar to diabetic ketoacidosis (Hess 2013; O’Brien 2010).

Diagnosis is based on the clinical history, physical examination and demonstration of persistent fasting hyperglycemia (increased blood glucose concentration) and glycosuria (presence of the glucose in the urine). Acute stress-induced hyperglycemia is not so important in the differential diagnosis as in cats, and that’s why the measurement of blood fructosamine level is not required in dogs for diagnosis of canine diabetes mellitus (Nelson 2004; Reusch et al. 2010). Recognition of diabetes mellitus in dogs also requires diagnosis of other concurrent diseases which are almost always present in diabetic dogs (Nelson 2004), and in dogs with diabetic ketoacidosis almost always acute pancreatitis is present (Fleeman and Rand 2013).

The aim of the treatment is to limit or completely resolve clinical signs of the disease and prevent the life-threatening hypoglycemia (blood glucose concentration below reference interval) and development of complications such as diabetic ketoacidosis or hyperglycemic hyperosmolar syndrome. In contrast to the treatment of humans with diabetes mellitus, maintenance of euglycemia (normal blood glucose concentration) is not the aim of the therapy, and a glycemia level between 270 mg/dL and 90 mg/dL throughout the day is considered as an achievement of the main goals of the treatment i.e. resolving clinical signs and the assertion of good quality life (Reusch et al. 2010). Treatment of the other concurrent disease (or diseases) is also important for the successful therapy of canine diabetes mellitus (Nelson 2004). Insulin and nutritional therapy, daily physical exercise, reduction of body mass in overweight and obese dogs, and a break of treatment with diabetogenic drugs (e.g. glucocorticoids) if they were administered for any reasons, are the elements of the therapy of diabetic dogs (Reusch et al. 2010). It should also be emphasized that the owner of a diabetic dog should contribute in the monitoring of the level of glycemia and effects of the therapy by measuring body weight of the dog, daily water intake, blood and urinary glucose concentration (using a glucometer and urine dipsticks, respectively), the level of ketonuria (using ketone strips), and observe if the dog has clinical signs of hypoglycemia such as weakness, lethargy, ataxia (lack of coordination of muscle movements), local muscle fasciculation, tremors, seizures and coma (Fleeman and Rand 2013; Nelson 2004; Reusch et al. 2010).


Fleeman L., Rand J. Canine Diabetes Mellitus. In: Rand J., Behrend E.N., Gunn-Moore D. and Campbell-Ward M.L. (eds.) Clinical Endocrinology of Companion Animals. Wiley-Blackwell, Ames, 2013, pp. 143-168.

Hess R.S. Insulin Resistance in Dogs. Veterinary Clinics of North America: Small Animal Practice, 2010, 40, 309-316.

Hess R.S. Canine Diabetic Emergencies. In: Rand J., Behrend E.N., Gunn-Moore D. and Campbell-Ward M.L. (eds.) Clinical Endocrinology of Companion Animals. Wiley-Blackwell, Ames, 2013, pp. 201-208.

Nelson R.W. Canine diabetes mellitus. In: Mooney C.T. and Peterson M.E. (eds.) BSAVA Manual of Canine and Feline Endocrinology. 3 rd ed. British Small Animal Veterinary Association, Gloucester, 2004, pp. 112-128.

O’Brien M.A. Diabetic Emergencies in Small Animals. Veterinary Clinics of North America: Small Animal Practice, 2010, 40, 317-333.

Reusch C.E., Robben J.H., Kooistra H.S. Endocrine Pancreas. In: Rijnberk A. and Kooistra H.S. (eds.) Clinical Endocrinology of Dogs and Cats. An Illustrated Text. 2 nd ed. Schlütersche Verlagsgesellschaft, Hannover, 2010, pp. 155-185.

Rucinsky R., Cook A., Haley S., Nelson R., Zoran D.L., Poundstone M. AAHA Diabetes Management Guidelines for Dogs and Cats. Journal of the American Animal Hospital Association, 2010, 46, 215-224.

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