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Vol. 10, Issue 5 (2021)

Diabetes mellitus in canines: A concise review

Harneet Kour and Sushma Chhabra
Diabetes mellitus constitutes a major global public health problem in humans, and is also of concern in dogs. Diabetes mellitus (DM), or diabetes, is a condition that occurs when there is deficiency or absolute lack of insulin secretion. Insulin deficiency diabetes (Type I) is caused either by genetic disposition or autoimmune destruction of insulin producing beta cells, pancreatitis/ exocrine pancreatic disease or secondary chronic hyperglycemia. Insulin resistance or Type 2 DM adds a peripheral insulin resistance to the non-functional islets of Langerhans, where in addition to metabolic abnormalities and ambient factors, other contributing diseases play an important role, for example, hyperadrenocorticism in dogs where excessive cortisol production antagonizes insulin activity and acromegaly. The main clinical manifestations are polydipsia, polyuria, polyphagia, weight loss and glucosuria. The etiology of diabetes mellitus is similar in dogs, cats and humans and is probably multifactorial. An essential aspect of successful DM management is to ensure that the owner of a diabetic dog is capable of administering insulin, recognizing the clinical signs of inadequately managed DM, and monitoring blood glucose levels at home. Insulin therapy is the mainstay of treatment for clinical DM. Various biomarkers not only reflect well glycemic control in hematologic disorder, but also represent postprandial glucose fluctuation. Complementary treatments, notably the use of encapsulated islets, gene therapy, and others, are being investigated for their therapeutic utility in the effective management of diabetes. This review will highlight our existing understanding of canine diabetes diagnosis and management.
Pages: 1574-1583  |  468 Views  270 Downloads

The Pharma Innovation Journal
How to cite this article:
Harneet Kour, Sushma Chhabra. Diabetes mellitus in canines: A concise review. Pharma Innovation 2021;10(5):1574-1583.
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