The role of nutrition in the management of cats with diabetes mellitus
Abstract
As a species, cats have a different nutrient profile requirement to humans and dogs from whom, historically, nutritional information has been extrapolated. The greater understanding of the requirements of both the species and the disease process of diabetes mellitus means that it is now possible to recommend a specific nutrient profile and formulation to help nutritionally support cats with this prevalent disease. A strong link between obesity and feline diabetes mellitus means that weight management is an important part of managing the patient through the disease process and achieving good glycaemic control. Medical treatment with insulin remains the cornerstone of therapy for feline diabetes mellitus; however adaptation of the diet and providing consistency in the type and timings of food will also help in the long-term management process. Specific considerations should be made in relation to protein and carbohydrate content of the diet, not only to the overall quantity in the diet, but also the source and digestibility. It is recommended that cats should remain on a diet specifically formulated for the management of feline diabetes mellitus life-long (unless concurrent disease suggests otherwise), even if the patient enters remission.
Diabetes mellitus is a common but serious condition in cats resulting from an absolute or relative insulin deficiency. The majority of diabetic dogs are suffering from an absolute insulin deficiency caused by destruction of the pancreatic beta cells. In contrast, cats are more likely to have a relative insulin deficiency, resulting from insulin resistance, usually caused by obesity (Figure 1). Over time though, these cats can develop an absolute insulin deficiency as a result of progressive disruption of normal beta cell function.
Regardless of the aetiology, insufficient insulin action results in a persistent hyperglycaemia. As blood glucose levels exceed the renal threshold, glucose is lost in the urine causing an osmotic polyuria and compensatory polydipsia. At the same time, the majority of body cells are less able to take up glucose, amino acids and fatty acids and convert them to their storage forms, resulting in polyphagia and weight loss. Other symptoms frequently contribute to the clinical picture including short- and long-term complications such as diabetic ketoacidosis and diabetic neuropathy.
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