DIABETES MELLITUS IN CATS
Diabetes mellitus is one of the most common endocrine diseases in cats (mainly middle age and elderly cats). Most cases of the disease in cats are similar to human type 2 diabetes mellitus (80-95% of diabetic cats). This type of the disease is characterized in cats by tissue insulin resistance and decreased insulin secretion from β-cells (cells producing insulin) of the pancreatic islets (Rand and Marshall 2004; Reusch et al. 2010). The other types of diabetes mellitus occur rarely in cats. Secondary feline diabetes mellitus may be caused by:
- decrease of β-cell number as a result of pancreatitis or pancreas carcinoma
- induced tissue insulin resistance during the course of an other disease (acromegaly, hyperthyroidism, hyperadrenocorticism)
These disorders lead to a decrease of insulin secretion or increased tissue insulin resistance (Rand 2013; Rand and Marshall 2004).
Obesity, confinement indoors and physical inactivity, increasing age, neutered males, stress, high-fat and/or high-carbohydrate diet, hyperglycemia (chronic hyperglycemia leading to glucose toxicity and further loss of β-cells), and steroid drugs (especially long-acting) are risk factors for feline diabetes mellitus (Rand 2013; Rand and Marshall 2004; Rand and Marshall 2005; Rios and Ward 2008a). Moreover, Burmese cats, Maine coons, domestic longhair cats, Russian blue cats, and Siamese cats are breeds predisposed to diabetes mellitus (Rand 2013).
Polyuria (excessive urine production), polydipsia (increased thirst), polyphagia (increased appetite) and weight loss are the first clinical signs of diabetes mellitus in cats (Rand and Marshall 2004). These symptoms, except weight loss, are compensatory mechanisms of the cat that contribute to glycemic (blood glucose level) control (Reusch et al. 2010). In some cats however decreased appetite may be observed (Rand 2013). The owner of the cat may also observe inability to jump, progressive muscle weakness, and a lack of grooming resulting in an unkempt scurfy hair coat (Rand 2013; Rand and Marshall 2004). Untreated diabetes mellitus may lead to the development of diabetic ketoacidosis (uninhibited synthesis of ketone bodies in the liver) with clinical signs such as lethargy, dehydration, vomiting, tachypnea (rapid breathing), and an acetone smell to the breath (Rand and Marshall 2004). Weakness of the hind limbs and plantigrade posture (hocks touching the ground) are signs of diabetic peripheral neuropathy. Diabetes mellitus in cats (like in humans and dogs) may be also complicated by hyperglycemic hyperosmolar syndrome (characterized in the “Diabetes mellitus in dogs” bookmark) (O’Brien 2010).
Diagnosis in most cases is based on the clinical history, physical examination and demonstration of persistent fasting hyperglycemia (increased blood glucose concentration), glycosuria (presence of glucose in the urine) and ketonuria (presence of ketone bodies in the urine). Determination of the serum fructosamine concentration (serum protein irreversibly binding glucose reflecting the blood glucose concentration in the preceding 2-3 weeks) is useful in the differentiation between acute stress-induced hyperglycemia and persistent diabetic hyperglycemia (Rand 2013; Rand and Marshall 2004; Rios and Ward 2008b).
The goals of the treatment is to limit or completely resolve clinical signs of the disease and prevent life-threatening hypoglycemia (blood glucose concentration below reference interval), development of ketoacidosis, hyperglycemic hyperosmolar syndrome, chronic pancreatitis and diabetic peripheral neuropathy (O’Brien 2010; Rand and Marshall 2004; Rios and Ward 2008b). In newly diagnosed cats, achieving diabetic remission may be the goal of the therapy, however this is not possible in some cases (Rand 2013). In these cases, 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 achievement of the main goals of the treatment i.e. resolving clinical signs and the assertion of good quality life (Reusch et al. 2010). Insulin therapy, nutritional therapy and sometimes oral hypoglycemic drugs are used in the treatment of feline diabetes mellitus. It should also be emphasized that the owner of a diabetic cat should contribute in monitoring the level of glycemia and the effects of the therapy by measuring body weight of the cat, 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 cat has clinical signs of hypoglycemia such as weakness, lethargy, ataxia (lack of coordination of muscle movements), local muscle fasciculation, tremors, seizures and coma (Gunn-Moore and Simpson 2013; Rand 2013; Rand and Marshall 2004; Rios and Ward 2008b).
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Rand J.S., Marshall R.D. Diabetes Mellitus in Cats. Veterinary Clinics of North America: Small Animal Practice, 2005, 35, 211-224.
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.
Rios L., Ward C. Feline Diabetes Mellitus: Pathophysiology and Risk Factors. Compendium: Continuing Education for Veterinarians, 2008a, 30(12), E1-E7.
Rios L., Ward C. Feline diabetes mellitus: diagnosis, treatment, and monitoring. Compendium: Continuing Education for Veterinarians, 2008b, 30(12), 626-640.