Diabetes Mellitus in Dog and Cat

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Diabetes Mellitus in Dog and Cat

Diabetes Mellitus in Dog and Cat

                   Shveta Singh1,  Nripendra Singh2, Manisha Tyagi3, Lipika Sarma4

        

 1 Ph.D. Scholar, Department of Veterinary Medicine, C.V.Sc., Khanapara, Guwahati, AAU, Assam

 2Ph.D. Scholar, Department of Veterinary Anatomy, C.V.Sc. & A.H., OUAT, Bhubaneswar, Orrisa

 3Ph.D. Scholar, Division of Livestock Production Management, ICAR-NDRI Karnal, Haryana

4 Ph.D. Scholar, Department of Veterinary Physiology, C.V.Sc., Khanapara, Guwahati, AAU, Assam

A chronic disorder of carbohydrate metabolism due to relative or absolute insulin deficiency. Characterstics of Diabetes Mellitus are hyperglycemia, polyurea, polydypsia, polyphagia and glycosuria. Diabetes Mellitus is two types (a) Type 1 diabetes/ Insulin-Dependent diabetes (juvenile diabetes) caused by destruction of the beta cells of the pancreas. Dogs have only  type 1 diabetes (b) Type 2 (Insulin-independent) diabetes – Common in cats. Resistance to insulin caused by other medical conditions or by hormonal drugs. The condition is treatable, but if left untreated -can lead to cataract, neuropathy, malnutrition, ketoacidosis, dehydration, and death.

Predisposition and Susceptibility

Most cases of spontaneous diabetes occur in middle-aged dogs and cats. In dogs, females are affected twice as often as males.  Increased incidence in certain small breeds: Spitz, Samoyed Miniature Poodles, Dachshunds, Schnauzers, Cairn Terriers, Lhasa apso and Beagles etc. Obesity also predisposes to insulin resistance.

Etiology and Pathogenesis

Primary cause Sub-acute pancreatic necrosis (a) Pancreatic fibrosis (b) Chronic pancreatitis. Secondary cause- Autoimmmune disorder, hyperadrenocorticism, obesity, hypothyroidism, hepatitis & hypocalcemia. Pregnancy and diestrus predispose to Diabetes Mellitus.

Diabetes Mellitus caused by absolute/relative deficiency of insulin hormone (β-cells of islet of Langerhans). Reason of destruction of islet cells (due to immune destruction/severe pancreatitis in dogs or amyloidiosis in cats. Chronic relapsing pancreatitis with progressive loss of both exocrine and endocrine cells.

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In cats selective infiltration of islets with amyloid, glycogen, and collagen leads to destruction of islet cells and degenerative changes in β cells, is the most common pancreatic lesion. As cats age, a greater percentage of their islets contain amyloid.

In dogs with hyperadrenocorticism, and chronic administration of glucocorticoids or progestins. In dogs progesterone leads to release of growth harmone which causes hyperglycemia and insulin resistance. Obesity also predisposes to insulin resistance in both cats and dogs.

Hyperglucagonemia is the result of increased secretion of pancreatic glucagon, enteroglucagon, or both. Increased levels of glucagon mobilize hepatic stores of glucose and result in hyperglycemia and also cause ketoacidosis by stimulating oxidation of fatty acids in liver.

Infection with certain viruses in humans may be responsible for certain cases of rapidly developing diabetes mellitus.

In cats degenerative changes of α and β cells is common due to amyloid infiltration because cat can not process IAPP (Islets associated polypeptide) which is responsible for conversion to amyloid and leads to Diabetes type II.

Clinical manifestation

Initially Polyurea, polydypsia, polyphagia and later on loss of body condition, exhaustion on exercise. In advanced cases Bleeding and clotting time increases, delay in wound healing and Ketotic odour from breath and urine. In highly advanced cases coma, convulsions and death are observed.

Decreased resistance to bacterial and fungal infections and often develop chronic or recurrent infections such as cystitis, prostatitis, bronchopneumonia, and dermatitis (due to impaired chemotactic, phagocytic and antimicrobial activity related with decreased neutrophil)

Cataracts develop frequently in dogs (not cats) with poorly controlled diabetes mellitus. Lenticular opacities appear initially along the suture lines of lens fibers and are stellate (“asteroid”) in shape. Cataract formation in dogs is related to the unique sorbitol pathway by which glucose is metabolized in the lens, which leads to edema of the lens and disruption of normal light transmission.

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Emphysematous cystitis (rare) due to infection with glucose fermenting bacteria (E.coli, Proteus spp.etc).

Diagnosis

Based on persistent fasting hyperglycemia and glycosuria. The normal fasting value for blood glucose in dogs and cats is 75-120 mg/dL. In cats multiple blood and urine samples may be required to confirm stress induced hyperglycemia.

In cats stress induced hyperglycemia is common (serum fructosamine level is normal) measurement of serum glycosylated hemoglobin or fructosamine (or both) can assist in differentiating between stress-induced hyperglycemia and diabetes mellitus.

Treatment and Management

Treatment involves a combination of weight reduction, diet, insulin, and possibly oral hypoglycemic. Intact females to be neutered.

In cats high protein diet+oral hypoglycemic/insulin therapy. NPH, lente, or PZI insulin is preferred. In cats use of high protein, low carbohydrate levels in food. Newly diagnosed Cats Insulin Glargine (insulin of choice), used in conjunction with high protein and low CHO diet

In dogs diets that are high in fiber and complex carbohydrates. administer glimeperide and acarbose. Glipizide not to be used in thin or ketonuric cats.

Two doses of insulin a day NPH or lente @ 0.5 U/kg bid. Avoid diets rich in simple sugars. Insulin therapy-Initially NPH(Neutral Protamine Hagedorn)@0.5U/kg B.W, s/c,bid. (Blood glucose should not fall below 80mg/dL). If not regulated with NPH, then Basal insulin detemir is used @ 0.1U/kg B.W,bid.

In Diabetic Ketoacidosis  i/v fluids such as 0.9% NaCl or lactated Ringers solution, short acting(Crystalline Zinc Insulin), supplementing electrolyte especially Potassium.

Dietary management

  • Correction/management of obesity (Wt reduction improves glucose tolerance).
  • Feed low calorie – dense diet (to avoid sudden postprandial hyperglycemia).
  • Feed diets containing high fiber content, esp soluble fibers (gums, pectin etc.)
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Regular monitoring every month.

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