Canine diabetes symptoms and treatment

Canine diabetes is characterized by absolute or relative lack of insulin action and it affects approximately 1 in 200 dogs.

Causes of diabetes in dogs:
Failure of insulin production: immune-mediated islet cell destruction, chronic pancreatitis, or drug toxicity.

Insulin resistance: obesity, glucocorticoids, progestagen therapy, insulin antibodies, or hormonal antagonism (e.g., metestrus diabetes or hypercortisolemia/hyperadrenocorticism).

Symptoms of canine diabetes:
History:
- Primarily middle-aged to older dogs
- Polyuria / polydipsia
- Polyphagia
- Weight loss
- Vomiting
- Anorexia
- Depression / Weakness
- Recurring urinary tract infections

Findings:
- Ketotic breath
- Cataracts
- Hind-limb neuropathy
- Glucosuria with hyperglycemia (with or without ketonuria) confirms diagnosis
- Elevated alkaline phosphatase
- Abnormal glycosylated protein (e.g., hemoglobin, fructosamine) concentrations

Differential diagnosis of canine diabetes:
- Chronic renal failure, hyperadrenocorticism
- Stress, renal disease

Treatment of canine diabetes:
Objectives:
- Reduce hyperglycemia
- Prevent ketoacidosis
- Prevent secondary diseases (UTI, cataracts)
- Minimize hepatopathy
- Improve well-being

Medical diabetes treatment:
- Insulin replacement therapy is required for ketoacidotic or underweight dogs
- Sick anorectic animals: not necessary to finely control blood glucose initially; administer half the usual insulin requirement during recovery period.

Alternatives to insulin:
- Glipizide will stimulate insulin secretion
- Metformin decreases hepatic glucose production, stimulates glucose uptake
- Acarbose inhibits carbohydrate digestive enzymes, decreases postprandial blood glucose

Additions to drug therapy:
- Exercise
- Weight management
- Chromium tripicolinate improves glucose metabolism by potentiating insulin action
- L-Carnitine supplementation aids fatty acid breakdown and utilization, assists weight loss and decreases body fat.
- Do not supplement chromium and carnitine if included in diet.

Canine diabetes prognosis:
If the primary cause of insulin resistance can be identified and eliminated, diabetes may not persist. Measure blood insulin after glucose administration to assess insulin-producing capacity. Insulin-dependent dogs have a good prognosis if owners are dedicated to treatment and dietary management.

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A diagnosis of canine diabetes mellitus is 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, stress-induced hyperglycemia is a frequent problem, and multiple blood and urine samples may be required to confirm the diagnosis. Measurement of serum glycosylated hemoglobin or fructosamine (or both) can assist in differentiating between stress-induced hyperglycemia and diabetes mellitus. In all cases, a search should be made for drugs or diseases that predispose to diabetes.

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The feeding schedule of pets receiving insulin should be planned so that nutrients are delivered to the body during peak periods of exogenous insulin activity. This span will be determined by the type of insulin used and the time of day it is administered. Several small meals should be provided throughout the period of insulin activity, as opposed to feeding a single large meal. Feeding several small meals helps minimize postprandial fluctuations in blood glucose levels. Other factors that affect the degree of hyperglycemia that occurs following a meal include the composition of the food and the type of insulin administered.

If insulin is administered early in the morning, the first meal should be given immediately before the insulin injection. If the pet refuses to eat on any occasion, the insulin injection can be withheld, thereby preventing the subsequent possibility of hypoglycemia. The remaining three or four meals in the day can be given at equally spaced intervals, depending on the action of the insulin used. Taking blood samples and measuring blood glucose levels every 1 to 2 hours throughout a 24-hour period will indicate if the feeding schedule coincides adequately with insulin activity. If postprandial blood glucose levels rise above 180 milligrams, (mg)/deciliter (dl), the interval between feeding and insulin administration should be decreased. If hyperglycemia still occurs, the size of the meal should be decreased and/or the number of meals provided per day should be increased. Likewise, a meal should always be provided within 1 to 2 hours following the lowest blood glucose level.

Once an appropriate pet food and feeding schedule have been selected, the management program should be strictly adhered to. Pets that have previously been fed free-choice should be gradually switched to the new regimen. Although most dogs will adapt quickly, cats can be very resistant to changes in their feeding routine and in the type of food that is fed. This resistance can make dietary management of a diabetic cat difficult for some owners. Mixing the new food into the cat's previous food and changing to a meal-feeding regimen over a period of several weeks can help decrease these problems. Allowing cats to nibble over the period of insulin activity is also effective in some cases. Supplemental food should not be given, and feeding times should vary as little as possible. Periodic monitoring of blood glucose levels can be used to adjust the diet as the pet loses weight, changes the amount of exercise it gets, or requires adjustments in insulin dosage.

We also recommend this natural balanced real-meat dog food and natural dietary supplement for recovery.

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Diabetic dog food

The relationship between obesity and NIDDM in humans is well documentated. Studies with dogs and cats have shown that a similar relationship exists in these species. Baseline plasma insulin level and insulin response to a glucose load increase linearly in dogs as a function of their degree of obesity. This effect occurs in both healthy and diabetic dogs and cats. Similarly, a study with cats found that healthy but obese cats had normal fasting plasma glucose concentrations, but the study showed abnormal results on glucose tolerance tests and slightly elevated baseline serum insulin concentrations. Significant delays in initial insulin response and substantially increased insulin responses at a later phase of the glucose tolerance test were found in the overweight cats.

Decreased tissue sensitivity to insulin and impaired beta-cell responsiveness to stimuli are believed to be the cause of these changes. Specifically, the tissue of obese animals has decreased numbers of cellular insulin receptors, and the receptors that are present have reduced binding affinity. In some cases, a post-receptor, intracellular defect in insulin action also occurs. Ultimately, these changes decrease the body's baseline insulin and insulin secretion increase in an attempt to compensate for the obesity-induced cellular resistance to insulin.

Weight reduction and control is an important aspect of the dietary management of diabetic animals that are overweight. When obesity is reduced in dogs and cats with abnormal insulin-secretory responses, glucose tolerance often improves. In addition, weight loss in pets with IDDM can result in enhanced tissue sensitivity to insulin, resulting in lowered daily insulin requirements. When a diabetic pet is overweight, caloric intake should be designed for weight loss and the eventual maintenance of ideal body weight. A diet that contains a high proportion of complex carbohydrates and reduced fat provides decreased energy density. However, a diet that is low in energy density must also contain adequate levels of all nutrients in forms that are available for digestion and absorption.

A commercial diet that is formulated to be complete and balanced while containing moderate fiber levels, increased complex carbohydrates, and reduced fat is recommended. Adding complex carbohydrates or fiber to a normal diet in a attempt to decrease energy density is contraindicated because this practice may cause increased stool volume, loose stools, or diarrhea and can lead to nutrient imbalances. When weight loss is instituted with pets that have IDDM, the pet's blood glucose should be carefully monitored and adjustments in insulin made as glucose tolerance improves.

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Dietary goals for dogs and cats with Type 1 diabetes (also referred to as insulin-dependent diabetes or IDDM) are to improve regulation of blood glucose by delivering nutrients to the body during periods when exogenous insulin is active and to minimize postprandial fluctuations in blood glucose levels. Dietary management does not eliminate the need for insulin replacement therapy, but it can be used to improve glycemic control.

Dietary treatment for pets with Type 2 diabetes (also referred to as non-insulin-dependent diabetes or NIDDM) can be instrumental in improving glycemic control and preventing the need to institute exogenous insulin therapy. Factors that must be considered when developing an appropriate diet for a diabetic pet include the consistency and type of diet, its nutritional adequacy and nutrient composition, and the pet's caloric intake and feeding schedule.

Dogs and cats with diabetes should be fed food that contains consistent amounts and source of nutrients. Specifically, the type and quantity of nutrients that are delivered to the body should remain consistent from day-to-day, and the proportions of calories in the diet that are supplied by carbohydrate, protein, and fat should stay constant. For pets with IDDM, the provision of a consistent diet allows the insulin dosage to be adjusted to closely fit the needs of the animal. Similarly, if pets with NIDDM are being treated with oral hypoglycemic agents, the provision of a consistent diet is helpful in maintaining normal blood glucose levels.

Changes in the ingredients or nutrient composition of a diet can disrupt the tight coupling of blood glucose levels with insulin activity that is needed for proper glycemic control. Therefore, only pet foods that are prepared using a fixed formulation should be selected for diabetic pets. Manufacturers that use fixed formulations ensure that the nutrient composition and ingredients of a food remain consistent between batches. In contrast, manufacturers that use variable formulations will change ingredients depending on the availability and market prices. If information about the formulation type is not readily available, it can be obtained by contacting the manufacturer directly. Homemade diets should also be avoided with diabetic pets because of difficulties with maintaining nutrient consistency.

The type of commercial product that is fed is also of importance. Semimoist pet foods or snacks should not be fed to diabetic pets. Postprandial blood glucose and insulin responses have been shown to be highest when dogs are fed either canned or dry pet foods. This increase appears to be because of the high level of simple carbohydrate found in semimoist products. These nutrients require minimal digestion in the small intestine and are rapidly absorbed following a meal. In contrast, the digestible carbohydrates found in dry and canned foods are made up primarily of complex carbohydrates (starch). Starches require enzymatic digestion to simple sugars before they can be absorbed into the body. This process slows the rate of delivery of glucose to the bloodstream. Complex carbohydrates and certain types of fiber also affect the rate of food passage through the gastrointestinal tract and the absorption of other nutrients in the diet. Dry pet foods generally contain higher levels of both complex carbohydrates and plant fiber than semimoist or canned foods do.

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Diabetes mellitus is a chronic endocrine disorder that occurs in both dogs and cats. It is caused by the relative or absolute deficiency of the hormone insulin, which is produced by the beta cells of the pancreas. Insulin stimulates the transport of glucose and other nutrients across cell membranes for cellular use and is involved in a number of anabolic processes within the body. A lack of insulin activity leads to elevated blood glucose levels (hyperglycemia) and an inability of tissues to receive the glucose that they need (glucoprivation). Primary clinical signs include polyuria, polyphagya, polydipsia, and weight loss. Diagnosis is usually made using the initial signs of the disorder, which are the presence of a persistent hyperglycemia and a persistent or concurrent glycosuria.

It is estimated that diabetes has an incidence between 0.2% and 1% in dogs and cats seen at small animal clinics. A large proportion of these diabetic pets are obese at the time of diagnosis. In dogs, other factors that appear to be related to the development of diabetes are hormone abnormalities such as hypothyroidism and Cushing's syndrome, recurrent episodes of pancreatitis, pancreatic islet-cell destruction, stress, and genetic predisposition. In cats, the most significant risk factor for the development of diabetes is increasing age. Between 70% and 90% of diabetic cats are 7 years or older and more than 65% are 10 years or older. Other predisposing factors for cats include inactivity, presence of pancreatic neoplasia, long-term administration of progesterone or progestin, and possibly, genetics.

All of the clinical signs observed in pets with diabetes are associated with the short or long-term effects of hyperglycemia. The microvascular effects of diabetes contribute to the development of cataracts and renal disease. Polyneuropathy develops in some cases and can manifest as weakness, depression, or uninary and bowel incontinence. Bacterial infections are common in animals with poor glycemic control. All of these complications can be minimized or prevented through stringent control of blood glucose levels in diabetic animals.

The general therapeutic goals in diabetes management are to minimize post-prandial (after-meal) hyperglycemia, prevent hyperglycemia when insulin is being administered, resolve and minimize clinical signs, prevent or delay long-term complications, and improve overall health. These goals can be achieved through exogenous insulin administration, oral hypoglycemic agents, diet, weigh loss (if indicated) exercise, and the control of concurrent illness.

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