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Dietary treatment of diabetes mellitus in dogs and cats (Sponsored by Nestle Purina)
Dietary therapy is the key to proper management of the diabetic cat and dog.
Dietary therapy is the key to proper management of the diabetic cat and dog. Cats develop type II diabetes mellitus; therefore, feeding a low-carbohydrate, high-protein diet is essential for optimizing and utilizing the gluconeogenic capacity and obligate carnivore aspect of this species. In fact, cats fed low-carbohydrate, high-protein diets are more than twice as likely to go into remission and discontinue insulin injections compared with cats fed low-glycemic index, high-fiber diets. On the other hand, dogs develop type I diabetes mellitus which requires continuous insulin therapy. Dogs are more omnivorous than cats, and feeding a low-glycemic index, high-fiber diet is the key to good diabetic regulation. Dogs are susceptible to exocrine pancreatic disorders, such as pancreatitis and pancreatic insufficiency, therefore, fat content of the diet is important as well.
Feline diabetes mellitus
Diabetes mellitus is one of the most common feline endocrine diseases, affecting one in every 200 to 300 cats, or roughly 240,000 diagnosed cases per year.1 Despite the increasing frequency of the disease in the cat population, treatment of diabetic cats is frustrating and often associated with serious complications.
While insulin therapy and high-fiber diets have been mainstays of diabetes treatment, many diabetic cats experience complications associated with this therapy, such as hypoglycemia and progressive neuropathy.2-7 In a recent study, 10 percent of diabetic cats had documented hypoglycemia caused by an insulin overdose.6 Obese cats (>6 kg) were more likely to become hypoglycemic and lack autonomic warning signs of hypoglycemia. 6 Because of the difficulty in achieving adequate glycemic control with insulin therapy in cats, diabetic neuropathy is a common finding in diabetic cats. In one study, all diabetic cats suffered from subclinical forms of diabetic neuropathy as evidenced by impaired motor and sensory peripheral nerve conduction.7 In summary, current dietary and insulin therapy is associated with increased risk of severe hypoglycemia and often results in poorly-controlled diabetes and progressive neuropathy in cats with type II diabetes.
The latest clinical and histologic evidence suggests that type II diabetes is the most frequently occurring form of diabetes in cats and people.2-4 Type II diabetes in cats is characterized by an impaired ability to secrete insulin following a glucose stimulus and is caused by both a defect in pancreatic beta cells and by peripheral insulin resistance.2-4 The etiology of type II diabetes is undoubtedly multifactorial; obesity, genetics, diet, and islet amyloidosis are involved in the development of this form of diabetes in humans and cats.2-4 It is now recognized that the classic metabolic abnormalities found in type II diabetes—decreased insulin secretion and peripheral insulin resistance—may be consequences of abnormal amyloid production by pancreatic cells.2-4 Despite the prevalence of type II diabetes in cats, the advanced nature of their disease (amyloid deposition, glucose toxicity) often requires that insulin therapy be instituted.2
The cat is an obligate carnivore and, as such, is unique among mammals in its insulin response to dietary carbohydrates, protein, and fat. The feline liver exhibits normal hexokinase activity, but glucokinase activity is virtually absent.8 Glucokinase converts glucose to glycogen for storage in the liver and is important in decreasing postprandial glucose. Normal cats are similar to people in that glucokinase levels drop precipitously with persistent hyperglycemia in people with type II diabeties. Amino acids, rather than glucose, are the signal for insulin release in cats.9 In fact, a recent publication demonstrated more effective assessment of insulin reserve in cats using the arginine response test rather than a glucose tolerance test.10
Another unusual aspect of feline metabolism is the increase in hepatic gluconeogenesis seen after a meal. Normal cats maintain essential glucose requirements from gluconeogenic precursors (e.g., amino acids) rather than from dietary carbohydrates. As a result, cats can maintain normal blood glucose concentrations even when deprived of food for more than 72 hours.9 Furthermore, feeding has very little effect on blood glucose concentrations in normal cats.2,11 In summary, the cat is uniquely adapted to a carnivorous diet and is not metabolically adapted to ingestion of excess carbohydrates.
Low protein and excess carbohydrates in the diet equal catabolism
When type II diabetes occurs in cats, the metabolic adaptations to a carnivorous diet become even more deleterious, leading to severe protein catabolism; feeding a diet rich in carbohydrates may exacerbate hyperglycemia and protein wasting in these diabetic cats. In fact, in people with type II diabetes, the first recommendation is to restrict excess dietary carbohydrates such as potatoes and bread and to control obesity by caloric restriction.12 Furthermore, people with type II diabetes have improved glycemic control and nitrogen turnover during weight loss when a low-energy, highprotein diet is combined with oral hypoglycemic therapy.13
A low-carbohydrate, high-protein diet, which is similar to a cat's natural diet (mice), may ameliorate some of the abnormalities associated with feline diabetes. In initial studies using a canned highprotein, low-carbohydrate diet and the starch blocker acarbose, insulin injections were discontinued in 58 percent of cats, and those with continued insulin requirements were regulated on a much lower dosage (1 U twice daily).14 Comparison of canned high-fiber vs. low-carbohydrate diets in 63 client-owned diabetic cats showed that those fed low-carbohydrate diets were three times more likely to discontinue insulin injections.15
The diet formulation is critical in that most dry cat food formulations contain excessive carbohydrates; therefore, canned cat foods and preferably high-protein formulations should be used for initial treatment of diabetic cats. Because weight reduction also decreases insulin resistance, cats should be fed no more than 30 kcal/lb of ideal body weight in two equal meals per day. Initially, caution should be used when changing from dry to canned foods, as insulin requirements may decrease dramatically, and a reduction in insulin dosage may be required. Feeding either dry or canned highprotein, low-carbohydrate diets can improve glycemic control; however, cats fed canned high-protein, low-carbohydrate (less than 10 percent on a dry matter basis) diets are two to three times more likely to no longer require exogenous insulin injections.14-16
Diabetic nephropathy occurs in a large percentage of people with type II diabetes.17 Diabetic nephropathy, like other diabetic complications, is associated with poor glucose regulation. The earliest sign of diabetic nephropathy is microalbuminuria. Azotemia is a late consequence of diabetic nephropathy, but may be reversible with good diabetic regulation. Hyperglycemia increases the glomerular filtration rate and renal plasma flow, and may increase binding of plasma proteins to glomerular basement membranes.17 Elevation of tissue polyol concentrations resulting from hyperglycemia contributes to renal dysfunction. Thickening of the glomerular basement membranes and glomerular hypertension may also contribute to renal problems.17 If diabetic nephropathy is identified early and glycemic control improves, glomerular damage may be reversed. The incidence of diabetic nephropathy in cats is unknown, but recent studies indicate that the incidence might approach 50 to 60 percent of diabetic cats.18 Treatment using a low-carbohydrate diet, such as Purina Veterinary Diets DM Dietetic Management Feline Formula, combined with oral hypoglycemics or insulin may help prevent progression of nephropathy. Conversely, use of low-protein diets are contraindicated in diabetic cats with moderate or mild azotemia, as they may exacerbate the diabetes, leading to regulation problems. Unless the cat has advanced renal disease caused by infection, uroliths, or other disorders, dietary protein should not be restricted. Phosphorus binders may be indicated in severe cases of diabetic nephropathy.
Concurrent gastrointestinal disease is very common in diabetics, particularly diabetic cats. In one study, fewer than one-third of the cats died of diabetes.19 Thirty-nine of 42 cats presented with diabetic ketoacidosis had concurrent diseases, including hepatic lipidosis, cholangiohepatitis, pancreatitis, chronic renal failure, urinary tract infection, and neoplasia.20 In a similar survey of 104 diabetic cats 22 percent had concurrent diseases, the most common being hyperthyroidism, inflammatory bowel disease, and eosinophilic granuloma complex.21
Dietary therapy for concurrent disorders such as pancreatitis or inflammatory bowel disease may benefit from a high-protein, low-carbohydrate diet (Purina Veterinary Diets DM Feline Formula or Purina Veterinary Diets EN Feline Formula) combined with probiotics (e.g., Fortiflora—Nestlé Purina). Ancillary therapy should be directed at the specific underlying disorder.
The most common endocrinopathies of diabetic cats are, in order of frequency, hyperthyroidism, acromegaly, and hyperadrenocorticism.22-24 Diabetic cats suffering from hyperthyroidism will often have periods of hyperglycemia followed by periods of hypoglycemia as insulin dosages are adjusted upward. Serum fructosamine concentrations will be falsely lower in diabetic hyperthyroid cats due to increased protein turnover; therefore, poor regulation may be challenging to identify. Permanent therapy for hyperthyroidism, such as radioactive iodine or surgery, should be used to resolve the hyperthyroidism in cats with concurrent diabetes in order to improve diabetic regulation. In fact, many cats with concurrent hyperthyroidism and diabetes will go into remission and no longer require insulin following appropriate treatment of the hyperthyroidism.
Acromegaly in cats almost always presents first as insulin-resistant diabetes.23 Acromegalic cats can be identified using a serum somatomedin (insulin-like growth factor) test and computed tomography or magnetic resonance imaging of the pituitary gland.
Finally, hyperadrenocorticism is a rare cause of insulin resistance in the cat, but can be diagnosed using a low-dose dexamethasone suppression test (0.1mg/kg intravenously). Regardless of the concurrent endocrinopathy, cats with diabetes and concurrent disease should receive a high-protein, low-carbohydrate diet to ameliorate the consequences of high blood glucose.
Diabetes in dogs
Insulin-dependent diabetes mellitus (type I) is a diabetic state in which endogenous insulin secretion is insufficient to prevent ketone production. In type I diabetes, insulin secretion may be reduced or absent and can be readily corrected by exogenous insulin administration; in dogs, type I diabetes is caused by autoimmune destruction of the beta cells. Secondary diabetes in the dog may be due to pancreatitis or concurrent endocrinopathies.
Dogs suffering from diabetes range in age from 4 to 14 years with a peak incidence at 7 to 9 years.24 A genetic basis for diabetes is suspected in the keeshond and golden retriever. Other commonly affected breeds include miniature and toy poodles, dachshunds, miniature schnauzers, beagles, pulis, Cairn terriers and miniature pinschers. Most diabetic animals present with the classic clinical signs of polyuria and polydipsia. Weight loss is commonly observed in dogs. In some cases, polyphagia is also observed. In dogs, progressive polyuria, polydipsia and weight loss usually develop rapidly over a period of several weeks. Another common presenting complaint of diabetic dogs is acute onset of blindness caused by bilateral cataract formation. Physical examination findings of nonketotic diabetes in dogs are typically non-specific. In dogs, the most common physical examination findings are dehydration and muscle wasting or thin body condition. But about 25 to 30 percent of diabetic animals are obese upon initial examination. Hepatomegaly is usually observed in diabetic dogs. Cataracts are observed in approximately 40 percent of diabetic dogs. A diagnosis of diabetes should be based on the presence of clinical signs compatible with diabetes and evidence of fasting hyperglycemia and glycosuria. Common clinicopathologic features of diabetes in dogs include fasting hyperglycemia, hypercholesterolemia, increased liver enzyme activity (alkaline phosphatase, alanine aminotransferase), neutrophilic leukocytosis, proteinuria, increased urine specific gravity, and glycosuria.25
The goals of dietary therapy in diabetes for both cats and dogs are to provide sufficient calories to maintain ideal body weight and correct obesity or emaciation, to minimize postprandial hyperglycemia, and to facilitate ideal glucose absorption by timing meals to coincide with insulin administration.26 Caloric intake should be 60 to 70 kcal/kg per day for smaller dogs and 50 to 60 kcal/kg per day for larger dogs. Obese animals should have their body weight reduced gradually over a period of two to four months by feeding 60 to 70 percent of the calculated caloric requirements for ideal body weight. Underweight animals should be fed a high-caloric density food based on caloric intake for optimum body weight. Table 1 lists the carbohydrate, fiber, and protein content of some commercially available dog foods.
Table1. Macronutrient content of selected therapeutic dog foods suitable for treatment of diabetes mellitus
The feeding schedule should be adjusted to the insulin therapy. Dogs should be fed within two hours of Lente (long-acting) insulin administration or six hours of protamine zinc insulin administration. Feeding usually elevates the plasma glucose for less than 90 minutes. Meals should be timed so that maximal exogenous insulin activity occurs during the postprandial period; therefore, when a twice-daily insulin dosing regimen is used, the dog should be fed immediately before or after the insulin injection. Diets formulated for canine adult maintenance with moderate dietary fiber and carbohydrate content will be suitable for most diabetic dogs, for example, Purina Veterinary Diets DCO Dual Fiber Control canine formula. Most well-managed diabetic dogs require about the same amount of food per day as healthy nondiabetic dogs of similar age, gender, and lifestyle.
The protein content of the diet should be normal or increased in diabetic dogs, particularly in obese dogs. It has been shown that insulin resistance is reduced and lean body mass preserved in dogs fed higher-protein diets for weight loss.27 Higher-protein formulations may also beneft underweight diabetic dogs with significant muscle wasting or those suffering from concurrent exocrine pancreatic insufficiency. Low-glycemic index carbohydrates such as sorghum and barley are recommended. Readily absorbed carbohydrates such as rice and corn syrup have high glycemic indices and should be avoided. Foods with high sugar content (semi-moist foods) should not be used to improve the palatability of food prescribed for diabetic dogs.
Dietary fat restriction (<12 percent on a dry matter basis or <30 percent ME) is recommended for diabetic dogs with concurrent chronic pancreatitis or persistent hypertriglyceridemia (miniature schnauzers). Foods with a high fat content should not be used to improve the palatability of food prescribed for diabetic dogs. Instead, the low-carbohydrate, low-fat food may be made more palatable with agents such as warm low-fat chicken or beef broth.
One of the approaches to managing diabetes in dogs combines the use of nutritional components such as starch blends, carboxymethylcellulose, and fermentable fiber blends. Barley and sorghum can be used to blunt the postprandial rise in blood glucose, adjust posprandial insulin to appropriate levels, and to help blunt glucose surge. Fermentable fibers, such as fructooligosccharides, beet pulp, and gum arabic, increase production of short-chain fatty acids from the large intestine, which in turn increases glucagon-like peptide-1 (GLP-1) secretion and activity. GLP-1 is necessary for normal insulin secretion and for normal timing of insulin secretion after eating. Carboxymethylcellulose delays gastric emptying, further blunting the glucose surge that occurs after feeding. Diets with moderate dietary fiber content are recommended for diabetic dogs especially those that are overweight (crude fiber maximum 10 to 15 percent dry matter). High-fiber, restrictedfat diets should not be routinely recommended for diabetic dogs with a body condition score of less than 4/9.
In a survey of concurrent disorders in 221 diabetic dogs, over 40 percent had lipemia.28 Although hyperlipidemia can be caused by diabetes, a thorough evaluation of thyroid and adrenal status should be done to rule out common endocrinopathies as a cause of the hyperlipidemia, particularly if it is hypercholesterolemia. A fat-restricted diet should be considered for diabetic dogs with persistent hypertriglyceridemia. This often involves breeds such as the miniature schnauzer that have a defect in lipoprotein lipase activity. Hyperlipidemia is a cause of insulin resistance; therefore, dietary restriction of fat is essential for good diabetic regulation in these patients.
In the previously mentioned survey of concurrent disorders in 221 diabetic dogs, more than 70 percent had elevated liver enzyme activity, and 13 percent had acute pancreatitis.28 Acute pancreatitis may be one of the most difficult diseases to manage nutritionally and is complicated further when the dog is also diabetic. Low-fat formulations (<12 percent on a dry matter basis or <30 percent ME) may be helpful to feed dogs after repeated bouts of pancreatitis.
A less commonly reported or identified pancreatic disorder in dogs is exocrine pancreatic insufficiency. These patients often present with repeated bouts of diarrhea, anorexia, and hypoglycemia. Unlike young German shepherds with exocrine pancreatic insufficiency, diabetic dogs may have borderline pancreatic enzyme activity resulting in carbohydrate and fat malassimilation and diarrhea, but not overt steatorrhea. The condition is diagnosed using the commercially available trypsin-like immunoreactivity test; I also measure cobalamin and folate concentrations to look for deficiency or excess of these vitamins. Adding pancreatic enzymes and probiotics to the diet may help in restoring normal digestion and microbial floral in these patients. Diabetic dogs with reduced exocrine pancreatic function have an increased caloric requirement compared with healthy dogs.
In one study, 23 percent of the diabetic dogs had test results consistent with hyperadrenocorticism, and 9 percent were hypothyroid.28 Hypothyroidism is the most common endocrinopathy accompanying diabetes in dogs and can result in insulin resistance.29 Diabetic dogs should be evaluated for hypothyroidism at the time of diagnosis using thyrotropin (TT4) and endogenous canine thyroid stimulating hormone (TSH) assays. Low TT4 and high TSH results will confirm hypothyroidism, while low TT4 and normal or low TSH results are indicative of euthyroid sick syndrome.
Hyperadrenocorticism is a less common endocrinopathy associated with diabetes, but often results in the development of ketosis. Most dogs with both diseases develop hyperadrenocorticism before the onset of diabetes. Testing for hyperadrenocorticism may be complicated in diabetic patients with a large number of false positives resulting from the low dose dexamethasone suppression test. I prefer to screen for hyperadrenocorticism using an ACTH response test in stable diabetic (e.g., nonketotic) patients.
Hypoglycemia and hyperglycemia
The clinical signs of hypoglycemia in diabetics are initially consistent with epinephrine release to counter the hypoglycemia. Nervousness, anxiety, vocalization, muscle tremors, ataxia, and pupillary dilatation should alert the owner to the possibility of hypoglycemia. At this point, the animal should be offered food and the owner should seek veterinary advice. Late in the course of hypoglycemic shock, the animal may become recumbent, comatose, or experience seizure. If vascular access is not possible or if the owner is administering therapy, 50 percent dextrose (Karo syrup, pancake syrup) may be applied to the oral mucous membranes using a large syringe. When doing so, the owner should maintain a reasonable distance from the animal's teeth to prevent accidental injury from biting. The owner should then transport the animal to a veterinarian as soon as possible. At the veterinary office, the patient should receive a slow intravenous bolus of 50 percent dextrose (0.5 g/kg diluted 1:4).30 Thereafter, a continuous infusion of 5 percent dextrose should be administered until the animal can be fed. Many animals that experience insulin overdose will suffer cerebral edema and temporary blindness or behavior changes; often these signs are temporary and resolve after several weeks or months. Endogenous glucose stores (hepatic glycogen) may have been depleted by the insulin overdose and it may take several days for hyperglycemia to recur. In these cases, insulin therapy should be discontinued until hyperglycemia recurs.
Generally, hyperglycemia problems can be differentiated by the characteristics of the blood glucose curve and the insulin dosage (per dosing interval). If the patient is receiving >2.2 U/kg of insulin per dose, insulin resistance should be investigated. Causes of insulin resistance in dogs include hypothyroidism, hyperadrenocorticism, acromegaly, estrus, drug therapy, and infections. If the animal is receiving <2.2 U/kg per dose, the blood glucose curve will usually indicate one of the following: insufficient dosage of insulin, short duration of action of insulin, insulin-induced hypoglycemic hyperglycemia (Somogyi effect) and, insulin overlap or prolonged insulin action. Corrective actions include, respectively, increasing the insulin dose, changing to a longer acting insulin or twice daily insulin regimen, reduction of the insulin dose by 25 percent, or changing to a shorter duration insulin or insulin mixture (30 percent regular, 70 percent NPH, respectively). Causes of hyperglycemia and hypoglycemia in diabetic dogs are listed in Table 2.
Table 2. Causes of hyperglycemia and hypoglycemia in diabetic dogs
Exercise should be kept constant in diabetic animals. The owners should be instructed to walk the animal daily and avoid intermittent or unplanned episodes of strenuous exercise. Increasing exercise in obese diabetic animals will reduce insulin resistance and improve glycemic control. In fact, the best way to reduce insulin requirements and maintain steady glucose concentrations throughout the day in dogs is to exercise the dog for 20 to 30 minutes before the evening meal and insulin administration. I have been able to regulate very large and athletic breeds, such as racing greyhounds, by adjusting the insulin to the activity. For example, if a race or strenuous hike is planned, the morning insulin might not be given or only half the insulin is administered to avoid exerciseinduced hypoglycemia.
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