Please refer to these 2018 AAHA Diabetic Guidelines if you have a dog with Diabetes and EPI….. This is not a straight forward Diabetic situation and it is best to familiarize yourself with multi-faceted aspects of managing Diabetes especially in an EPI dog
Dealing with Unstable Diabetes
Aug -2018 Possible New Diabetic Treatment- -no insulin shots!
In: Encyclopedia of Canine Clinical Nutrition, Pibot P., Biourge V. and Elliott D.A. (Eds.). International Veterinary Information Service, Ithaca NY (www.ivis.org), Last updated: 31-Mar-2008; A4206.0308
Diabetes Mellitus: Nutritional Strategies
Diabetes mellitus is a common endocrine disease of dogs and requires life-long therapy. Nutritional management is an important part of the treatment regimen and feeding guidelines based on evidence from well-designed clinical studies are essential. The first part of this chapter provides an understanding of the pathogenesis of diabetes in dogs, which is required before evaluation of issues relating to nutritional management. This allows comparison of the current, evidence-based, nutritional recommendations for human patients with types of diabetes analogous to canine diabetes. The second part reviews the available evidence from feeding studies in dogs and provides detailed analysis of the recommendations for dietary fiber, carbohydrate, fat, protein, and selected micronutrients in diabetic dogs. The final summary uses the American Diabetes Association grading system to rank the scientific basis of the nutritional recommendations for canine diabetes.
1. Diabetes in Dogs
Prevalence of Diabetes Mellitus in Dogs
Diabetes mellitus is one of the most frequent endocrine diseases affecting middle-aged and older dogs, and the prevalence is increasing. Thirty years ago, 19 in 10,000 dogs visiting veterinary hospitals were diagnosed with diabetes mellitus (Marmor et al., 1982; Guptill et al., 2003). By 1999, the prevalence in the same veterinary hospitals had increased three-fold to 58 per 10,000 dogs (Figure 1) (Guptill et al., 2003).
Clinical Sequelae of Diabetes in Dogs
Insulin deficiency results in altered carbohydrate, fat, and protein metabolism. Abnormal carbohydrate metabolism manifests as hyperglycemia and glycosuria and is responsible for the polyuria, polydipsia, and cataract formation seen in diabetic dogs. The hyperlipidemia, ketone production, and hepatic changes seen in these dogs primarily results from altered fat metabolism. Decreased tissue utilization of glucose, amino acids, and fatty acids causes lethargy, weight loss, reduced stimulation of the satiety center, poor coat, and reduced immunity that is characteristic of untreated diabetic dogs.
Cataract formation is the most common, and one of the most important, long-term complications associated with diabetes in dogs (Beam et al., 1999) (Figure 2a and Figure 2b). Cataracts are irreversible and can progress quite rapidly (Figure 3a–Figure 3c). About 30% of diabetic dogs already have reduced vision at presentation (Graham & Nash, 1997a). Cataracts will develop within 5 – 6 months of diagnosis in the majority of diabetic dogs and, by 16 months, approximately 80% will have significant cataract formation (Beam et al., 1999). Importantly, the risk of cataract development seems to be unrelated to the level of hyperglycemia but increases with age (Salgado et al., 2000). Thus, dietary manipulation is not likely to influence the rate or severity of cataract development in diabetic dogs.
Figure 2a. Diabetic cataract associated with uveitis in a dog. Advanced cataract in an aging dog. Hyperemia is present in the sclera, indicating moderate uveitis. (©RIE Smith).
Figure 2b. Diabetic cataract associated with uveitis in a dog. Severe uveitis in a diabetic dog. The eye is red and painful, with the presence of mucopurulent ocular discharge and posterior synechia.
Figure 3a Development of diabetic cataracts in a dog (from Fleeman & Rand 2000). An eleven-year-old crossbred dog photographed shortly after diagnosis of diabetes mellitus. (©RIE Smith).
Figure 3b. Development of diabetic cataracts in a dog. The same dog three months after initial diagnosis of diabetes mellitus. Diabetic cataracts have rapidly developed and the dog’s owner reported sudden vision loss. (©RIE Smith).
Figure 3c. Development of diabetic cataracts in a dog. The same dog following phacoemulsification surgery to remove the cataract from the right eye. (©RIE Smith).
Treated diabetic dogs have a similar chance of survival as compared to non-diabetic dogs of the same age and gender, although the hazard of death occurring is greatest during the first 6 months of therapy (Graham & Nash, 1997b). Most diabetic dogs are middle-aged and older and are prone to diseases that commonly affect this age group. Consequently, many suffer concurrent problems that need to be managed in combination with the diabetes. For diabetic dogs receiving insulin therapy, the nutritional requirements of any concurrent disease may need to take precedence over the dietary therapy for diabetes. Regardless of the diet fed, glycemic control can still usually be maintained with exogenous insulin therapy.
If concurrent illness causes transient inappetence, it is generally advisable to administer half the usual insulin dose to reduce the risk of hypoglycemia. Diabetic dogs with a reduced appetite will often eat if they are hand-fed highly palatable food by their owner. If there is a more severe concurrent illness causing prolonged inappetence, diabetic dogs should be hospitalized for blood glucose concentration monitoring and treatment with a rapid-acting insulin preparation and intravenous fluids supplemented with glucose and potassium (Feldman et al., 2004a).
Severe hypoglycemia resulting from insulin overdose can cause irreversible brain damage and death, and avoidance of insulin-induced hypoglycemia is one of the primary aims of therapy in diabetic dogs. Dietary manipulation that reduces the risk of insulin-induced hypoglycemia affords important clinical benefit for diabetic dogs. Severe hypoglycemia has been reported in a diabetic dog that was fed ad libitum and received insulin at grossly irregular intervals (Whitley et al., 1997). Commercial dog foods usually result in postprandial elevation of plasma glucose for less than 90 minutes following consumption by dogs (Nguyen et al., 1998a) and meals should ideally be timed so that maximal exogenous insulin activity occurs during the postprandial period (Church, 1982). Thus, dogs should be fed within 2 hours of administration of lente insulin or within 6 hours of protamine zinc insulin (Stenner et al., 2004) (Figure 4). In practice, a feasible compromise is to feed the dog immediately following the insulin injection. This considerably simplifies the home treatment regimen for most dog owners while still allowing good glycemic control to be readily achieved. In addition, many owners prefer this regimen because they feel their pet is rewarded for submitting to the injection.
Because the daily insulin-dosing regimen tends to be fixed for diabetic dogs, it is important that a predictable glycemic response is achieved following each meal. Ideally, every meal should contain the same ingredients and calorie content, and should be fed at the same time each day. It is crucial that the diet fed is palatable so that food intake is predictable. The major determinant of the postprandial glycemic response in dogs is the starch content of the meal (Nguyen et al., 1998b) so particular care should be applied to ensure consistent source and content of dietary starch.
The importance of avoiding an insulin overdose cannot be over-emphasized. Every person in the diabetic dog’s household needs to be aware of this life-threatening complication, which can rapidly develop into a serious emergency. If some insulin is spilt during the injection it should never be “topped up”, even if it appears that the dog has received no insulin. If the owner is ever uncertain about whether or not to give an insulin dose, the safest option is to withhold the injection, as the consequences of missing a single insulin dose are negligible. If mild signs of hypoglycemia develop, the owner should feed a meal of the dog’s usual food. If the dog is unwilling or unable to eat, syrup containing a high glucose concentration can be administered orally. Suitable syrups are marketed for use by human diabetics. When the dog recovers, food should be fed as soon as possible. No more insulin should be given to the dog and the owner should discuss the case with a veterinarian before the next injection is due. A 50% reduction in insulin dose is usually recommended in these circumstances.
Successful management of 94% of diabetic dogs is achieved with twice-daily insulin dosing (Hess & Ward, 2000). High doses of insulin and episodes of hypoglycemia are more common in diabetic dogs that receive insulin only once-daily (Hess & Ward, 2000). Although treatment regimens comprising once-daily insulin injections are considered by some to be simpler and more convenient, most of these regimens involve feeding two meals each day, one soon after the insulin injection and another at the time of peak insulin activity about 8 hours later. Given the length of the usual working day, it may actually be more convenient for people to feed the second meal 12 hours after the first. Experienced owners rarely report any difficulty with the administration of insulin injections and, if they are required to be at home to feed the dog, it is little more effort to give the dog an insulin injection at the same time. As a result, many clinicians favor treatment regimens that involve administration of the same dose of insulin along with feeding of the same sized meal every 12 hours.
The owners of diabetic dogs should be aware that a consistent insulin-dosing and feeding routine is optimal. Conservative, fixed-dose, twice-daily insulin therapy, in conjunction with a palatable diet containing a consistent content and source of dietary starch, which is fed at defined times in relation to insulin administration, is likely to be associated with reduced risk of hypoglycemia in diabetic dogs.
Pathogenesis of Diabetes in Dogs
The current classification of human diabetes mellitus is based on pathogenesis, and thus provides a rational foundation for understanding treatment issues. Adoption of these criteria for canine diabetes will afford a similar benefit for veterinarians. Human diabetes is divided into type 1, type 2, other specific types of diabetes, and gestational diabetes (The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997). At present, there are no internationally accepted criteria for the classification of canine diabetes. If the criteria established for human diabetes were applied to dogs, at least 50% of diabetic dogs would be classified as type 1. The remainder are likely to have “other specific types of diabetes” resulting from pancreatic destruction or chronic insulin resistance, or they have diestrus-induced diabetes.
Type 1 Diabetes
Type 1 diabetes appears to be the most common form of diabetes in dogs, and is characterized by pancreatic beta cell destruction leading to absolute insulin deficiency. In people, this usually occurs via cell-mediated, autoimmune processes and is associated with multiple genetic predispositions and poorly defined environmental factors (The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997). The majority of diabetic dogs have absolute insulin deficiency (Montgomery et al., 1996). The etiology of beta cell destruction is often unknown, although there is evidence that in approximately 50% of diabetic dogs it is caused by immune-mediated processes similar to human type 1 diabetes (Alejandro et al., 1988; Hoenig & Dawe; 1992; Davison et al., 2003a, Davison et al., 2003b).
Evidence is mounting for a genetic basis for canine diabetes. An association with major histocompatibility complex alleles on the dog leukocyte antigen gene strongly suggests that the immune response has a role in the pathogenesis of diabetes mellitus (Kennedy et al., 2003; Davison et al., 2003a; Rand et al., 2004).
Although genetic susceptibility appears to be a prerequisite, multiple environmental factors likely initiate beta cell autoimmunity, which once begun, then proceed by common pathogenic pathways (Kukreja & Maclaren, 1999). Similar to canine diabetes, the incidence rate of type 1 diabetes in people is rising (Onkamo et al., 1999), a trend that has been explained on the basis of increased contacts with adverse environmental factors (Kukreja & Maclaren, 1999). There is a highly significant seasonal incidence of diagnosis of both human type 1 diabetes (Gamble & Taylor, 1969; Fleegler et al., 1979) and canine diabetes (Atkins & MacDonald, 1987), with the incidence peaking in winter, indicating that environmental influences may have a role in disease progression just prior to diagnosis.
The rate of progression to absolute insulin deficiency is quite variable in human patients. It can be rapid in young children and much slower in middle-aged and older people. This latter group has the latent autoimmune diabetes of adults (LADA) form of type 1 diabetes, which is characterized by gradual beta cell destruction over months or years and is not associated with obesity (Zimmet et al., 1994). Distinct autoantibody patterns are recognized in the acute onset and slowly progressive (LADA) forms of human type 1 diabetes (Zimmet et al., 1994; Seissler et al., 1998), indicating a different pathogenesis for the two forms of the disease.
The rate of progression to absolute insulin deficiency has not been studied in dogs, but epidemiological factors closely match those of human patients with the LADA form of type 1 diabetes, who are usually not obese and tend to be middle-aged and older. Most affected dogs are over 7 years of age and the onset of clinical signs is typically insidious, ranging from weeks to months in duration (Ling et al., 1977). This has prompted speculation that there may also be similarities between the pathogenesis of canine diabetes and human LADA.
Other Types of Canine Diabetes
Association Between Diabetes and Pancreatitis in Dogs
Extensive pancreatic damage, which likely results from chronic pancreatitis, is responsible for the development of diabetes in approximately 28% of diabetic dogs (Alejandro et al., 1988) and thus is the most common “other specific type” of diabetes in dogs. Beta cell loss is being investigated in non-diabetic dogs with chronic pancreatitis and preliminary findings indicate that some have reduced beta cell function and appear to be pre-diabetic (Watson & Herrtage, 2004). Serum canine pancreatic lipase immunoreactivity (cPLI) is a sensitive marker for pancreatic inflammation in dogs (Steiner, 2003). Increases in serum cPLI concentration have been reported in 5 of 30 (17%) newly diagnosed diabetic dogs, although none of these dogs had serum cPLI concentrations above the diagnostic cut-off value for pancreatitis (Davison et al., 2003b).
In long-term diabetic dogs with no clinical evidence of exocrine pancreatic disease, serum cPLI concentrations in the diagnostic range for pancreatitis were found in 2 of 12 (17%) dogs, with a further 4 (33%) dogs recording increases in cPLI that did not reach the diagnostic cut-off value for pancreatitis, and an additional 2 (17%) dogs having laboratory evidence of exocrine pancreatic insufficiency (unpublished data). This indicates that subclinical exocrine pancreatic disease is common in diabetic dogs.
The association between canine diabetes and pancreatitis warrants particular attention because beta cell autoimmunity, pancreatic inflammation, and regulation of gut immunity might be linked in disease pathogenesis. The gut immune system likely plays a central role in the pathogenesis of human type 1 diabetes because accumulating evidence suggests that affected persons have aberrant regulation of gut immunity (Vaarala, 1999, Akerblom et al., 2002). The gut and the pancreas are probably immunologically linked, as well as anatomically linked, and influenced by environmental factors such as intestinal microflora, infections, and dietary factors (Vaarala, 1999).
Hypertriglyceridemia has been proposed as a possible inciting cause of canine pancreatitis (Williams, 1994) and is commonly seen in diabetic dogs (Ling et al, 1977). Obesity affects one-quarter to one-third of dogs presented to veterinary practices (Edney & Smith, 1986), and is also associated with an increased risk of pancreatitis (Hess et al., 1999). Environmental factors such as feeding high-fat diets, lipemia and disturbances in lipid metabolism, have been implicated as potential etiological factors in dogs with obesity-associated pancreatitis (Simpson, 1993), and likely play a role in the development of pancreatitis in diabetic dogs. More detailed discussion on canine pancreatitis and hyperlipidemia can be found in Chapter 5 and Chapter 7 of this encyclopedia.
Adult Dachshund presenting an excess of weight. No epidemiological data examining the relationship between canine diabetes and obesity have been published since 1960 (Krook et al.), and an association between obesity and diabetes in dogs is not currently recognized. (©Clouquer).
Role of Insulin Resistance in Canine Diabetes
Diabetes induced by insulin resistance states are less common “other specific types” of canine diabetes.
Disease conditions such as hyperadrenocorticism (Peterson, 1984) and acromegaly (Selman et al., 1994) result in insulin resistance, and may induce diabetes in dogs. Iatrogenic causes of insulin resistance that might lead to induced diabetes include chronic corticosteroid therapy (Campbell & Latimer, 1984). As most dogs do not develop overt diabetes with chronic corticosteroid therapy or spontaneous hyperadrenocorticism, for overt diabetes to develop it might require underlying reduced beta cell function resulting from immunological processes or chronic pancreatitis.
Although obesity causes insulin resistance in dogs, there are no published data clearly indicating that obesity is a risk factor for canine diabetes.
Obesity is a well-established risk factor for type 2 diabetes in cats and people. In contrast, there are no well-documented studies demonstrating convincingly that type 2 diabetes is a significant disease entity in dogs. In dogs, obesity causes insulin resistance (Rocchini et al., 1999; Villa et al., 1999, Mittelman et al., 2002), which leads to hyperinsulinemia and impaired glucose tolerance (Mattheeuws et al., 1984, Henegar et al., 2001). These effects are particularly pronounced when obesity is induced by feeding a diet high in saturated fat (Truett et al., 1998). Dogs fed a high-fat diet develop insulin resistance that is not compensated for by increased insulin secretion, resulting in more severe glucose intolerance (Kaiyala et al., 1999). Despite the evidence that obesity causes impaired glucose tolerance, it appears that very few dogs develop overt diabetes as a consequence of obesity-induced insulin resistance.
Diestrus- and Gestation-associated Diabetes
Gestational diabetes is another classification of diabetes recognized in human patients. In women, it is defined as any degree of glucose intolerance with onset or first recognition during pregnancy (The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 1997). If overt diabetes persists after the pregnancy ends, then it is reclassified as type 1, type 2, or another specific type of diabetes. Reduced insulin sensitivity occurs in healthy bitches by day 30 – 35 of gestation (McCann, 1983) and becomes more severe during late pregnancy (Concannon, 1986). The luteal phase of the non-pregnant cycle of the bitch is similar in duration to the 9 weeks of pregnancy and it is generally agreed that the hormone profiles during diestrus and pregnancy, are essentially identical (Concannon et al., 1989; Feldman et al., 2004b). Progesterone elevation causes glucose intolerance and overt diabetes during diestrus in bitches (Eigenmann et al., 1983, Scaramal et al., 1997). Progesterone also stimulates the mammary gland of bitches to produce growth hormone, which is a potent inducer of insulin resistance (Selman et al., 1994).
The periodic influence of diestrus-associated insulin resistance might contribute to the increased risk of female compared with male dogs for developing diabetes (Marmor et al., 1982; Guptill et al., 2003).
Classification of canine diabetes based on the current understanding pathogenesis is summarized in Table 1.
If diabetes is diagnosed in a bitch during either pregnancy or diestrus, it probably should be classified as of being comparable to human gestational diabetes. If diabetes persists after pregnancy or diestrus ends, then it should be reclassified as type 1 or another specific type of diabetes. (©Lanceau).
|Table 1. Classification of Canine Diabetes Mellitus Based on Current Understanding of Pathogenesis|
|Form of canine diabetes mellitus||Analogous form of human diabetes mellitus||Estimated proportion of diabetic dogs||Pathogenesis||Clinical features|
|Type 1 diabetes||Latent Autoimmune Diabetes of Adults (LADA) form of type 1 diabetes||50%||– Autoimmune destruction of pancreatic beta cells
– Genetic susceptibility related to the major histocompatibility complex on the dog leukocyte antigen gene
– Most likely initiated in susceptible individuals by environmental factors that interact with gut immunity
|– Middle-aged and older dogs
– Not associated with obesity
– Permanent, absolute insulin deficiency
|Extensive damage from chronic pancreatitis||Other specific types of diabetes||30%||Chronic pancreatitis causing widespread destruction of both endocrine and exocrine pancreatic tissue||– Onset of diabetes typically occurs many months before onset of exocrine insufficiency
– Permanent, absolute insulin deficiency
|Diabetes associated with insulinresistant states||Other specific types of diabetes||20%||– Concurrent disease or therapy causing insulin resistance
– Some dogs developing diabetes in association with insulin-resistant states might have underlying reduced beta cell function because of autoimmune destruction or chronic pancreatitis
|– Occurs in dogs with insulin resistance, e.g., hyperadrenocorticism, corticosteroid therapy
– Absolute or relative insulin deficiency
|Diestrus-associated diabetes||Gestational diabetes||Prevalence dependent on proportion of intact bitches in the population||– Progesterone causes insulin resistance
– Progesterone also stimulates growth hormone production by the mammary gland, which further contributes to insulin resistance
– Might have underlying reduced beta cell function due to autoimmune destruction or chronic pancreatitis
|– Occurs in intact bitches during diestrus or pregnancy
– Absolute or relative insulin deficiency
– Remission of diabetes is possible when diestrus or pregnancy ends
|Not reported in dogs||Type 2 diabetes||0%||– Impaired insulin secretion and insulin resistance
– Obesity is a risk factor
– Although overt type 2 diabetes is not reported in dogs, the insulin resistance of obesity might have the potential to precipitate signs of overt diabetes in dogs with beta cell destruction associated with other forms of diabetes, such as chronic pancreatitis
Nutritional Perspectives Based on Pathogenesis of Diabetes in Dogs
Understanding the pathogenesis of diabetes in dogs provides a logical foundation for understanding issues relating to nutritional management of this disease. Recently, the American Diabetes Association released a position statement comprising a large meta-analysis presenting evidence-based nutrition principles and recommendations for the treatment and prevention of human diabetes (Franz et al., 2002a). Consideration of the evidence-based recommendations for human patients with types of diabetes comparable to canine diabetes provides a rational perspective for dietary recommendations for diabetic dogs.
Dietary Carbohydrate and Type 1 Diabetes
Perspective gained from the dietary carbohydrate recommendations for human type 1 diabetics provide relevant perspective for canine diabetics because at least 50% of diabetic dogs appear to have analogous disease. Most relevant is perhaps the current recommendation regarding consumption of dietary fiber by human type 1 diabetics. After decades spent researching the effects of dietary fiber on the glycemic and lipemic responses of diabetic people, it is interesting that the current recommendation is that consumption of fiber is to be encouraged in all people and that those with type 1 diabetes require no more dietary fiber than non-diabetic people (Franz et al., 2002a). This suggests that there might also be no clinical benefit of feeding a diet with increased levels of fiber to diabetic dogs compared with feeding “typical”, moderate-fiber diets formulated for adult maintenance.
With regard to the glycemic effects of carbohydrates, there is strong evidence in human diabetics that the total amount of carbohydrate in meals and snacks is more important than the source or type (Franz et al., 2002a). Additionally, there is a strong association between the pre-meal insulin dosage required and the postprandial glycemic response to the carbohydrate content of the meal, regardless of the glycemic index, fiber, fat, or caloric content of the meal (Franz et al., 2002a). As a regimen of fixed daily insulin dosages is typically used to manage diabetic dogs, it is rational to provide a consistent amount of carbohydrate in the meals fed each day.
Dietary Fat and Type 1 Diabetes
The primary goal regarding dietary fat in human patients with diabetes is to decrease intake of saturated fat and cholesterol to reduce the risk of coronary heart disease (Franz et al., 2002a). As coronary heart disease is not recognized as a significant clinical entity in dogs, it might not be relevant to extrapolate dietary fat recommendations for human patients to diabetic dogs. For most human type 1 diabetics, effective insulin therapy returns serum lipid levels to normal and usually lowers plasma triglyceride concentrations (Franz et al., 2002a). However, for obese individuals with type 1 diabetes, there is strong evidence that restricted intake of saturated fats, incorporation of monounsaturated fats into the diet, modest weight loss, and increased physical activity may be beneficial (Franz et al., 2002a). The same recommendations might afford clinical benefit for obese diabetic dogs.
Dietary Protein and Type 1 Diabete
The protein composition of the recommended diet for people with diabetes is the same as that recommended for the non-diabetic population (Franz et al., 2002a). However, if microalbuminuria or persistent proteinuria develop, then protein restriction might help slow the progression of diabetic nephropathy in these people (EASD, 1995).
Diabetes with Exocrine Pancreatic Disease
Approximately 60% of human type 1 diabetics have reduced exocrine pancreatic function and it is now recognized that diabetes secondary to exocrine pancreatic disease might be more frequent in people than previously realized (Hardt et al., 2000). Despite this, no specific dietary recommendations are given in the current American Diabetes Association position statement regarding diabetic patients with concurrent exocrine pancreatic disease. Human diabetics with hypertriglyceridemia have increased risk of acute pancreatitis and current management recommendations include a fat-restricted diet (Athyros et al., 2002).
Dietary Recommendations for Gestational Diabetes
In the supplemental American Diabetes Association position statement focusing on gestational diabetes (Franz et al., 2002b), it is noted that restriction of dietary carbohydrate has been shown to decrease maternal postprandial glucose levels (Major et al., 1998). Similarly, bitches with diestrus-associated insulin resistance might benefit from a carbohydrate-restricted diet. This would likely reduce postprandial blood glucose fluctuations, helping to alleviate the hyperinsulinemia associated with diestrus, thus preserving beta cell function and reducing the risk of overt diabetes. There is some evidence that reduced intake of total fat, particularly saturated fat, in people might improve insulin sensitivity and reduce the risk for insulin resistance-associated diabetes (Franz et al., 2002a). Potentially, feeding a fat-restricted diet to bitches with diestrus-associated insulin resistance might improve insulin sensitivity and reduce the risk of overt diabetes. As both fat and carbohydrate restriction may be recommended for these animals, a high-protein diet is a rational choice.
Importantly, nutrient-restricted diets should never be recommended for pregnant bitches unless there is strong scientific evidence for both maternal and fetal benefit.
Dietary Recommendations for Older Diabetics
There are no evidence-based nutritional recommendations for aging diabetic persons and they must be extrapolated from what is known for the general population (Franz et al., 2002a). There is strong evidence that energy requirements for older adults are less than those for younger adults, however it is pointed out that under-nutrition is more likely than over-nutrition in elderly people. Therefore, caution should be exercised when prescribing weight-loss diets (Franz et al., 2002a).
There are no evidence-based nutritional recommendations for aging diabetic dogs. Caution should be exercised when prescribing low-calorie diets to older dogs because this might result in excessive loss of body condition. (©Lanceau).
- 1. Akerblom HK, Vaarala O, Hyoty H et al. Environmental factors in the etiology of type 1 diabetes. Am J Med Genet. 2002; 115:18-29. – PubMed –
- 2. Alejandro R, Feldman E, Shienvold FL et al. Advances in canine diabetes mellitus research: Etiopathology and results of islet transplantation. J Am Vet Med Assoc 1988; 193:1050-1055. – PubMed –
- 3. Anderson RA. Chromium, glucose tolerance, and diabetes. Biol Trace Elem Res 1992; 32:19-24. – PubMed –
- 4. Anderson RA. Chromium, glucose intolerance and diabetes. J Am Coll Nutr 1998; 17:548-555. – PubMed –
- 5. Athyros VG, Giouleme OI, Nikolaidis NL et al. Long-term follow-up of patients with acute hypertriglyceridemia-induced pancreatitis. J Clin Gastroenterol 2002; 34:472-475. – PubMed –
- 6. Atkins CE, MacDonald MJ. Canine diabetes mellitus has a seasonal incidence: Implications relevant to human diabetes. Diabetes Res 1987; 5:83-87. – PubMed –
- 7. Bauer JE, Maskell IE. Dietary fibre: Perspectives in clinical management. In: Wills JM, Simpson KW (eds). The Waltham book of clinical nutrition of the dog and cat. Oxford, New York, Tokyo: Pergamon, 1995; 87-104.
- 8. Beam S, Correa MT, Davidson MG. A retrospective-cohort study on the development of cataracts in dogs with diabetes mellitus: 200 cases. Vet Ophtalmol 1999; 2:169-172. – PubMed –
- 9. Bednar GE, Patil AR, Murray SM et al. Starch and fiber fractions in selected food and feed ingredients affect their small intestinal digestibility and fermentability and their large bowel fermentability in vitro in a canine model. J Nutr 2000; 131:276-286. – PubMed –
- 10. Blaxter AC, Cripps PJ, Gruffydd-Jones TJ. Dietary fibre and post prandial hyperglycaemia in normal and diabetic dogs. J Small Anim Pract 1990; 31:229-233.
- 11. Bouchard GF, Sunvold GD. Implications for starch in the management of glucose metabolism. In current perspectives in weight management. In: Proceedings of the 19th Annu Vet Med Forum Am Coll Vet Intern Med; 2001:16-20.
- 12. Camire ME. Chemical changes during extrusion cooking. Recent Advances. Adv Exp Med Biol 1998; 434:109-121. – PubMed –
- 13. Campbell KL, Latimer KS. Transient diabetes mellitus associated with prednisone therapy in a dog. J Am Vet Med Assoc 1984; 185:299-301.
- 14. Center SA. Carnitine in weight loss. In:Current perspectives in weight management In: Proceedings of the 19th Annu Vet Med Forum Am Coll Vet Intern Med 2001:36-44.
- 15. Church DB. Canine diabetes mellitus: Some therapeutic considerations. In: Veterinary Annual. 22nd ed.; Bristol: Scientechnica 1982:235-240.
- 16. Concannon PW. Canine pregnancy and parturition. Vet Clin North Am Small Anim Pract 1986; 16:453-475. – PubMed –
- 17. Concannon PW, McCann JP, Temple M. Biology and endocrinology of ovulation, pregnancy and parturition in the dog. J Reprod Fertil Suppl 1989; 39:3-25. – PubMed –
- 18. Davis M. Dietary fibre and post prandial hyperglycaemia. J Small Anim Pract 1990; 31:461.
- 19. Davison LJ, Fleeman LM. Pathogenesis of canine diabetes mellitus: Current research directions (abstract). In: Proceedings of the Annu Meeting Soc Comp Endocrino 2003a.
- 20. Davison LJ, Herrtage ME, Steiner JM et al. Evidence of anti-insulin autoreactivity and pancreatic inflammation in newly diagnosed diabetic dogs (abstract). J Vet Intern Med 2003b; 17:395.
- 21. EASD (Diabetes and Nutrition Study Group of the EASD). Nutritional recommendations for individuals with diabetes mellitus. Diab Nutr Metab 1988; 1:145-149.
- 22. EASD (Diabetes and Nutrition Study Group of the EASD). Recommendations for the nutritional management of patients with diabetes mellitus. Diab Nutr Metab 1995; 8:1-4.
- 23. Edney ATB, Smith PM. Study of obesity in dogs visiting veterinary practices in the United Kingdom. Vet Rec 1986; 118:391-396. – PubMed –
- 24. Eigenmann JE, Eigenmann RY, Rijnberk A et al. Progesterone-controlled growth hormone overproduction and naturally occurring canine diabetes and acromegaly. Acta Endocrinol 1983; 104:167-176. – PubMed –
- 25. Feldman EC, Nelson RW. Diabetic ketoacidosis. In: Canine and feline endocrinology and reproduction. 3rd ed. St Louis: Saunders, 2004a; 580-615. – Available from amazon.com –
- 26. Feldman EC, Nelson RW. Ovarian cycle and vaginal cytology. In: Canine and feline endocrinology and reproduction. 3rd ed. St Louis: Saunders, 2004b:752-774. – Available from amazon.com –
- 27. Fleegler FM, Rogers KD, Drash A et al. Age, sex, and season of onset of juvenile diabetes in different geographic areas. Pediatrics 1979; 63:374-379. – PubMed –
- 28. Fleeman LM, Rand JS. Long-term management of the diabetic dog. Waltham Focus 2000; 10:1 6-23.
- 29. Fleeman LM, Rand JS. Diets with high fiber and moderate starch are not advantageous for dogs with stabilized diabetes compared to a commercial diet with moderate fiber and low starch (abstract). J Vet Intern Med 2003; 17:433.
- 30. Fox GN, Sabovic Z. Chromium picolinate supplementation for diabetes mellitus. J Fam Pract 1998; 46:83-86. – PubMed –
- 31. Franz MJ, Bantle JP, Beebe CA et al. Evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications (technical review). Diabetes Care 2002a; 25:148-198. – PubMed –
- 32. Franz MJ, Bantle JP, Beebe CA et al. Gestational diabetes mellitus (position statement). Diabetes Care 2002b; 25:S94-S96.
- 33. Gamble DR, Taylor KW. Seasonal incidence of diabetes mellitus. BMJ 1969; 3:631-633.
- 34. Graham PA, Maskell IE, Nash AS. Canned high fiber diet and postprandial glycemia in dogs with naturally occurring diabetes mellitus. J Nutr 1994; 124:2712S-2715S.
- 35. Graham PA, Maskell IE, Rawlings JM et al. Influence of a high fibre diet on glycaemic control and quality of life in dogs with diabetes mellitus. J Small Anim Pract 2002; 43:67-73. – PubMed –
- 36. Graham PA, Nash AS. Rates of blindness and other complications in diabetic dogs (abstract). J Vet Intern Med 1997a; 11:124.
- 37. Graham PA, Nash AS. Survival data analysis applied to canine diabetes mellitus (abstract). J Vet Intern Med. 1997b ;11:142.
- 38. Gross KL, Wedekind K, Kirk CA, et al. Effect of dietary carnitine or chromium on weight loss and body composition of obese dogs (abstract). J Anim Sci 1998; 76:175.
- 39. Guptill L, Glickman L, Glickman N. Time trends and risk factors for diabetes mellitus in dogs: Analysis of veterinary medical data base records (1970-1999). Vet J 2003; 165:240-247. – PubMed –
- 40. Hardt PD, Krauss A, Bretz L et al. Pancreatic exocrine function in patients with type 1 and type 2 diabetes mellitus. Acta Diabetol 2000; 37:105-110. – PubMed –
- 41. Henegar JR, Bigler SA, Henegar LK et al. Functional and structural changes in the kidney in the early stages of obesity. J Am Soc Nephrol 2001; 12:1211-1217. – PubMed –
- 42. Hess RS, Kass PH, Shofer FS et al. Evaluation of risk factors for fatal acute pancreatitis in dogs. J Am Vet Med Assoc 1999; 214:46-51. – PubMed –
- 43. Hess RS, Ward CR. Effect of insulin dosage on glycemic response in dogs with diabetes mellitus: 221 cases (1993-1998). J Am Vet Med Assoc 2000; 216:217-221. – PubMed –
- 44. Hess RS, Kass PH, van Winkle TJ. Association between diabetes mellitus, hypothyroidism or hyperadrenocorticism, and atherosclerosis in dogs. J Vet Intern Med 2003:17:489-494. – PubMed –
- 45. Hoenig M, Dawe DL. A qualitative assay for beta cell antibodies. Preliminary results in dogs with diabetes mellitus. Vet Immunol Immunopathol 1992; 32:195-203. – PubMed –
- 46. Hoenig M, Laflamme DP, Klaser DA et al. Glucose tolerance and lipid profiles in dogs fed different fiber diets. Vet Ther 2001; 2:160-169.
- 47. Jarvi AE, Karlstrom BE, Granfeldt YE et al. The influence of food structure on postprandial metabolism in patients with non-insulin-dependent diabetes mellitus. Am J Clin Nutr 1995; 61:837-842. – PubMed –
- 48. Jeejeebhoy KN. The role of chromium in nutrition and therapeutics and as a potential toxin. Nutr Rev 1999; 57:329-335. – PubMed –
- 49. Kaiyala KJ, Prigeon RL, Kahn SE et al. Reduced beta-cell function contributes to impaired glucose tolerance in dogs made obese by high-fat feeding. Am J Physiol 1999; 277:E659-E667. – PubMed –
- 50. Karr-Lilienthal LK, Merchen NR, Grieshop CM et al. Selected gelling agents in canned dog food affect nutrient digestibilities and fecal characteristics of ileal cannulated dogs. J Nutr 2002; 132:1714S-1716S.
- 51. Katz SA, Salem H. The toxicology of chromium with respect to its chemical speciation: a review. J Appl Toxicol 1993; 13:217-224. – PubMed –
- 52. Kealy RD, Lawler DF, Ballam JM et al. Effects of diet restriction on life span and age-related changes in dogs. J Am Vet Med Assoc 2002; 220:1315-1320. – PubMed –
- 53. Kennedy LJ, Davison LJ, Barnes A et al. Susceptibility to canine diabetes mellitus is associated with MHC class II polymorphism (abstract). In: Proceedings of the 46th Annu Congress British Sm Anim Vet Assoc 2003:563.
- 54. Kimmel SE, Michel KE, Hess RS et al. Effects of insoluble and soluble dietary fiber on glycemic control in dogs with naturally occurring insulin-dependent diabetes mellitus. J Am Vet Med Assoc 2000; 216:1076-1081.
- 55. Krook L, Larsson S, Rooney JR. The interrelationship of diabetes mellitus, obesity, and pyometra in the dog. Am J Vet Res 1960; 21:121-124.
- 56. Kukreja A, Maclaren NK. Autoimmunity and diabetes. J Clin Endocrinol Metab 1999; 84:4371-4378. – PubMed –
- 57. Liljeberg HG, Granfeldt YE, Bjorck IM. Products based on a high fiber barley genotype, but not on common barley and oats, lower postprandial glucose and insulin responses in healthy humans. J Nutr 1996; 126:458-466.
- 58. Ling GV, Lowenstine LJ, Pulley T et al. Diabetes mellitus in dogs:A review of initial evaluation, immediate and long-term management, and out-come. J Am Vet Med Assoc 1977; 170:521-530.
- 59. Major CA, Henry MJ, De Veciana M et al. The effects of carbohydrate restriction in patients with diet-controlled gestational diabetes. Obstet Gynecol 1998; 91:600-604. – PubMed –
- 60. Marmor M, Willeberg P, Glickman LT et al. Epizootiologic patterns of diabetes mellitus in dogs. Am J Vet Res 1982; 43:465-470. – PubMed –
- 61. Massimino SP, McBurney MI, Field CJ et al. Fermentable dietary fiber increases GLP-1 secretion and improves glucose homeostasis despite increased gastrointestinal glucose transport capacity in healthy dogs. J Nutr 1998; 128:1786-1793.
- 62. Mattheeuws D, Rottiers R, Kaneko JJ et al. Diabetes mellitus in dogs: Relationship of obesity to glucose tolerance and insulin response. Am J Vet Res 1984; 45:98-103. – PubMed –
- 63. McCann JP, Concannon PW. Effects of sex, ovarian cycles, pregnancy and lactation on insulin and glucose response to exogenous glucose and glucagon in dogs (abstract). Biol Reprod 1983; 28:41.
- 64. Mittelman SD, Van-Citters GW, Kirkman EL et al. Extreme insulin resistance of the central adipose depot in vivo. Diabetes 2002; 51:755-761. – PubMed –
- 65. Montgomery TM, Nelson RW, Feldman EC et al. Basal and glucagon-stimulated plasma c-peptide concentrations in healthy dogs, dogs with diabetes mellitus, and dogs with hyperadrenocorticism. J Vet Intern Med 1996; 10:116-122. – PubMed –
- 66. Murray SM, Fahey GCJr, Merchen NR et al. Evaluation of selected high-starch flours as ingredients in canine diets. J Anim Sci 1999; 77:2180-2186. – PubMed –
- 67. Nelson R, Briggs C, Scott-Moncrieff JC et al. Effect of dietary fiber type and quantity on control of glycemia in diabetic dogs (abstract). J Vet Intern Med 2000; 14:376.
- 68. Nelson RW, Duesberg CA, Ford SL et al. Effect of dietary insoluble fiber on control of glycaemia in dogs with naturally acquired diabetes mellitus. J Am Vet Med Assoc 1998; 212:380-386. – PubMed –
- 69. Nelson RW, Ihle SL, Lewis LD et al. Effects of dietary fiber supplementation on glycemic control in dogs with alloxan-induced diabetes mellitus. Am J Vet Res 1991; 52:2060-2066. – PubMed –
- 70. Nelson RW, Sunvold GD. Effect of carboxymethylcellulose on postprandial glycaemic response in healthy dogs. In: Reinhart GA, Carey DP (eds). Recent advances in canine and feline nutrition. Vol II. Wilmington, USA: Orange Frazer Press, 1998:97-102.
- 71. Nguyen P, Dumon H, Biourge V et al. Measurement of postprandial incremental glucose and insulin changes in healthy dogs: Influence of food adaptation and length of time of blood sampling. J Nutr 1998a; 128:2659S-2662S.
- 72. Nguyen P, Dumon H, Biourge V et al. Glycemic and insulinemic responses after ingestion of commercial foods in healthy dogs: Influence of food composition. J Nutr 1998b; 128:2654S-2658S.
- 73. Onkamo P, Vaananen S, Karvonen M et al. Worldwide increase in incidence of type 1 diabetes the analysis of the data on published incidence trends. Diabetologia 1999; 42:1395-1403.
- 74. Peterson ME. Decreased insulin sensitivity and glucose tolerance in spontaneous canine hyperadrenocorticism. Res Vet Sci 1984; 36:177-182. – PubMed –
- 75. Rand JS, Fleeman LM, Farrow HA et al. Canine and feline diabetes: Nature or nurture? J Nutr 2004; 134:2072S-2080S. – PubMed –
- 76. Ravina A, Slezak L, Rubal A et al. Clinical use of the trace element chromium (III) in the treatment of diabetes mellitus. J Trace Elem Exp Med 1995; 8:183-190. – PubMed –
- 77. Rocchini AP, Mao HZ, Babu K et al. Clonidine prevents insulin resistance and hypertension in obese dogs. Hypertension 1999; 33:548-553. – PubMed –
- 78. Rodriguez J, Bruyns J, Askanazi J et al. Carnitine metabolism during fasting in dogs. Surgery 1986; 99:684-687.
- 79. Salgado D, Reusch C, Spiess B. Diabetic cataracts:Different incidence between dogs and cats. Schweiz Arch Tierheilkd 2000; 142:349-353.
- 80. Scaramal JD, Renauld A, Gomez NV et al. Natural estrous cycle in normal and diabetic bitches in relation to glucose and insulin tests. Medicina (Buenos Aires) 1997; 57:169-180.
- 81. Schachter S, Nelson RW, Kirk CA. Oral chromium picolinate and control of glycemia in insulin-treated diabetic dogs. J Vet Intern Med 2001; 15:379-384.
- 82. Seissler J, de Sonnaville JJ, Morgenthaler NG et al. Immunological heterogeneity in type 1 diabetes: Presence of distinct autoantibody patterns in patients with acute onset and slowly progressive disease. Diabetologia 1998; 41:891-897.
- 83. Selman PJ, Mol JA, Rutteman GR et al. Progestin treatment in the dog 1. Effects on growth hormone, insulin-like growth factor 1 and glucose homeostasis. Eur J Endocrinol 1994; 131:413-421.
- 84. Simpson KW. Current concepts of the pathogenesis and pathophysiology of acute pancreatitis in the dog and cat. Compend Contin Educ Pract Vet 1993; 15:247-253.
- 85. Sottiaux J. Atherosclerosis in a dog with diabetes mellitus. J Small Anim Pract 1999; 40:581-584.
- 86. Spears JW, Brown TT, Sunvold GD et al. Influence of chromium on glucose metabolism and insulin sensitivity. In: Reinhart GA, Carey DP (eds). Recent advances in canine and feline nutrition, volume II. 1998 Iams Nutrition Symposium Proceedings. Wilmington, USA: Orange Frazer Press, 1998:103-113.
- 87. Stamler J, Vaccaro O, Neaton JD et al. Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the multiple risk factor intervention trial. Diabetes Care 1993; 16:434-444.
- 88. Steiner JM, Williams DA. Development and validation of a radioimmunoassay for the measurement of canine pancreatic lipase immunoreactivity in serum of dogs. Am J Vet Res 2003; 64:1237-1241.
- 89. Stenner VJ, Fleeman LM, Rand JS. Comparison of the pharmacodynamics and pharmacokinetics of subcutaneous glargine, protamine zinc, and lente insulin preparations in healthy dogs (abstract). J Vet Intern Med 2004; 18:444-445.
- 90. Struble AL, Feldman EC, Nelson RW et al. Systemic hypertension and proteinuria in dogs with diabetes mellitus. J Am Vet Med Assoc 1998; 213:822-825.
- 91. Sunvold GD, Bouchard GF. The glycaemic response to dietary starch. In: Reinhart GA, Carey DP (eds). Recent advances in canine and feline nutrition. Vol II. Wilmington; USA: Orange Frazer Press, 1998:123-131.
- 92. Sunvold GD, Vickers RJ, Kelley RL et al. Effect of dietary carnitine during energy restriction in the canine (abstract). FASEB J 1999; 13:A268.
- 93. The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Report of the expert committee on the diagnosis and classification of diabetes mellitus. Diabetes Care 1997; 20:1183-1197.
- 94. Truett AA, Borne AT, Monteiro MP et al. Composition of dietary fat affects blood pressure and insulin responses to dietary obesity in the dog. Obes Res 1998; 6:137-146.
- 95. Twomey LN, Pethick DW, Rowe JB et al. The use of sorghum and corn as alternatives to rice in dog foods. J Nutr 2002; 132:1704S-1705S.
- 96. Vaarala O. Gut and the induction of immune tolerance in type 1 diabetes. Diabetes Metab Res Rev 1999; 15:353-361.
- 97. Villa E, Gonzalez-Albarran O, Rabano A et al. Effects of hyperinsulinemia on vascular blood flows in experimental obesity. J Steroid Biochem Mol Biol 1999; 69:273-279.
- 98. Watson PJ, Herrtage ME. Use of glucagon stimulation tests to assess beta-cell function in dogs with chronic pancreatitis. J Nutr 2004; 134:2081S-2083S.
- 99. Whitley NT, Drobatz KJ, Panciera DL. Insulin overdose in dogs and cats: 28 cases (1986-1993). J Am Vet Med Assoc 1997; 211:326-30.
- 100. Wiberg ME, Nurmi A-K, Westermarck E. Serum trypsin like immunoreactivity measurement for the diagnosis of subclinical exocrine pancreatic insufficiency. J Vet Intern Med 1999; 13:426-432.
- 101. Williams DA. Diagnosis and management of pancreatitis. J Small Anim Pract 1994; 35:445-454.
- 102. Zimmet PZ, Tuomi T, Mackay IR et al. Latent autoimmune diabetes mellitus in adults (LADA): The role of antibodies to glutamic acid decarboxylase in diagnosis and prediction of insulin dependency. Diabet Med 1994; 11:299-303.
NEW STRATEGIES IN THE MANAGEMENT OF CANINE DIABETES MELLITUS
Michael E Herrtage MA BVSc DVSC DVR DVD DSAM DECVIM DECVDI MRCVS
Department of Veterinary Medicine,
University of Cambridge
Diabetes mellitus is a heterogeneous condition in the dog rather than a single disease entity. The
incidence of diabetes mellitus is similar for the dog, with the reported frequency varying from 1 in
100 to 1 in 500.
beta cells of the islets of Langerhans in the pancreas. Carbohydrate metabolism and in particular
blood glucose concentration is controlled by the balance between the action of catabolic hormones,
for example glucagon, cortisol, catecholamines and growth hormone on the one hand, and the
principal anabolic hormone, insulin, on the other. A relative or absolute deficiency of insulin
results in decreased utilisation of glucose, amino acids and fatty acids by peripheral tissues,
particularly liver, muscle and adipose tissue. Failure of glucose uptake by these cells leads to
hyperglycaemia. Once the renal threshold for glucose reabsorption is exceeded, an osmotic
diuresis ensues with loss of glucose, electrolytes and water in the urine. Compensatory polydipsia
prevents the animal becoming dehydrated. The loss of glucose leads to catabolism of the body’s
reserves especially of fat. Excessive fat catabolism leads to the production and accumulation of
ketone bodies (acetoacetic acid, ß-hydroxybutyric acid and acetone) and the onset of diabetic
ketoacidosis. In diabetic ketoacidosis, the dog is unable to maintain an adequate fluid intake and
becomes rapidly dehydrated due to the uncontrolled osmotic diuresis. The dehydration and
acidosis requires emergency care if the animal is to survive.
In man, diabetes is classified as type I, insulin-dependant diabetes mellitus (IDDM), type 2, noninsulin-
dependant diabetes mellitus (NIDDM) type 3 due to other causes. Type 1 diabetes is
characterised by a combination of genetic susceptibility and immunological destruction of beta
cells, with progressive and eventually complete insulin insufficiency. The presence of circulating
autoantibodies against insulin, the beta cell, and/or glutamic acid decarboxylase (GAD) usually
precedes the development of hyperglycaemia or clinical signs. Type 2 diabetes mellitus is
characterised by insulin resistance and “dysfunctional” beta cells; defects believed to be genetic in
origin are evident for a decade or longer before hyperglycaemia and clinical signs of diabetes
develop, and the deleterious effects can be accentuated by environmental factors such as obesity.
This classification has not proved very useful in veterinary medicine since nearly all dogs with
diabetes mellitus require insulin therapy regardless of the underlying aetiology require treatment
Diabetes mellitus is a disease of middle-aged dogs with a peak incidence around 8 years of age.
Genetic predisposition to diabetes has been found in Keeshunds and Samoyeds. Cairn terriers,
poodles and dachshunds may also be over-represented, although a recent survey showed over half
the diabetic dogs were Labrador retrievers, collies and Yorkshire terriers. Entire females are more
frequently affected than males and this is due mainly to the induction of growth hormone secretion
by progesterone and other progestogens.
Polyuria, polydipsia, increased appetite and weight loss develop over a few weeks in
uncomplicated cases. In entire bitches, this usually occurs during the metoestrus phase of the
Hepatomegaly, muscle wasting and infections of the urinary or respiratory tracts may be noted on
clinical examination. Ulcerative skin lesions and cutaneous xanthomata have occasionally been
reported. If the diabetes remains uncontrolled, an accumulation of ketone bodies may occur which
causes metabolic acidosis and leads to depression, anorexia, vomiting, rapid dehydration. Coma
and death may result from severe hypovolaemia and circulatory collapse.
Urine analysis reveals persistent glycosuria and often ketonuria. Despite the high solute load in
the urine, which would tend to increase the specific gravity of the urine, many older dogs may
have impaired renal concentrating power and thus the specific gravity of the urine is variable,
typically ranging between 1.015 and 1.045. Bacterial cystitis is common and occasionally may
involve gas-producing organisms which can cause emphysematous cystitis.
Plasma biochemistry reveals a fasting hyperglycaemia (> 10 mmol/l) and hyperlipidaemia. In
some patients the blood will be lactescent due to lipaemia. Liver enzymes are usually raised and
liver function tests such as bile acid concentrations may be abnormal. In cases where diabetes is
associated with pancreatitis, amylase and lipase concentrations may be elevated.
In diabetic ketoacidosis, there are serious derangements in fluid, electrolyte and acid-base status.
The most frequent abnormalities are pre-renal azotaemia, hyponatraemia and metabolic acidosis.
The cat appears to be less prone to developing diabetic ketoacidosis.
Routine stabilisation of diabetes mellitus in the dog
The primary goal of diabetes therapy is to maintain normoglycaemia and thereby control the signs
that occur secondary to hyperglycaemia and glycosuria which result in the development of
complications. Complications of diabetes mellitus include: hypoglycaemia, ketoacidosis, cataract
formation, hepatic lipidosis, pancreatitis, infections, retinopathy, diabetic nephropathy, diabetic
neuropathy and skin disease. The essentials of good stabilisation of diabetes mellitus requires
understanding by the owner, and adherence to a regular daily routine that involves diet, insulin
administration and regular, controlled exercise.
Stabilisation can be carried out satisfactorily at home, but particularly if the patient is ketotic, it
may be preferable to hospitalise the animal during stabilisation since it is easier to monitor blood
glucose more closely.
Most diabetic dogs are presented with complete islet cell degeneration and atrophy. Therefore
diabetes mellitus in dogs is insulin-dependent. Rarely, bitches may be presented during the
metoestrus phase of the oestrus cycle before islet cell exhaustion has occurred. If
ovariohysterectomy is performed in these patients immediately the signs of diabetes become
apparent, there can be complete resolution of the disease. However, in the majority of bitches this
opportunity is missed or goes unnoticed and permanent damage to the islet cells occurs.
Dietary therapy. Appropriate dietary therapy is an essential part of the management of diabetes.
The diet must be well-balanced and constant in both composition and amount fed at each meal. It
is therefore most convenient to use a commercial diet. Canned or dry foods which contain
digestible complex carbohydrates should be fed as slow digestion minimises the fluctuations in
post-prandial blood glucose concentrations. Semi-moist foods which contain a predominance of
easily assimilated carbohydrates in the form of disaccharides and propylene glycol should be
avoided because of marked post-prandial hyperglycaemia. There is evidence that diets with high
fibre content improve glycaemic control by delaying starch hydrolysis and glucose absorption
thereby reducing post-prandial fluctuations in blood glucose. High fibre diets are also beneficial in
correcting obesity. However, there may be disadvantages in using high fibre diets such as reduced
palatability and the fact the low caloric density may cause the patient to lose excessive weight or
fail to gain weight in those patients already below ideal body weight. The author tends to reserve
high fibre diets for those patients that are difficult to stabilise and/or are obese.
Finally, the feeding schedule should be designed to enhance the action of insulin and minimise
post-prandial hyperglycaemia. The daily caloric intake should occur when insulin is present in the
circulation and capable of handling glucose absorbed from the intestine. Several small meals are
preferable to one large feed as these will help minimise post-prandial hyperglycaemia and thus
help to control fluctuations in blood glucose. The author routinely recommends two equal meals
fed at times to coincide with insulin activity. In cases that prove difficult to stabilise 3–4 smaller
meals are fed during the day. Titbits and scavenging must be avoided as they tend to destabilise
Insulin therapy. For routine stabilisation in the dog insulin zinc suspension (lente) which contains
a mixture of 30% insulin zinc suspension (amorphous) and 70% insulin zinc suspension
(crystalline) is the preparation of choice in the UK. When given by subcutaneous injection, it is an
intermediate acting insulin with an onset of activity at 1–2 hours, peak activity around 6–12 hours
and a duration of action of between 18 and 26 hours in the dog. The times for peak activity and
duration of action vary with the individual, but in most dogs once daily administration is adequate.
Lente insulin is usually given as a single morning injection at the same time or just before the first
meal with the second meal given 6–8 hours later to coincide with peak insulin activity. An initial
dose of between 0.5–1.0 unit/kg is used. Insulin is probably best dosed on body surface area
rather than a simple weight basis. Thus small dogs (<15 kg) tend to require 1.0 unit/kg and larger
dogs (>25 kg) receive 0.5 unit/kg. Although the subcutaneous route is ideal for long term use, the
intramuscular route may be used initially, especially in mildly dehydrated or ketotic animals,
because absorption from subcutaneous depots in these patients may be slow and erratic.
Insulin should be administered using specific 0.5 ml or 1.0 ml syringes calibrated in units (100 or
40 units/ml depending on the preparation). Insulin preparations should be stored in a refrigerator
at 2–8oC because they are adversely affected by heat or freezing. Preparations should be rolled
gently to re-suspend the particles before use.
A diabetic patient will usually take 2–4 days to respond fully to a dose of insulin or a change in
preparation. It is important to avoid increasing the dose too quickly before equilibration has
occurred as this can lead to a sudden and precipitous fall in blood glucose due to overdosage with
insulin. In most cases, adjustments in the insulin dose should be made in small changes of one to
four units per injection.
The type of preparation and frequency of administration may require alteration in those patients
that prove difficult to stabilise with this standard routine. However, it is good for the clinician to
become familiar with one type of insulin preparation and only change from that preparation if the
insulin is the cause of the instability.
Ideally monitoring should consist of serial blood glucose concentrations as tighter diabetic control
can be gained than with urine glucose estimations. Initially at least two blood glucose estimations
should be made, one before insulin is administered and the second just before the second feed.
Once the dog appears fairly stable more frequent blood samples should be taken throughout the
day to assess the degree of stabilisation. An assessment of daily water intake can also provide
useful information about the degree of diabetic control.
Blood glucose concentrations should ideally be maintained between 5 and 9 mmol/l. The blood
glucose concentration will usually be highest in the morning before insulin is administered and
lowest just before the second feed. A trace of glucose in the morning urine sample may be
acceptable but the urine should be negative at other times in the day. However, it is important to
remember that urine glucose may not reflect the blood glucose concentration at the same point in
time and if the urine glucose is negative, the blood glucose concentration could be hypoglycaemic
(< 3.0 mmol/l), normoglycaemic or hyperglycaemic (> 5.5 mmol/l).
Although the author’s clients monitor urine for glucose and ketones regularly, he does not
advocate adjusting daily insulin dosages on the basis of morning urine glucose measurements.
Instead, he prefers to continue with a fixed insulin dosage unless the patient remains unstable for
more than several days.
Measurement of glycated proteins such as fructosamine and glycosylated haemoglobin is used
increasingly in the dog to monitor the response to treatment. The irreversible, non-enzymatic
glycation process occurs throughout the life span of the protein, mainly albumin in the case of
fructosamine, and is proportional to the glucose concentration over that time. These
measurements reflect the average blood glucose concentration over the preceding one to two
weeks in the case of serum fructosamine and two to three months in the case of glycosylated
haemoglobin. Fructosamine concentrations less than 400 mmol/l indicate good glycaemic control
whereas concentrations above 500 mmol/l are found in newly diagnosed or poorly controlled
diabetics. Glycosylated haemoglobin is less routinely available as an assay. Well controlled
diabetic dogs have between 4 and 6 per cent glycosylated haemoglobin, whereas poorly controlled
diabetics have concentrations greater than 7 per cent.
A diabetic record should be kept by the owner for each patient as alterations to stability can be
assessed more easily over a period of time. Insulin requirements will be increased by infection,
oestrus particularly the metoestrus phase to the cycle, pregnancy and ketoacidosis. It is
recommended that entire bitches should undergo ovariohysterectomy to avoid insulin resistance at
Trying to control Diabetes in an EPI pet can be quite the challenge, and often requires much more understanding of how to work with concurrent pancreatic conditions vs. just trying to managing Diabetes. Some tips to consider when dealing with both EPI + Diabetes are listed below. Diabetes can become life-threatening very quickly…… so please always work with your vet when dealing with Diabetes.
In addition, some EPI + Diabetes cases need more-in-depth analysis of a complicated situation. If you vet needs to consult with an endocrinologist specialist, please suggest that he or she contact Dr. Mark Petersen. Dr. Petersen is one of the top USA small animal endocrinologist and will consult with vets. His website with contact information is: https://www.drmarkepeterson.com/endocrine-clinic/
For Pet Owners
I strongly advise all Diabetic Pet owners to check out the K9-Diabetes group: http://k9diabetes.com/
…even if you prefer not to join the k9-Diabetes Forum… This site has the most comprehensive, current and valid Diabetic site for dogs.
Pet owners can also view Dr. Petersen’s endocrinology blog… Specifically the pancreas “blo” that may help them better understand why it can be so convoluted dealing with EPI + Diabetes and how to better ascertain what might be going on and why current treatment is not working: https://endocrinevet.blogspot.com/search/label/Pancreas
Also…. specifically check out these particular endocrinology references
- Blois SL, Dickie E, Kruth SA, et al. Multiple endocrine diseases in dogs: 35 cases (1996-2009). J Am Vet Med Assoc 2011;238:1616-1621.
- Ford SL, Nelson RW, Feldman EC, et al. Insulin resistance in three dogs with hypothyroidism and diabetes mellitus. J Am Vet Med Assoc 1993;202:1478-1480.
- Hess RS, Saunders HM, Van Winkle TJ, et al. Concurrent disorders in dogs with diabetes mellitus: 221 cases (1993-1998). J Am Vet Med Assoc 2000;217:1166-1173.
intervention to better ascertain what is going on and how to treat the concurrent conditions.