Genetic Welfare Problems of Companion Animals

An information resource for prospective pet owners

Yorkshire Terrier

Yorkshire Terrier

Diabetes Mellitus

Related terms: Canine diabetes mellitus, DM, Diabetic Ketoacidosis

VeNom term:  Diabetes mellitus (VeNom code: 658).

Related conditions: Cataract, Pancreatitis, Hyperadrenocorticism

Outline: Diabetes mellitus is a hormonal disorder that occurs when there is a failure to adequately control blood sugar levels. Dogs that have the condition are unable to use blood sugar as an energy source for the cells in their body as they would normally, and therefore the level of sugar in the blood increases. The most common signs of diabetes mellitus are excessive thirst and urination with weight loss.

The onset of diabetes mellitus occurs most commonly in middle aged or older dogs. Left untreated, diabetes mellitus can lead to complications including a severe illness called diabetic ketoacidosis where the body begins to break down body tissue, such as fats and muscle, to use as a source of energy in place of blood sugars. This process produces toxins that can cause dehydration, nausea and vomiting and can be life-threatening if left untreated. Diabetic dogs are generally reliant on dietary management and daily injections of the hormone insulin for the rest of their lives.

There is evidence of a genetic basis for the development of diabetes mellitus, and the Yorkshire terrier dog breed has been shown to be at increased risk of the condition compared with the general dog population.


Summary of Information

(for more information click on the links below)

1. Brief description

Diabetes mellitus is a hormonal disorder which results in high levels of sugar (glucose) in the blood. Glucose is an important source of energy in the body. In animals that are diabetic, the cells in the body are unable to absorb glucose properly, and this leads to an increase in the blood. In dogs, the most common reason for high blood sugar levels is because they are not producing sufficient amounts of the hormone, insulin that controls the uptake of glucose by cells. The pancreas is the organ that produces insulin and, commonly, dogs with diabetes mellitus have a damaged pancreas. This is similar to a form of type-1 diabetes in humans.

Dogs with high levels of glucose in the blood excrete excess glucose from the body via the kidneys, which results in frequent and copious urination. This dehydrates the body so that the dog becomes thirsty, drinks more frequently and drinks larger amounts. The condition leads to weight loss, slow wound healing, poor coat condition and the dog may show increased appetite and lethargy. Over time, the dog may also suffer damage to its small blood vessels and nerves, leading to cataracts in the eye.

 The major signs of diabetes mellitus are excessive drinking and urination (called polydipsia and polyuria), weight loss, increase in appetite and lethargy. Cataract development and consequent blurred vision are also common in dogs with diabetes. If the initial signs of diabetes mellitus go unnoticed, dogs may develop a severe and life-threatening condition called diabetic ketoacidosis, which occurs when the body breaks down fats and tissue to produce glucose to such a degree that the by-products of this process, ketones, have built up to a toxic level and the blood has become acidic.

2. Intensity of welfare impact

Diabetes mellitus is often a lifelong condition, and the dog’s quality of life may suffer over a long duration. Dogs with diabetes may suffer from excessive thirst and urination, weight loss, increase in appetite and lethargy. Over time, if the levels of insulin and glucose are not well-balanced, dogs may develop cataracts which affect vision. Owners of dogs with diabetes mellitus are most concerned about the condition itself, loss of vision, episodes of low blood sugar (termed hypoglycaemic episodes) causing lethargy, and long-term future care (Niessen et al 2012). Dogs that are over-weight are more prone to developing diabetes and bitches may be more susceptible to the condition than males.

If dogs develop diabetic ketoacidosis, the symptoms are more severe and include dehydration, nausea and vomiting, and this can be life-threatening without emergency treatment. Progression to a more complicated diabetic condition is often associated with other diseases that can be painful for the animal (Davison et al 2005; Hume et al 2006; Mattin et al 2014), with the most common being inflammation of the pancreas (pancreatitis), urinary tract infection and hyperadrenocorticism (called ‘Cushings’ in humans), which involves excess production of the hormone cortisol (important for metabolism and regulation of body processes). This causes symptoms such as abdominal distension, loss of muscle mass and strength, lethargy, loss of fur, and thinning and calcification of the skin.

3. Duration of welfare impact

The onset of diabetes mellitus occurs generally in middle-aged and older dogs, typically between 5-12 years of age (Catchpole et al 2005; Marmor et al 1982). In one study of 439 diabetic dogs, the average (median) age of onset was 9.9 years and the average (median) survival time after diagnosis was 17.3 months (Mattin et al 2014). Using Swedish insurance records, it has been estimated that 1 in 100 dogs reaching 12 years of age will develop diabetes mellitus (Fall and colleagues 2007). Diabetic dogs often require insulin treatment throughout their entire life (Fleeman and Rand 2001) and diabetes can be managed through dietary control, by regular provision of food portions and using specially formulated high-fibre foods, by oral hypoglycaemic drugs and/or by regular (daily or twice daily) injections of insulin.

4. Number of animals affected

Overall, the estimated prevalence of diabetes mellitus in the overall UK dog population was 34 cases per 10,000 dogs (0.34%) based on clinical data from veterinary practices (Mattin et al 2014). In Sweden, the overall incidence of diabetes mellitus was 13 new cases per 10,000 dog years at risk (Fall et al 2007). In the United States of America and Canada, the number of cases of diabetes mellitus in dogs presented to veterinary teaching hospitals increased from 19 cases per 10,000 admissions in 1970 to 64 cases per 10,000 in 1999 (Guptill et al 2003).

Studies of the UK dog population suggests that Yorkshire terriers are consistently overrepresented in diabetic dog populations versus non-diabetic populations (Mattin et al 2014; Catchpole et al 2005).

5. Diagnosis

The major presenting signs of diabetes mellitus are excessive thirst (polydipsia), excessive urination (polyuria) and weight loss (Doxey et al 1985). Diagnosis of diabetes mellitus is based on testing for abnormally high levels glucose and ketones in the urine (glycosuria and ketonuria) and persistently high levels of glucose in the blood (hyperglycaemia) (Fleeman and Rand 2001). Testing for fructosamine, a product of glucose and protein reactions in the blood can assist in longer-term diagnosis and management of diabetes mellitus.

6. Genetics

Canine diabetes mellitus is a complex genetic disorder, caused by a number of different genes and influenced by environmental factors also. In Yorkshire terriers, a number of genes have been identified as likely to contribute to the high risk of developing diabetes mellitus in this breed (Short et al 2010), but the mode of inheritance is not straight-forward. Further research is required to determine the role and relationship between diabetes susceptibility genes in different breeds.

7. How do you know if an animal is a carrier or likely to become affected?

The precise cause of the increased risk of diabetes mellitus in specific breeds is not known, and there are currently no genetic tests that can determine whether an animal is susceptible to the development of the condition.

8. Methods and prospects for elimination of the problem

Both genetic and environmental (e.g. diet) factors play a role in canine diabetes, and it is therefore unlikely that a genetic approach alone will eliminate this particular condition. It is not advisable to breed from dogs affected by diabetes mellitus, or from those with affected relatives within breeds that have increased susceptibility, including grandparents, siblings, previous offspring and siblings of parents.


For further details about this condition, please click on the following:
(these link to items down this page)


1. Clinical and pathological effects

Diabetes mellitus is a hormonal disorder which results in high levels of sugar (glucose) in the blood. Glucose is an important source of energy in the body and is produced when carbohydrates in food are broken down during digestion. The glucose can either be absorbed directly by cells and metabolised to release energy or converted in the liver to glycogen and stored for later use. In animals that are diabetic, the cells in the body are unable to absorb glucose properly, and this leads to an increase of sugar in the blood. The cause of canine diabetes mellitus is thought to involve multiple factors and most often occurs in dogs due to reduced insulin production (insulin deficiency) but it can also occur when the cells in the body stop absorbing insulin (insulin resistance). The pancreas is the organ that produces the hormone insulin and commonly, dogs that have diabetes mellitus are found to have damage to the cells in the pancreas that produce insulin (pancreatic beta cell destruction). This means that insulin is produced at lower levels than is required for the normal functioning of the body (insulin deficiency diabetes; Atkins et al 1988; Hoenig and Dawe 1992; Watson 2003). This is similar to a form of type-1 diabetes in humans.

Another cause of diabetes is insulin resistant diabetes, which is less common in dogs, and occurs when cells in the body have become unresponsive to the insulin hormone that is produced, due to a decrease in activity of the insulin receptors on the cells of tissue. This is diagnosed when dogs have both a high level of glucose (hyperglycemia) and a high level of insulin in their blood (hyperinsulinaemia). It is commonly associated with hormonal changes; for example in female dogs, increased levels of the sex hormone progesterone related to their season may cause short-term diabetes mellitus because the progesterone hormone blocks insulin from entering cells of the body (Drouin et al 2009).

In a condition called hyperadrenocorticism, dogs have unusually high levels of the hormone cortisol (hyperadrenocorticism), which is involved in metabolism, and this hormone may also block insulin receptors and therefore contribute to the development of diabetes mellitus. The symptoms of diabetes mellitus are the same for both insulin deficient and insulin resistant types but the treatment plans may differ. Since there may be a delay between the onset of diabetes and time of diagnosis, some dogs start with insulin resistant diabetes and then progress to insulin deficiency diabetes, presumably due to further damage to insulin producing beta cells (Catchpole et al 2005).

Where there are high levels of glucose in the blood, excess glucose is excreted from the body via the kidneys and this produces the characteristic signs of diabetes as dogs that have high levels of blood sugar need to urinate frequently and produce large volumes of urine when they do so. The body becomes dehydrated and dogs become thirsty, drink more frequently and drink larger amounts to replace the fluid lost. The deficiency in insulin production has the effect that the uptake and storage of glucose is impaired and therefore the cells in the body gain energy from other sources, eg fats and proteins. This may lead to weight loss, poor wound healing and coat condition due to loss of immune system function (Peikes et al 2001), and the dog may show increased appetite and lethargy (Doxey et al 1985; Fleeman and Rand 2001). Over time, the dog may also suffer damage to its small blood vessels and nerves, leading to cataracts in the eye. Cataract development which causes blurred vision is very common in diabetic dogs (Beam et al 1999). Normally, the lens of the eye absorbs glucose from fluids within the eyeball and metabolises it for energy and excess sugar is converted to another sugar, sorbitol. When there is excess sugar (glucose and sorbitol), water is pulled into the lens tissue which causes the cloudiness and loss of clarity in the lens.

If the initial signs of diabetes mellitus go unnoticed, dogs may develop a condition called diabetic ketoacidosis, which occurs when the body has been breaking down fats and tissue to produce glucose to such a degree that the by-product of this process, ketones, have built up to a toxic level and the blood has become acidic. Anorexia, vomiting and dehydration can develop and the condition is life threatening without appropriate therapy (Catchpole et al 2005).

There is some evidence that females are at greater risk of developing diabetes mellitus, and this is likely due to the hormonal changes that occur during the oestrus cycle (Davison et al 2005; Marmor et al 1982), and two studies have described the effects of neuter-sex status (neutered males being more at risk than entire males; Guptill et al 2003; Mattin et al 2014). However, sex predispositions have not been fully explored for diabetes risk, and there are many confounding factors (eg weight, age or hormonal balance).

Return to top

2. Intensity of welfare impact

Since diabetes mellitus is often a lifelong condition, the dog’s quality of life may suffer, although, in general, if managed well, diabetic dogs can have a good quality of life. In an international survey of owners of dogs with diabetes mellitus, 84% perceived that the condition had a negative impact on their dog’s quality of life (Niessen et al 2012), with major issues being concerns about the condition itself, loss of vision, episodes of low blood sugar (“hypoglycaemic episodes”) which cause lethargy, and long-term future care.

Causes of welfare concern for diabetic dogs would be excessive thirst (polydipsia), weight loss, lethargy and cataract development, which may impact on quality of life. Cataracts, in particular, are common and these may cause anxiety, confusion and increased risk of injury due to vision loss, although many dogs are able to learn to cope with failing vision and especially if the cataract development is gradual. In one study, 75% of diabetic dogs had developed cataracts (Beam et al 1999). Of these dogs, the majority developed cataracts within 5-6 months of the time of diagnosis of the diabetes, and approximately 80% of dogs developed cataracts within 16 months of diagnosis (Beam et al 1999).

If the initial signs of diabetes mellitus go unnoticed, dogs may develop severe illness (diabetic ketoacidosis), with anorexia, vomiting and dehydration; and is life threatening without emergency treatment. In a study of 127 dogs diagnosed with diabetic ketoacidosis at the time of initial diagnosis of diabetes mellitus, 30% of dogs did not survive (Hume et al 2006). Progression to a more complicated diabetic condition is often associated with other diseases, with the most common being pancreatitis and urinary tract infection, both of which can be painful. Hyperadrenocorticism is also associated with, and has similar outward signs to diabetes mellitus, (Davison et al 2005; Hume et al 2006; Mattin et al 2014). In a recent study, diabetic dogs with pancreatitis and ketoacidosis had increased risk of death (Mattin et al 2014).

Return to top

3. Duration of welfare impact

The onset of diabetes mellitus occurs generally in middle-aged and older dogs, typically between 5-12 years of age (Catchpole et al 2008; Marmor et al.1982). Some dogs may develop the condition earlier if life although this is uncommon (ie 10% of 1536 dogs developed diabetes mellitus at under 7 years of age: “Juvenile diabetes mellitus”; Catchpole et al 2013).

In one study of 439 diabetic dogs, the median age of onset of 9.9 years and the median survival time after diagnosis was 17.3 months (Mattin et al 2014). The highest mortality rate has been reported during the first 6 months from diagnosis (Nelson and Reusch 2014). Using Swedish insurance records, Fall and colleagues (2007) estimated that 1 in 100 dogs reaching 12 years of age would develop diabetes mellitus.

Diabetes mellitus can be managed with diet, hypoglycaemic agents and/or daily insulin therapy although diabetic dogs often require insulin treatment throughout their entire life (Fleeman and Rand 2001).

Return to top

4. Number of animals affected

The estimated prevalence of diabetes mellitus in the UK dog population is 34 cases per 10,000 dogs (0.34%) based on clinical data from veterinary practices (Mattin et al 2014). From insurance records in Sweden, the overall incidence of diabetes mellitus was 13 cases per 10,000 dog years at risk (Fall et al 2007). In the United States of America and Canada, the prevalence of diabetes mellitus in dogs presented to veterinary teaching hospitals increased from 19 cases per 10,000 admissions in 1970 to 64 cases per 10,000 in 1999 (Guptill et al 2003).

In a study of veterinary clinic data in the UK, Yorkshire terriers had the greatest odds of a diabetes mellitus diagnosis, which was almost 5 times higher than crossbreed dogs (Mattin et al 2005; odds ratio: 4.56, 95% confidence interval: 1.79-11.64). In another study, which compared data from the UK national canine diabetes register with insurance data, the number of Yorkshire terriers with diabetes mellitus was disproportionally greater than the number of Yorkshire terriers in the general insurance population, and therefore Yorkshire terriers had a high relative risk of diabetes mellitus compared to the overall population (Catchpole et al 2005; odds ratio: 3.69; 95% confidence interval: 2.55-5.35).

Return to top

5. Diagnosis

The major presenting signs of diabetes mellitus are polydipsia, polyuria and weight loss (Doxey et al 1985). Diagnosis of diabetes mellitus is based on the presence of glycosuria, ketonuria and persistent hyperglycaemia (glucose >9 mmol/l; Fleeman and Rand 2001).

Diagnostic tests target plasma glucose levels or pancreatic beta cell function, including radioimmunoassays for canine insulin and C-peptide. Measures of high serum fructosamine and glycated haemoglobin are increasingly being used to diagnose and monitor therapy (Jensen 1995). Other useful biochemical markers include serum trypsin-like immune-reactivity and canine pancreatic lipase immunoreactivity, indicative of exocrine pancreatic disease.

Return to top

6. Genetics

Canine diabetes mellitus is considered a complex inherited disorder, since its development is influenced by several different genes and environmental factors. In humans, the major histocompatibility complex genes are strongly associated with type-1 diabetes and latent autoimmune diabetes in adults (Grant et al 2010), thus studies on the genetic mechanisms for diabetes mellitus in dogs have focused on similar areas, the dog leucocyte antigen (DLA) genes. On these gene sequences, several alleles or groups of alleles have been identified as associated with a higher risk of diabetes mellitus in dogs (Kennedy et al 2006), and those that carry two separate high risk gene sequences have a substantially increased risk of diabetes mellitus compared to dogs that only carry one type of high risk allele, or none. It should be noted that these gene associations are not necessarily specific for diabetes mellitus and similar DLA genotypes have also been associated with increased susceptibility to hypothyroidism (underactive thyroid gland) and hypoadrenocorticism (low production of the hormone cortisol) in dogs (Kennedy et al 2006; Hughes et al 2010). Therefore, expression of these genes should be considered to be a general risk factor for immune-mediated disease, and other genes and environmental factors might then influence the nature and target of the condition.

Diabetes susceptible breeds such as the Yorkshire terrier demonstrated a different genotype profile for genes associated with insulin production compared to ‘resistant’ breeds in which diabetes is uncommon (Boxer, German shepherd dog, Golden retriever; Short et al 2007). Cytokine gene polymorphisms, associated with cell signalling in the body (which might influence the uptake of glucose or insulin in the cells) were linked with diabetes mellitus in Yorkshire terriers (and other small breeds; Miniature poodles, Cairn terriers, Miniature schnauzers, Cavalier King Charles spaniels; Short et al 2007). However, this does not provide the full picture of how diabetes mellitus is inherited, and it is likely there are other genes and environmental factors at play. Further research is required to determine the role and relationship between diabetes susceptibility genes in different breeds.

Return to top

7. How do you know if an animal is a carrier or likely to become affected?

Although there are clear breed-related predispositions for canine diabetes mellitus, the cause of the increased risk in specific breeds is not currently known. At present, there are no genetic tests which can determine whether an animal is susceptible to diabetes mellitus development.

Return to top

8. Methods and prospects for elimination of the problem

The mode of inheritance of diabetes mellitus is difficult to determine, likely because of the multiple factors of development, and it may be specific to certain breeds or breed groups, or on a case by case basis. Both genetic and environmental (eg diet) factors play a role in canine diabetes, although specific environmental risk factors have not yet been systematically evaluated in diabetic dogs. It is therefore unlikely that a genetic approach alone will eliminate the condition. For such complex inherited disorders, a multi-strategy approach using health screening schemes, pedigree breed information and genome-wide estimated breeding values is recommended to reduce the problem (Farrell et al 2015). Since dogs in this breed have an increased susceptibility to the condition, it is not advisable to breed from those dogs affected by diabetes mellitus, or from those with affected relatives, including grandparents, siblings, previous offspring and siblings of parents.

Return to top

9. Acknowledgements

UFAW thanks Dr Emma Buckland (BSc, PhD), Dr David Brodbelt (MA VetMB PhD DVA DipECVAA MRCVS) and Dr Dan O’Neill (MVB BSc, MSc, PhD, MRCVS) for their work in compiling this section.

Return to top

10. References

Atkins CE, LeCompte PM, Chin HP, Hill JR, Ownby CL and Brownfield MS (1988) Morphologic and immunocytochemical study of young dogs with diabetes mellitus associated with pancreatic islet hypoplasia. American Journal of Veterinary Research 49: 1577–81

Beam S, Correa MT and Davidson MG (1999) A retrospective-cohort study on the development of cataracts in dogs with diabetes mellitus: 200 cases. Veterinary Ophthalmology 2: 169–172

Catchpole B, Adams JP, Holder AL, Short AD, Ollier WER and Kennedy LJ (2013) Genetics of canine diabetes mellitus: are the diabetes susceptibility genes identified in humans involved in breed susceptibility to diabetes mellitus in dogs? The Veterinary Journal 195: 139–47. doi:10.1016/j.tvjl.2012.11.013

Catchpole B, Kennedy LJ, Davison LJ and Ollier WER (2008) Canine diabetes mellitus: From phenotype to genotype. Journal of Small Animal Practice 49: 4-10

Catchpole B, Ristic JM, Fleeman LM and Davison LJ (2005) Canine diabetes mellitus: can old dogs teach us new tricks? Diabetologia 48: 1948–56. doi:10.1007/s00125-005-1921-1

Davison LJ, Herrtage ME and Catchpole B (2005) Study of 253 dogs in the United Kingdom with diabetes mellitus. The Veterinary Record 156: 467–471

Doxey DL, Milne EM and Mackenzie CP (1985) Canine diabetes mellitus: a retrospective survey. Journal of Small Animal Practice 26: 555–561. doi:10.1111/j.1748-5827.1985.tb02232.x

Drouin P, Blickle JF, Charbonnel B, Eschwege E, Guillausseau PJ, Plouin PF, Daninos JM, Balarac N and Sauvanet JP (2009) Diagnosis and classification of diabetes mellitus. Diabetes Care 32 Suppl 1: S62–7. doi:10.2337/dc09-S062

Fall T, Hamlin HH, Hedhammar A, Kämpe O and Egenvall A (2007) Diabetes mellitus in a population of 180,000 insured dogs: incidence, survival, and breed distribution. Journal of Veterinary Internal Medicine 21: 1209–1216. doi:10.1111/j.1939-1676.2007.tb01940.x

Farrell LL, Schoenebeck JJ, Wiener P, Clements DN and Summers KM (2015) The challenges of pedigree dog health: approaches to combating inherited disease. Canine Genetics and Epidemiology 2: 3. doi:10.1186/s40575-015-0014-9

Fleeman LM and Rand JS (2001) Management of Canine Diabetes. Veterinary Clinics of North America: Small Animal Practice 31: 855–880. doi:10.1016/S0195-5616(01)50003-0

Grant SFA, Hakonarson H and Schwartz S (2010) Can the genetics of type 1 and type 2 diabetes shed light on the genetics of latent autoimmune diabetes in adults? Endocrine Reviews 31: 183–93. doi:10.1210/er.2009-0029

Guptill L, Glickman L and Glickman N (2003) Time Trends and Risk Factors for Diabetes Mellitus in Dogs: Analysis of Veterinary Medical Data Base Records (1970–1999). The Veterinary Journal 165: 240–247. doi:10.1016/S1090-0233(02)00242-3

Hoenig M and Dawe DL (1992) A qualitative assay for beta cell antibodies. Preliminary results in dogs with diabetes mellitus. Veterinary Immunology and Immunopathology 32: 195–203

Hughes AM, Jokinen P, Bannasch DL, Lohi H and Oberbauer AM (2010) Association of a dog leukocyte antigen class II haplotype with hypoadrenocorticism in Nova Scotia Duck Tolling Retrievers. Tissue Antigens 75: 684–90. doi:10.1111/j.1399-0039.2010.01440.x

Hume DZ, Drobatz KJ and Hess RS (2006) Outcome of Dogs with Diabetic Ketoacidosis: 127 Dogs (1993-2003). Journal of Veterinary Internal Medicine 20: 547–555. doi:10.1111/j.1939-1676.2006.tb02895.x

Jensen A (1995) Glycated blood proteins in canine diabetes mellitus. Veterinary Record 137: 401–405. doi:10.1136/vr.137.16.401

Karvonen M, Viik-Kajander M, Moltchanova E, Libman I, LaPorte R and Tuomilehto J (2000) Incidence of childhood type 1 diabetes worldwide. Diabetes Mondiale (DiaMond) Project Group. Diabetes Care 23: 1516–26

Kennedy LJ, Davison LJ, Barnes A, Short AD, Fretwell N, Jones CA, Lee AC, Ollier WER and Catchpole B (2006) Identification of susceptibility and protective major histocompatibility complex haplotypes in canine diabetes mellitus. Tissue Antigens 68: 467–476

Marmor M, Willeberg P, Glickman LT, Priester WA, Cypess RH and Hurvitz AI (1982) Epizootiologic patterns of diabetes mellitus in dogs. American Journal of Veterinary Research 43: 465–70

Mattin M, O’Neill D, Church D, McGreevy PD, Thomson PC and Brodbelt D (2014) An epidemiological study of diabetes mellitus in dogs attending first opinion practice in the UK. The Veterinary Record 174: 349. doi:10.1136/vr.101950

Moalem S, Storey KB, Percy ME, Peros MC and Perl DP (2005) The sweet thing about Type 1 diabetes: a cryoprotective evolutionary adaptation. Medical Hypotheses 65: 8–16. DOI:10.1016/j.mehy.2004.12.025

Nelson RW and Reusch CE (2014) Animal models of disease: classification and etiology of diabetes in dogs and cats. The Journal of Endocrinology 222: T1–9. DOI:10.1530/JOE-14-0202

Niessen SJM, Powney S, Guitian J, Niessen APM, Pion PD, Shaw JAM and Church DB (2012) Evaluation of a Quality-of-Life Tool for Dogs with Diabetes Mellitus. Journal of Veterinary Internal Medicine 26: 953–961. DOI:10.1111/j.1939-1676.2012.00947.x

Peikes H, Morris DO and Hess RS (2001) Dermatologic disorders in dogs with diabetes mellitus: 45 cases (1986–2000). Journal of the American Veterinary Medical Association 219: 203-208. DOI: 10.2460/javma.2001.219.203

Rand JS, Fleeman LM, Farrow HA, Appleton DJ and Lederer R (2004) Canine and feline diabetes mellitus: nature or nurture? The Journal of Nutrition 134: 2072S–2080S. DOI:134/8/2072S

Short AD, Catchpole B, Kennedy LJ, Barnes A, Fretwell N, Jones C, Thomson W and Ollier WER (2007) Analysis of candidate susceptibility genes in canine diabetes. The Journal of Heredity 98: 518–25. DOI:10.1093/jhered/esm048

Short AD, Saleh NM, Catchpole B, Kennedy LJ, Barnes A, Jones CA, Fretwell N, and Ollier WER (2010) CTLA4 promoter polymorphisms are associated with canine diabetes mellitus. Tissue Antigens 75: 242–52. DOI:10.1111/j.1399-0039.2009.01434.x

Watson PJ (2003) Exocrine pancreatic insufficiency as an end stage of pancreatitis in four dogs. The Journal of Small Animal Practice 44: 306–12. DOI: 10.1111/j.1748-5827.2003.tb00159.x

© UFAW 2015


Credit for main photo above:

http://depositphotos.com/13265541/stock-photo-yorkshire-terrier-in-city-park.html ©Depositphotos.com/tandemich