Juvenile diabetes mellitus in a cocker spaniel: a case study

A three-month-old female intact cocker spaniel was presented to a primary care veterinary clinic with a three-day history of polyuria, polydipsia and polyphagia.

On physical examination, no abnormalities were noted. Blood work documented marked hyperglycaemia (25.2mmol/L; reference interval [RI] 4.4mmol/L to 6.6mmol/L), and urinalysis documented severe glucosuria. Repeat testing the following day confirmed persistent hyperglycaemia  (29.7mmol/L).

Insulin therapy was started (0.5IU/kg subcutaneous injection twice daily) and the dose was increased to 0.6IU/kg based on repeat blood glucose curves at the primary care practice over the following days. However, the owner reported ongoing uncontrolled signs of diabetes mellitus (polyuria, polydipsia) and difficulties administering SC insulin injections. Three days later, the patient developed diabetic ketosis (ketones 0.6mmol/L, pH 7.424) which was managed with intravenous soluble insulin (0.05 units/kg/hr), leading to a clinical improvement. The patient was discharged to receive an increased dose of lente insulin (0.75IU/kg twice daily) and referral for further investigations and management was arranged.

On presentation, physical examination documented moderate muscle wasting and a reduced body condition score (2 out of 9).

An ophthalmic examination revealed bilateral posterior subcapsular cataracts. Complete blood count was unremarkable. Serum biochemistry documented hyperglycaemia (28.7mmol/L) hyperphosphataemia (2.81mmol/L; RI 0.8mmol/L to 1.9mmol/L), hypercholesterolaemia (10.6 mmol/L; RI 3.5mmol/L to 7.2mmol/L), increased alkaline phosphatase activity (294IU/L; RI 20IU/L to 200IU/L) and ketonaemia (3.7 mmol/Lm; RI less than 0.2mmol/L). Blood gas analysis revealed a pH of 7.373. Urinalysis documented severe glucosuria, and ketonuria.

Management of diabetic ketosis included IV fluid therapy to correct hydration status, followed by the initiation of a constant rate infusion of neutral insulin once the patient was adequately hydrated. A glucose monitor was placed for continuous interstitial glucose monitoring. Abdominal ultrasound, performed under sedation, documented no abnormalities.

Once blood ketone levels normalised, the patient was transitioned to SC injections of intermediate-acting lente insulin at 0.55IU/kg.

After a few days of hospitalisation and insulin dose adjustment, the dog was discharged to continue the lente insulin at 1.1IU/kg by subcutaneous injection every 12 hours. Based on diabetic clinical score and readings from the interstitial glucose monitor, the dog’s dose was optimised over the coming days. Three months post-treatment, the patient remained clinically stable, with no clinical evidence of inadequate glycaemic control.

Discussion

Diabetes mellitus (DM) is a common endocrine disorder characterised by persistent hyperglycaemia due to insufficient insulin production, impaired insulin action or both. In humans, it is classified into type 1, or “insulin dependent” (IDDM), and type 2, or “non-insulin dependent” (NIDDM). Canine DM most closely resembles human type 1 diabetes, characterised by chronic hypoinsulinaemia and a complete requirement of exogenous insulin for glycaemic control (Ettinger and Feldman, 2017).

While most dogs are diagnosed  between the ages of five to 15, juvenile-onset diabetes is rare (Ettinger and Feldman, 2017) and occurs in dogs younger than one year of age (Feldman and Nelson, 2014). All reported cases of juvenile diabetes mellitus in dogs have been type 1, or IDDM. Increased serum insulin concentration may suggest an underlying insulin-antagonistic disorder, potentially indicating type 2 diabetes (Feldman and Nelson, 2014). However, considering the favourable response to exogenous insulin, no such disorder was suspected in our patient, and serum insulin concentration measurement was not deemed necessary.

In humans, type 1 diabetes (T1D) typically develops in early childhood due to significant insulin deficiency, primarily caused by autoimmune destruction of beta cells. However, in dogs with juvenile diabetes, insulitis – recognised as the key pathological feature of beta cell autoimmune attack – has only been documented once to date (Jouvion et al, 2006).

In a case series, seven Labrador retriever puppies developed diabetes mellitus between eight and 24 weeks of age, with some cases showing familial links, but genetic screening of three candidate genes found no causative mutations (Raffan et al, 2015). In humans and dogs, DM is regarded as a multifactorial disease influenced by genetic and environmental factors (Ettinger and Feldman, 2017).

Exocrine pancreatic insufficiency (EPI) is an uncommon complication of DM, usually developing as a consequence of chronic pancreatitis in diabetic dogs (Johnson-Pitt et al, 2024). Reports exist of juvenile diabetic dogs presenting with concurrent EPI (Alvarez et al, 2015). Clinical signs of EPI overlap with those of DM (weight loss and polyphagia), but are accompanied by gastrointestinal signs (diarrhoea, steatorrhea). Decreased serum trypsin-like immunoreactivity (TLI) concentration can aid in diagnosis. Our patient had a history of diarrhoea for one week prior to diagnosis of juvenile diabetes, which resolved with supportive care. Serum TLI concentration was within normal limits, excluding exocrine pancreatic insufficiency  (31.9µg/L; RI 5µg/Lto 35µg/L). Further studies are needed to explore the link between juvenile DM and EPI.

Pancreatitis should always be considered in the newly diagnosed diabetic patient (Feldman and Nelson, 2014). Ultrasonographic examination of our patient documented a pancreas of normal size and appearance. Canine pancreatic lipase immunoreactivity (cPLI) test was normal (115µg/L; RI less than 180µg/L).

Cataract formation is the most common long-term complication in diabetic dogs (Feldman and Nelson, 2014). The patient had evidence of subcapsular cataracts on ophthalmological examination. The pathogenesis likely involves the accumulation of sorbitol and galactitol, which are potent hydrophilic agents that cause an influx of water into the lens, leading to swelling, rupture of lens fibres, and cataract development. Once initiated, this process is irreversible and can progress rapidly (Feldman and Nelson, 2014; Ettinger and Feldman, 2017). Poorly controlled hyperglycaemia might have contributed to cataract formation in our patient.

A paucity of literature exists regarding the specific management strategies and prognosis for cases of canine juvenile diabetes. It is suspected that initial stabilisation and management of juvenile diabetics might be more challenging considering the insulin antagonistic effects of growth hormone and rapidly changing bodyweight as the patient grows, and subsequent requirement for frequent insulin dose adjustment. We suspect this patient developed diabetic ketosis due to poor glycaemic control, as a consequence of difficulties with administration of insulin.

Another potential contributing factor to insulin resistance is rising serum progesterone in dioestrus, which stimulates growth hormone production from mammary tissue which, along with progesterone, has insulin antagonistic effects. No evidence was present to suggest this patient was in dioestrus, and ovariohysterectomy was recommended at six months of age.

Conclusion

This case report describes the successful management of juvenile diabetes in a three-month-old dog. Juvenile diabetes is a rare condition – in a UK study, only four out of 253 diabetic dogs were younger than one year old, and few cases have been reported in the literature (Davison et al, 2005). Little is known about its possible aetiology, optimal management and prognosis. Since dogs from the same litter have been diagnosed with juvenile diabetes, a genetic association has been suggested (Davison et al, 2005) and investigated (Raffan et al, 2015), but no definitive conclusions have been reached.

Further studies are needed to clarify this possible connection. While insulin dosage recommendations are somewhat standardised in adult dogs with DM, no studies have determined the appropriate type and dosage of insulin for young dogs.

Additionally, the prognosis for dogs with juvenile DM remains uncertain. In adult dogs, several factors influence prognosis, including the owner’s commitment, ease of glycaemic regulation, presence of concurrent disorders, and comorbidities. A high mortality rate exists within the first six months, with one in 10 diabetic pets euthanised at diagnosis (Niessen et al, 2017). In a large study conducted in Sweden, among dogs that survived at least 30 days after diagnosis, the three-year survival rate was 33% (Fall et al, 2007).

Further research is needed to better understand the management and prognosis associated with juvenile DM.

Have you diagnosed DM in a young dog? If so, we would love to hear from you. We are conducting various research projects looking at this unusual condition. Please email [email protected] if you would like to be involved.

• This article appeared in Vet Times (2025), Volume 55, Issue 44, Pages 14-16.