Diabetes mellitus

What it is

Diabetes mellitus is an endocrine disease in which the beta cells of the pancreatic islets do not produce enough insulin for the body's needs. In most cats it resembles human type 2 diabetes: insulin resistance (from obesity, inactivity, age or drugs) and progressive beta cell failure coexist. Amyloid derived from islet amyloid polypeptide (amylin) is deposited in feline islets and contributes to beta cell loss. Sustained hyperglycaemia is itself toxic to beta cells (glucotoxicity) and suppresses insulin secretion; this is why, if glycaemia is controlled early, some function can recover.

Other causes are acromegaly from a growth hormone-secreting pituitary adenoma, which causes severe insulin resistance, pancreatitis, hyperadrenocorticism and diabetogenic drugs (long-acting corticosteroids, progestogens).

Who it affects

Middle-aged and older cats, especially neutered males, obese and indoor cats. The Burmese is predisposed in some populations.

Anatomy involved

• Pancreas: the islets of Langerhans, scattered through the pancreas, contain the insulin-producing beta cells; diabetic cats show islet amyloidosis, vacuolation and beta cell loss. In the cat the pancreatic duct joins the common bile duct before opening into the duodenum, so pancreatitis and cholangitis often coexist.
• Liver: hepatic lipidosis may develop.
• Peripheral nerves: diabetic neuropathy of the tibial nerve causes a plantigrade stance, with the hocks touching the ground.
• Kidneys: glucosuria predisposes to urinary tract infection.

Clinical signs

Polyuria and polydipsia, polyphagia and weight loss; sometimes the litter is wetter than usual. Pelvic limb weakness and a plantigrade stance in some cats. If diabetic ketoacidosis develops: anorexia, vomiting, dehydration, lethargy and collapse, an emergency.

Diagnosis

• Persistent hyperglycaemia and glucosuria in a cat with compatible signs.
• Cats have marked stress hyperglycaemia that can exceed the renal threshold; fructosamine (which reflects average glycaemia over the previous weeks) therefore helps confirm the diagnosis.
• Urinalysis and urine culture: glucosuria, ketonuria and infection.
• Complete blood work, total T4 in older cats and, when insulin resistance is marked, IGF-1 measurement for acromegaly.

Treatment

• Intermediate- or long-acting insulin, such as glargine or lente insulin, usually twice daily, adjusted with blood glucose curves, ideally at home or with continuous interstitial glucose monitors to avoid stress hyperglycaemia.
• A high-protein, low-carbohydrate diet, preferably wet, and gradual weight loss in obese cats.
• Withdrawal of diabetogenic drugs.
• In some countries oral SGLT2 inhibitors (bexagliflozin, velagliflozin) are licensed for newly diagnosed cats that still produce insulin; they increase urinary glucose loss, but must not be used in cats with ketosis because of the risk of ketoacidosis with normal or mildly increased glucose.

A substantial proportion of cats go into diabetic remission, no longer needing insulin, especially when good glycaemic control is achieved in the first months after diagnosis. Hypoglycaemia from insulin overdose is the most dangerous complication of treatment. Ketoacidosis is treated in hospital with fluids, regular insulin and potassium and phosphate correction.

Key studies

• iCatCare consensus (Taylor et al., 2025): the current reference guideline. It covers treatment with insulin or SGLT2 inhibitors, continuous glucose monitoring and the management of complications, and highlights hypersomatotropism as a common underlying cause.
• Niessen et al. (2015), screening of 1221 diabetic cats in the United Kingdom with serum IGF-1: 26.1% had values above 1000 ng/mL, and 89% of those that underwent CT had a pituitary tumour. The estimated prevalence of hypersomatotropism was 24.8%; most of these cats did not show the typical signs of acromegaly, and their clinicians had strongly suspected it in only 24% of cases.
• Gostelow et al. (2014), systematic review of 22 studies on diabetic remission. The evidence was moderate to poor (few randomised or blinded trials, small samples). No single factor predicts remission, it has been achieved with several insulins and protocols, and reducing dietary carbohydrate may help but needs further study.
• Bennett et al. (2006), randomised trial in 63 diabetic cats fed a canned low-carbohydrate, low-fibre food or a moderate-carbohydrate, high-fibre food for 16 weeks, with owners blinded to the diet. More cats on the low-carbohydrate food stopped needing insulin (68% versus 41%).
• Niessen et al. (2024), randomised, open-label non-inferiority trial of once-daily oral velagliflozin against twice-daily lente insulin in 127 cats. Velagliflozin was non-inferior at day 45 (treatment success in 54% versus 42%). With velagliflozin the commonest adverse event was loose faeces (38%) and 4 of 61 cats (7%) developed ketoacidosis; with insulin it was hypoglycaemia (53%).
• Behrend et al. (2024, SENSATION), open-label trial of velagliflozin as sole treatment in 252 cats. At day 180, 81% of the cats remaining had glucose or fructosamine within the reference range. Ketoacidosis occurred in 7.1%, more often in cats previously treated with insulin (18.4%) than in newly diagnosed cats (5.1%); 78% of these cats were euglycaemic, and most episodes of ketosis appeared in the first 14 days.