Section 1: Overview of Diabetes Mellitus in Cats
Top 3 Takeaways
- Insulin resistance (IR) and glucose toxicity play key roles in feline DM pathogenesis.
- Effective management involves lowering blood glucose (BG) concentrations and mitigating factors contributing to IR.
- Select insulins and SGLT2 inhibitors are licensed for the management of feline DM.
Feline DM pathogenesis is multifactorial, with numerous processes affecting pancreatic beta cell function and viability. However, most feline diabetes develops when insulin resistance places prolonged stress on pancreatic beta cells that may already be genetically vulnerable. (see Box: Causes of Insulin Resistance).1 Diet formulation and exocrine pancreatic disease may also contribute to the development of DM.2 Because, in part, of the impact of IR, feline DM shares strong similarities with human type 2 DM, although not all cats fit this pattern and many require exogenous insulin.
The initial consequence of IR is increased insulin secretion. At first this maintains euglycemia but simultaneously drives the accumulation
of poorly soluble amylin within pancreatic islets. Progressive amyloidosis impairs beta cell function, which compromises insulin secretion and increases BG. Many diabetic cats appear to spend months in a subclinical/preclinical period, in which BG is significantly elevated but remains below the threshold for glucosuria (~250–300 mg/dL).3
Although the systemic effects of moderate hyperglycemia in cats have not been established, glucose toxicity—a complex process that causes widespread compromise to cellular function—occurs in people with BG >200 mg/dL.4 Feline beta cells appear to be particularly vulnerable
to glucose toxicity and either decrease insulin production or undergo apoptosis.5,6 When insulin secretion is no longer sufficient to keep BG below the renal threshold, clinical signs of DM (polyuria [PU], polydipsia [PD], polyphagia [PP], and weight loss) become apparent. The other classic manifestation of glucose toxicity in cats is peripheral neuropathy.7 This primarily impacts the rear limbs and causes a plantigrade stance that limits cats’ ability to run and jump.
Treating feline DM relies on controlling hyperglycemia by giving insulin or an SGLT2 inhibitor, and by mitigating factors causing IR. In some cats, beta cell function may recover, and medical therapy can be withdrawn; this process is referred to as diabetic remission.8
Causes of Insulin Resistance in Cats a,b
- Obesity
- Sarcopenia (suspected)
- Sedentary lifestyle
- Inflammatory/infectious conditions
- Stomatitis/gingivitis
- Degenerative joint disease
- Chronic enteropathy
- Chronic pancreatitis
- Urinary tract infection
- Medications
- Glucocorticoids
- Progestogens
- Endocrinopathy
- Hyperthyroidism
- Hypothyroidism (infrequent in cats)
- Hypersomatotropism (acromegaly)
- Hypercortisolism
a. Gostelow R, Hazuchova K. Pathophysiology of prediabetes, diabetes, and diabetic remission in cats. Vet Clin North Am Small Anim Pract 2023;53(3):511–29.
b. Freeman LM. Cachexia and sarcopenia: emerging syndromes of importance in dogs and cats. J Vet Intern Med 2012;26(1):3–17.
The 2026 AAHA Diabetes Management Guidelines for Cats are generously supported by Adapet Medical, Boehringer Ingelheim, Dechra, and Merck Animal Health.
Citations
- Gostelow R, Hazuchova K. Pathophysiology of prediabetes, diabetes, and diabetic remission in cats. Vet Clin North Am Small Anim Pract 2023; 53(3):511–29.
- Gostelow R, Hazuchova K. Pathophysiology of prediabetes, diabetes, and diabetic remission in cats. Vet Clin North Am Small Anim Pract 2023; 53(3):511–29.
- Rand JS. Pathogenesis of feline diabetes. Vet Clin North Am Small Anim Pract. 2013;43(2):221–231.
- Giaccari A, Sorice G, Muscogiuri G. Glucose toxicity: the leading actor in the pathogenesis and clinical history of type 2 diabetes–mechanisms and potentials for treatment. Nutr Metab Cardiovasc Dis 2009;19(5):365–77.
- Zini E, Osto M, Franchini M, et al. Hyperglycaemia but not hyperlipidaemia causes beta cell dysfunction and beta cell loss in the domestic cat. Diabetologia 2009;52:336–46.
- Link KR, Allio I, Rand JS, et al. The effect of experimentally induced chronic hyperglycaemia on serum and pancreatic insulin, pancreatic islet IGF-I and plasma and urinary ketones in the domestic cat (Felis felis). Gen Comp Endocrinol 2013;188:269–81.
- Mizisin AP, Shelton GD, Burgers ML, Powell HC, Cuddon PA. Neurological complications associated with spontaneously occurring feline diabetes mellitus. J Neuropathol Exp Neurol. 2002;61(10):872–884.
- Gostelow R, Hazuchova K. Pathophysiology of prediabetes, diabetes, and diabetic remission in cats. Vet Clin North Am Small Anim Pract 2023; 53(3):511–29.