Feline diabetes is a NAVLE staple. The key things that distinguish cat DM from dog DM: cats get Type 2 (insulin resistance + islet amyloid), cats can go into diabetic remission, cats use glargine as first-line insulin, and the plantigrade stance is unique to diabetic neuropathy in cats. Know these distinctions cold.
Pathophysiology
Cats develop Type 2 DM—islet amyloid polypeptide (IAPP) deposition in pancreatic islets combined with peripheral insulin resistance. Obese male neutered cats are at highest risk. Predisposing conditions: obesity, physical inactivity, glucocorticoid therapy, acromegaly (up to 25% of diabetic cats may have elevated IGF-1—screen refractory cases), pancreatitis, and concurrent UTI (glucosuria promotes bacterial growth).
Stress hyperglycemia: Cats can have blood glucose >300 mg/dL from stress alone. Fructosamine distinguishes true DM from stress hyperglycemia—fructosamine reflects 2–3 week average glucose and is not affected by acute stress.
Clinical Signs
Classic PU/PD, polyphagia with weight loss. The pathognomonic sign unique to cats: plantigrade stance—walking on the hocks due to diabetic peripheral neuropathy. This is rare in dogs and classic for feline DM. Hepatomegaly from hepatic lipidosis secondary to uncontrolled diabetes is common. Poor coat quality.
Diagnosis
Blood glucose >250 mg/dL on multiple occasions OR persistently elevated fructosamine (>400 μmol/L = poor control; 350–400 = fair; <350 = good). Urinalysis: glucosuria (renal threshold ~280 mg/dL), +/- ketonuria. Renal threshold is important—a cat with chronic kidney disease may have glucosuria without hyperglycemia (proximal tubular dysfunction).
Insulin Comparison
Diabetic Remission
Diabetic remission is unique to cats (dogs do NOT go into remission). Definition: blood glucose <180 mg/dL without insulin for ≥4 weeks. Remission rates: up to 80–90% with early glargine therapy + high-protein, low-carbohydrate diet (canned food preferred). Key factors: early diagnosis before significant islet cell loss, weight loss in obese cats, optimal glycemic control. Remission is not permanent—cats can relapse, especially with stress, obesity, or glucocorticoid therapy.
Diabetic Ketoacidosis (DKA)
Triggers: infection, pancreatitis, stress, inadequate insulin dose. Signs: anorexia, vomiting, lethargy, acetone breath, dehydration. Labs: hyperglycemia, metabolic acidosis (low pH, low bicarb), ketonuria/ketonemia, hypokalemia (the critical electrolyte).
Treatment: IV 0.9% NaCl (fluid resuscitation), potassium supplementation in IV fluids, regular insulin CRI (0.05–0.1 IU/kg/hr). DO NOT use long-acting insulin (glargine) in DKA—use only regular insulin. Potassium must be supplemented with insulin because insulin drives K+ into cells and will worsen existing hypokalemia, risking respiratory muscle weakness and cardiac arrhythmias.