Diagnose & Treat Feline Diabetes Mellitus

Alice Huang, VMD, DACVIM, Purdue University School of Veterinary Medicine

ArticleLast Updated October 20127 min readPeer Reviewed
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  • Diabetes mellitus (DM), classified as type I or type II, is a treatable condition caused by complete or relative insulin deficiency.

  • Most diabetic cats have type II, characterized by β-cell dysfunction and peripheral insulin resistance.

  • Type I diabetes, uncommon in cats, results from immunologic destruction of β cells, leading to complete insulin insufficiency.

  • Reversion to noninsulin-dependent diabetic mellitus (NIDDM) state is more likely with type II diabetes, as some causes of peripheral insulin resistance are reversible and islet cell dysfunction is variable in these cases.


  • In uncomplicated DM, urinary and immune systems are most commonly affected. 

  • Long-standing, uncontrolled DM can lead to complications (eg, polyneuropathy, hepatic disease [hepatic lipidosis], bacterial infections).


  • Up to 1% of cats in the United States and Australia are affected.


  • Burmese cats are overrepresented in Australia, New Zealand, and the UK.1,2

  • Most cats are diagnosed ≥7 years of age.3,4

  • Males are more frequently affected.4


  • Multiple causes of peripheral insulin resistance have been identified (see Causes of Insulin Resistance in Cats):

  • Obesity.

  • Concurrent disease.

  • Diet.

  • Drugs. 

  • Direct β-cell loss can be secondary to chronic amyloid deposition or pancreatitis but does not cause DM; instead, conditions that lead to β-cell loss may increase susceptibility to DM when faced with peripheral insulin resistance.

Risk Factors

  • Risk factors for DM include obesity, male gender, advanced age, and renal transplantation.<sup3-5 sup>


  • Insulin deficiency results in hyperglycemia by causing uninhibited hepatic glucose production, impaired glucose tissue entry, and accelerated protein and lipid catabolism.

  • Persistent hyperglycemia results in glycosuria when the renal tubular threshold for glucose excretion exceeds 200–300 mg/dL in cats.

  • Ultimately, endothelial damage, immunosuppression, and glucose toxicity (ie, negative effects of chronic hyperglycemia) occur. 

  • Glucose toxicity initially suppresses insulin secretion (reversible), but eventually can cause permanent β-cell loss, thereby perpetuating diabetic disease. 

  • Increased proteolysis can lead to muscle wasting and poor wound healing. 

  • As accelerated lipid catabolism persists, hepatic lipidosis develops; ketoacidosis can occur secondary to enhanced ketone body production. 

Related Article: Feline Diabetes: Initial Management



  • Patients with DM may have a history of polyuria, polydipsia, polyphagia, weight loss, lethargy, lack of grooming, and/or plantigrade posture.

Physical Examination

  • Lackluster coat.

  • Obese despite history of weight loss.

  • Hepatomegaly.

  • Signs of polyneuropathy (eg, plantigrade posture, pelvic limb weakness). 

  • Findings related to concurrent disease or diabetic ketoacidosis (DKA).


Definitive Diagnosis

  • Based on clinical signs, history, and documentation of persistent hyperglycemia and glycosuria

  • Stress hyperglycemia can complicate diagnosis, suggesting consideration of serum fructosamine measurement.

  • Normal serum fructosamine is 200–360 µmol/L.

  • Diabetic levels are frequently >400 µmol/L.

  • For evaluation of persistent glycosuria, owners may collect urine for glucose strip testing or use Glucotest flakes in litter box.

Differential Diagnosis

  • Hyperthyroidism, chronic kidney disease, and exocrine pancreatic insufficiency can result in classic complaints (eg, polyuria, polydipsia, polyphagia, weight loss).

  • Stress hyperglycemia must be considered in a hyperglycemic cat.

  • Concurrent diseases (eg, pancreatitis, renal failure, infection) may complicate the diagnosis.

Laboratory Findings

  • Mild anemia.

  • Hypercholesterolemia.

  • Hypertriglyceridemia.

  • Mild increases in serum alanine transaminase (ALT) and alkaline phosphatase (ALP).

  • Less common findings:

  • Trace to small amounts of ketones in urine.

  • Evidence of urinary tract disease (pyuria, hematuria, bacteriuria) on urinalysis. 

  • Nonspecific hepatic changes seen via abdominal imaging.

Postmortem Findings

  • Hepatic lipidosis.

  • Pancreatic amyloid deposits.

  • Concurrent disease.


Inpatient or Outpatient

  • Healthy diabetics ± minimal ketonuria can be managed on outpatient basis. 

  • Hospitalization may be required with DKA or concurrent disease.

Nutritional Aspects

  • Dietary therapy may minimize postprandial blood glucose fluctuations. 

  • Diets should be palatable to ensure predictable consumption.

  • A consistent feeding schedule is more important than timing between insulin administration.

  • Owners may feed q12h, at time of insulin administration, or small amounts throughout the day.

  • The ideal dietary composition is debatable, as low-carbohydrate/high-protein and high-fiber/low-fat (and occasionally adult-maintenance) diets can result in good glycemic control when used with insulin.6

  • Low-carbohydrate diets result in higher remission rates.<sup7,8  sup>         

  • Both diets can induce remission.

  • Dietary glycemic control is not different in insulin-dependent cats.     

  • Overweight cats require a weight-reduction program, as obesity is a reversible cause of insulin resistance.

  • Compared with dry foods, canned foods are generally  preferred, as they typically have a lower carbohydrate content.

Alternative Therapy

  • Few insulin alternatives are available. 

  • Although most diabetic cats are insulin-dependent, there is higher NIDDM incidence  in cats than dogs. 

  • Oral hypoglycemic agents may be considered for diabetic cats; however, studies evaluating their efficacy are sparse.

Clinical Remission

  • Up to 60% of cats enter diabetic remission with insulin and dietary therapy.

  • Remission may not be permanent (median, 11 months).<sup9     sup>     

  • Approximately 30% of cats in remission will revert to a diabetic state and require reinstitution of insulin therapy.<sup9,10     sup>            

  • Remission rates increase in cases with good glycemic control within 6 months of diagnosis.<sup9   sup>

Client Education

  • Treatment is lifelong; owners should be prepared for complications or remissions. 

  • At-home insulin therapy, dietary management, and careful monitoring are cornerstones of successful management.

  • Insulin administration.

  • Insulin storage.

  • Syringe sizes and use (U-40 vs U-100).

  • Weight reduction (if necessary) and consistent diet and feeding schedule facilitate glycemic control.



  • Short-acting insulin (eg, regular insulin) is primarily used in the hospital for clinically ill diabetics or DKA cases, as increased potency increases risk for hypoglycemia.

  • Long-acting insulin, the mainstay of therapy, should be administered immediately after diagnosis.

  • Common insulin choices for cats are human recombinant types:

  • Protamine zinc insulin (PZI) (ProZinc, prozinc.us).11    

  • Only insulin FDA approved for cats.

  • U-40 syringe.

  • Insulin glargine (Lantus, lantus.com).12      

  • In conjunction with a low-carbohydrate/high-protein diet, may comparatively increase likelihood for diabetic remission.12 

  • U-100 syringe.    

  • Neutral protamine Hagedorn (NPH) insulin (duration short in cats).

  • U-100 syringe.

  • Lente insulin (Vetsulin, vetsulin.com) is currently unavailable. 

  • PZI and glargine result in similar glycemic control and can induce remission.10    

  • Insulin should be administered q12h rather than q24h, as duration of effect is often unpredictable and shorter than expected in cats.

  • Hypoglycemia can occur with insulin therapy.

Related Article: Persistent Hyperglycemia in Diabetic Dogs & Cats


Patient Monitoring

  • Clients should monitor for changes:

  • Polyuria.

  • Polydipsia.

  • Appetite.

  • Weight. 

  • Hypoglycemia (eg, disorientation, wobbliness, tremors, seizures).

  • Signs of concurrent disease (eg, pollakiuria, stranguria, hematuria, anorexia, vomiting, skin infections, weakness).


  • Iatrogenic hypoglycemia.

  • DKA and severe electrolyte abnormalities (uncontrolled diabetics).

  • Can be fatal, particularly in presence of severe pancreatitis.   

  • Polyneuropathy (from chronic hyperglycemia) frequently resolves with good glycemic control.

Future Follow-up

  • Twelve-hour blood glucose curves (BGCs) should be performed q10–14days from each insulin dose adjustment until patient appears healthy and blood glucose is relatively controlled.   

  • BGC measurements should be 100–300 mg/dL.

  • Fructosamine measurements:

  • For cats experiencing stress hyperglycemia.

  • For cats with good glucose control based on the initial BGC. 

  • For fractious cats in which BGCs are difficult to perform.  

  • Owners can be taught to perform at-home BGCs (AlphaTrak, alphatrakmeter.com).

  • May minimize stress hyperglycemia.

  • However, at-home BGCs may not represent significantly lower stress hyperglycemia than clinic-generated curves.13,14

  • Advantage of at-home glucose monitoring includes the ability to frequently monitor cats that are difficult to regulate.

  • Once well-controlled, BGCs and/or fructosamine may be performed q3–6mo or more, based on owner observations (eg, changes in polyuria, polydipsia, appetite, weight).

  • Urine cultures should be performed regularly (eg, q3–6mo) regardless of whether the urinalysis suggests infection.15

In General

Relative Cost

  • Diagnostic workup for uncomplicated DM: $$

  • Treatment and follow-up care for uncomplicated DM: $$–$$$ monthly

  • Diagnostic workup for complicated DM: $$$$–$$$$$

  • Treatment and follow-up care for complicated DM: $$$–$$$$$


  • Fair with diligent care and monitoring.

  • Can be stabilized with appropriate treatment, although diabetic remission may result in a waxing/waning course of disease.

  • Dependent on owner commitment, ease of glycemic control, and possible concurrent diseases. 

  • Many cats can do well for months to years with diligent care.


  • Minimizing circumstances for insulin resistance (eg, obesity, inactivity).

  • Not all obese cats become diabetic, and many diabetic cats are of normal size.

Future Considerations

  • More studies to evaluate the impact of diet on diabetic control are necessary. 

  • Remission studies directly comparing insulin types would be valuable. 

  • Given the changing insulin market, continued investigation into alternative insulin types for diabetic cats is important.

Tx at a Glance

  • Long-acting insulin should be administered immediately after diagnosis.

  • Insulin should be administered q12h rather than q24h.

  • Concurrent dietary and medical therapy is often best.

Two Dietary Options 

  • Low-carbohydrate/high-protein diet.

  • High-fiber/low-fat diet.

Two Medical Options

  • PZI (0.25 Units/kg SC q12h after a meal).

  • Insulin glargine (0.25 Units/kg SC q12h after a meal).

ALP = alkaline phosphatase, ALT = alanine transaminase, BGC = blood glucose curve, DKA = diabetic ketoacidosis, DM = diabetes mellitus, NIDDM = noninsulin-dependent diabetes mellitus, NPH = neutral protamine Hagedorn, PZI = protamine zinc insulin