diabetes mellitus

Many domesticated cats eat kibble diets high in carbohydrates, leading over time to the development of diabetes mellitus. Feeding a species-appropriate diet that’s low in carbs and high in protein creates better health and can even cause diabetes to go into remission.

The most common form of diabetes in cats is Type 2 diabetes. Also called diabetes mellitus, it results from prolonged inappropriate dietary practices. Chronic improper nutrition(i.e high carbohydrate consumption for a long period) can dramatically change the health of the cat’s body, and there is no more obvious example of this than the high incidence of diabetes mellitus in domesticated cats.


We need to be providing cats with food that comes as close as possible to the wild or feral feline diet. Recent research involved an analysis of the combined carcasses of wild rodents and small birds, revealing 67% water content, 62% crude protein,11% crude fat, 14.8% ash, and 2% carbohydrate (nitrogen-free extract). The average energy content of the prey was3,929 kcal/kg DM.4 Interestingly, a diet of wild rodents and small birds exceeded the recommended allowances provided by the Nutrient Requirements for Dogs and Cats(NRC 2006)5 for fat, crude protein, and essential amino acids. Most importantly, the feral cat diet consisted of only 2% carbohydrates.

Many domesticated cats receive standard commercial dry kibble diets. Up to 60% of the energy provided by these diets comes from carbohydrates (mean 41%).6 Compared with dogs and humans, cats have a reduced capacity to metabolize a high glucose load, resulting in higher blood glucose concentrations after a carbohydrate load. Cats also have an extended postprandial period of eight to 15 hours as compared with two to three hours for humans and three to six hours for dogs.2 Glucose metabolism in cats is unique, with limited liver enzyme activity, delayed gastric emptying, reduced small intestinal disaccharidase activity, and reduced and delayed insulin secretion, leading to inherent carbohydrate intolerance.


In a five-year study of 193,563 cats, the incidence of diabetes mellitus was one in 200 cats, with certain breeds being at higher risk, including Tonkinese, Norwegian Forest and Burmese.1 Although genetic susceptibilities have an influence, obesity is the most important acquired risk factor. In fact, overweight cats have a 4.6 times greater risk of developing diabetes than cats of normal weight.2

Shockingly, approximately 20% of obese cats over eight years of age are prediabetic, with impaired glucose tolerance or impaired fasting glucose.2 With time, obese cats can develop altered expression of several insulin-signalling genes and glucose transporters, and can be leptin-resistant. Diabetic cats also form amyloid deposits within the islets of the pancreas, and develop glucotoxicity when exposed to prolonged hyperglycemia.3


Healthy cats tend to have consistent blood glucose concentrations because, being carnivores, they are very adept at making glucose from the amino acids they consume inmeat-based diets. This happens as a constant process in the carnivore’s body.

There are two ways to get glucose into a cat’s body — one is via a dietary source of carbohydrates or sugars, and the other involves a conversion called gluconeogenesis, where the amino acids from protein are converted into glucose. The body has little ability to conserve amino acids, so they need to be used throughout the day, either as a component of protein synthesis or converted to glucose. Carnivores maintain a constant state of gluconeogenesis throughout the day, with a slight increase immediately after eating. Therefore, they can also maintain constant steady blood glucose levels throughout the day. In contrast to omnivores, the gluconeogenesis pathway is always available to carnivores for developing glucose.

As mentioned above, the combination of rodents and small birds has a carbohydrate concentration of 2%. Kibble is notoriously high in carbohydrates because it is necessary to form and hold the pieces together during the extrusion process. This means the carbohydrate content of kibble can be as high as 60%. The carbohydrate is broken down into glucose via pancreatic enzymes (e.g. amylase). The glucose is absorbed and transported via the portal vein to the liver.

Within the liver, the glucose is phosphorylated into the active metabolizable glucose-6-phosphate. The phosphorylation process requires two enzymes:

  • Glucokinase, which becomes active in high blood glucose levels.
  • Hexokinase, which becomes active in low blood glucose levels.

As carnivores, cats have minimal glucokinase activity and high hexokinase activity rates. Also, glucokinase in the cat cannot be upregulated (i.e. increased during times of high blood glucose). Again, cats have a reduced capacity to metabolize a high glucose load, with an extended postprandial period of eight to 15 hours.7,8,9 All this makes sense because we know that cats are carnivores and should eat high-meat diets, developing glucose via gluconeogenesis (the conversion of excess amino acids into glucose) rather than spikes of glucose from dietary carbohydrates.

So what happens when cats eat a high-carbohydrate dry kibble diet? The cat’s liver does not have the enzymes to convert high blood glucose into the active metabolic form of glucose (glucose-6-phosphate). Therefore, after a cat eats a kibble meal, the blood glucose remains high for a long time, much higher than an omnivore’s. Carnivores cannot rapidly respond to spikes in blood sugars and are subject to longstanding hyperglycemia.

Chronic high blood glucose leads to a cascade of physiologic events. High blood glucose signals the release of insulin from the pancreas. Eventually, the losing“blood glucose battle” leads to insensitivity of insulin receptors in the tissue, then the buildup of hyper-produced and released insulin leading to hyperinsulinemia. Hyperinsulinemia and hyperglycemia lead to abnormal fat deposition, obesity and constant unrelenting hunger, nerve damage, kidney and liver issues, non-healing wounds, cataracts, and repeated urinary tract infections due to excreted glucose in the urine.

And the vicious cycle continues. The obese “carboholic” cat is created by feeding a species-inappropriate diet high in carbohydrates.

In 60% of diabetic cats, pancreatitis is present at the time of diagnosis, based on biochemical and imaging findings, though few have clinical signs.9,10,11 Chronic hyperinsulinemia leads to amyloid buildup in the chronically inflamed pancreas, and in turn lead’s to the loss of insulin production — hence the need for insulin medications.


As any pet parent of an obese “carboholic” kitty knows, it is difficult to convert these cats to a species-appropriate, high meat protein, low carbohydrate diet. They refuse to eat. The pancreas is in overdrive, producing insulin, and the tissue that is insulin resistant is screaming for energy. The cat is hungry, doesn’t feel well, and is frankly resistant to all dietary changes.

So start slowly, adding small amounts of fresh meat and ground organs to the cat’s kibble. Gradually decrease the carbohydrate-laden kibble and add more and more fresh real meats. As the cat’s metabolism starts to correct, blood sugar decreases and becomes normalized, insulin receptors become more sensitive and provide the tissue with the energy it needs. The cat will become less ravenous, happier and healthier. He will feel better and become more active, and his body weight will normalize.

diabetes mellitus


Feed cats as the carnivorous creatures they are. Cats have a small amount of metabolic flexibility in the utilization of dietary carbohydrates, so diets with less than 12% metabolizable energy are recommended. This is especially important for cats with obesity, as well as older cats, susceptible breeds, and those with chronic corticosteroid needs. The highest remission rates in diabetic cats (>80%)are reported with very low carbohydrate diets(<6% ME) in combination with protocols aimed at achieving normal or near-normal blood glucose concentrations.12

The exciting news is that the goals for managing diabetes mellitus in the cat have changed from attaining glycemic control to achieving diabetic remission. Remission rates of up to 68% have been published. The used of low-carbohydrate foods improves the odds of achieving diabetic remission by four times.13

The normalization of blood glucose and body weight, and the remission of diabetes, are linked. This goal can be achieved through slow gradual energy restriction and a suitable weight loss diet with the macronutrient profile shifted from high dietary carbohydrates to low carbohydrates, moderate fat, and high protein. One recommendation is: fat <4 g/100 kcal, carbohydrates<3 g/100 kcal, and protein >10 g/kcal.14

One of the basic premises of integrative medicine is the healing nature of proper nutrition. In cats, returning to a species-appropriate carnivorous diet can not only result in better health and well-being, but even a remission of diabetes mellitus.



  1. O’Neill DG, Gostelow r, Orme C, Church DB, Niessen SJM, Verheven K, and Brodbelt DC.Epidemiology of Diabetes Mellitus among 193,435 Cats Attending Primary-Care Veterinary Practices in England, J Vet Intern Med, 2016 Jul-Aug;30(4):964-972, 2016.
  2. Gottlieb S, Rand J. Managing feline diabetes: current perspectives,Vet Med(Auckl) 2018;9: 33-42.
  3. Nelson RW, Reusch C.Classification and etiology of diabetes in dogs and cats.
  4. Kremen NA, Calvert CC, Larsen JA, Baldwin RA, Hahn TP, Fascetti AJ. Body composition and amino acid concentrations of select birds and mammals consumed by cats in northern and central California. J Anim Sci. 2013;91(3):1270–1276.
  5. Nutrient Requirements of Dogs and Cats– Animal Nutrition Series, National Research Council of the National Academies, 95, 2006.
  6. Debraekeleer J. Appendix L: nutrient profiles of commercial dog and cat foods. In: Hand M, Thatcher C, Remillard R, Roudebush P, editors.Small Animal Clinical Nutrition. 4th ed. Topeka,KS: Mark MorrisInstitute; 2000. pp. 1074–1083.
  7. American Diabetes Association Diagnosis and classification of diabetes mellitus. Diabetes Care.2014;37(Suppl 1): S81–S90.
  8. Hewson-Hughes AK, Gilham MS, Upton S, Colyer A, Butterwick R, Miller AT. Post-prandial glucose and insulin profiles following glucose-loaded meal in cats and dogs.Br J Nutr.2011;106(Suppl 1):S101–S10.
  9. Elliott KF, Rand J, Fleeman LM, et al. A diet lower in digestible carbohydrate results in lower postprandial glucose concentrations compared with a traditional canine diabetes diet and an adult maintenance diet in healthy dogs. Res Vet Sci. 2012;93(1):288–295.
  10. Appleton DJ, Rand JS, Sunvold GD. Insulin sensitivity decreases with obesity, and lean cats with low insulin sensitivity are at greatest risk of glucose intolerance with weight gain.J FelineMed Surg. 2001;3(4):211–228.
  11. Zini E, Hafner M, Kook P, Lutz TA, Ohlerth S, Reusch CE. Longitudinal evaluation of serum pancreatic enzymes and ultrasonographic findings in diabetic cats without clinically relevant pancreatitis at diagnosis. J Vet Intern Med. 2015;29(2):589–596.
  12. Marshall RD, Rand JS, Morton JM. Treatment of newly diagnosed diabetic cats with glargine insulin improves glycemic control and results in higher probability of remission than protamine zinc and lente insulins. J Feline Med Surg. 2009;11(8):683–691.
  13. Kirk CA. Feline diabetes mellitus: low carbohydrates versus high fiber?J.cvsm. 2006.09.04
  14. Zoran DL, Rand JS. The role of diet in the prevention and management of feline diabetes.VetClinNorth Am Small Anim Pract. 2013;43(2):233–243


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