Feline Health Alert  ---  Diabetes and Dry Cat Food [See Fleming's note at end of article]. Written by Dr. Debbie Greco, DVM, PhD. Animal Medical Center, NYC.

Diabetes mellitus is one of the most common endocrine diseases affecting 1 in every 200-300 cats; nearly 240,000 cases of feline diabetes mellitus are diagnosed annually.¹ Despite the prevalence of diabetes in the cat population and the increasing frequency of the disease, treatment of diabetic cats is frustrating and often associated with tremendous complications. While insulin therapy and high fiber diets are the mainstay of treatment of diabetes mellitus in cats, many diabetic cats experience complications, such as hypoglycemia and progressive neuropathy, associated this therapy.^2-7 In a recent study, 10% of diabetic cats had documented hypoglycemia caused by an insulin overdose.⁶ Obese cats (>6 kg) were much more likely to become hypoglycemic and lack autonomic warning signs of hypoglycemia.⁶Because of the difficulty in achieving adequate glycemic control with insulin therapy in cats, diabetic neuropathy is a common attending condition in diabetic cats. In one study, all diabetic cats suffered from subclinical forms of diabetic neuropathy as evidenced by impaired motor and sensory peripheral nerve conduction.⁷ In summary, current dietary and insulin therapy is associated with increased risk of severe hypoglycemia and often results in poorly controlled diabetes associated with progressive neuropathy in cats with type II diabetes mellitus.

The latest clinical and histological evidence now suggest that type 2 diabetes mellitus (DM) is the most frequently occurring form of DM in cats and humans.^2-4 Type 2 DM in cats is characterized by an impaired ability to secrete insulin following a glucose stimulus and is caused by both a defect in pancreatic beta cells and by peripheral insulin resistance.^2-4 Although the etiology type 2 DM is undoubtedly multifactorial; obesity, genetics, diet and amyloidosis of the islets are involved in the development of this form of DM in humans and cats.^2-4 It is now recognized that the classic metabolic abnormalities found in type 2 DM, decreased insulin secretion and peripheral insulin resistance, may be consequences of abnormal amyloid production by pancreatic cells.^2-4 Despite the presence of type 2 diabetes in many diabetic cats, the advanced nature of their disease (amyloid deposition, glucose toxicity) often requires that insulin therapy be instituted.²

Insulin is often used to treat diabetes mellitus in cats and dietary fiber may be used to improve diabetic control in cats.⁸ In one study, 23 client-owned diabetic cats were fed canned high insoluble fiber or low fiber diets in a 16 week crossover design.⁸ Only 13 of the 23 cats finished the study and 9 of the 13 showed improvement on the high fiber diet.⁸ A significant effect of the insoluble fiber diet was found on mean daily caloric intake, mean fasting blood glucose (FBG) and mean glycosylated hemoglobin (Glib).⁸ However, the effect on caloric intake was significant suggesting that the effects on mean FBG and Glib could have resulted from a reduction in caloric intake alone. Furthermore, this study looked at canned high fiber diets rather than dry high fiber diets. The carbohydrate content of dry diets, especially those containing high insoluble fiber, is approximately 36-40%. In contrast, the canned high fiber diets are approximately 23% carbohydrate as fed. It is entirely possible that the improvement in glycemic control in these patients could have been due to a change from dry to canned cat food.

The cat is an obligate carnivore and as such is unique among mammals in its insulin response to dietary carbohydrates, protein and fat. The feline liver exhibits normal hexokinase activity but glucokinase activity is virtually absent.⁹ Glucokinase converts glucose to glycogen for storage in the liver and is important in "mopping" up excess post-prandial glucose. Normal cats are in fact similar to diabetic humans because glucokinase levels drop precipitously with persistent hyperglycemia in human beings suffering from type 2 diabetes mellitus. Amino acids, rather than glucose, are the signal for insulin release in cats.¹⁰ In fact, a recent publication demonstrated more effective assessment of insulin reserve in cats using the arginine response test rather than a glucose tolerance test. Another unusual aspect of feline metabolism is the increase in hepatic gluconeogenesis seen after a normal meal. Normal cats maintain essential glucose requirements from gluconeogenic precursors (i.e., amino acids) rather than from dietary carbohydrates. As a result, cats can maintain normal blood glucose concentrations even when deprived of food for over 72 hrs;^10; furthermore, feeding has very little effect on blood glucose concentrations in normal cats.^2,12In summary, the cat is uniquely adapted to a carnivorous diet and is not metabolically adapted to ingestion of excess carbohydrate.***  When type 2 diabetes occurs in cats, the metabolic adaptations to a carnivorous diet become even more deleterious leading to severe protein catabolism; feeding a diet rich in carbohydrates may exacerbate hyperglycemia and protein wasting in these diabetic cats. In fact, in human beings with type 2 diabetes, the first recommendation is to restrict excess dietary carbohydrates such as potatoes and bread and to control obesity by caloric restriction.¹³ Furthermore, human beings with type 2 diabetes mellitus have been shown to have improved glycemic control and improvement in nitrogen turnover during weight loss when a low- energy diet (high protein) was combined with oral hypoglycemic therapy.¹⁴

A low-carbohydrate, high-protein diet which is similar in fact to a cat's natural diet (mice) may ameliorate some of the abnormalities associated with diabetes mellitus in the cat. Initial studies using a canned high protein/low carbohydrate diet (Hill's feline growth) and the starch blocker acarbose have shown that 58%of cats discontinue insulin injections and those with continued insulin requirements could be regulated on a much lower dosage (1U BID).¹⁵ Comparison of canned high fiber vs low carbohydrate diets showed that cats fed low carbohydrate diets were 10 times more likely to discontinue insulin injections.¹⁶

The diet formulation is critical in that most dry cat food formulations contain excessive carbohydrates; therefore, canned cat foods and preferably high protein or kitten formulations should be used for initial treatment of diabetic cats. Weight reduction also decreases insulin resistance and cats should be fed no more than 30 kcal/lb of ideal body weight in two equal meals per day. Caution should be used when initially changing from dry to canned foods as insulin requirements may decrease dramatically; a reduction in insulin dosage may be required. Cats develop Type II diabetes mellitus which is characterized by insulin resistance, obesity and pancreatic amyloid deposition. The unique nutritional requirements of cats suggest that reduction in dietary carbohydrate load in diabetic cats may decrease insulin demands and pancreatic exhaustion leading to resolution of the insulin dependent state. Improved glycemic control can be achieved using canned high fiber or high protein/low carbohydrate diets; however, cats fed high protein/low carbohydrate diets are 10 times more likely to discontinue exogenous insulin injections.

[Fleming's note: There are many such papers out there. Feeding dry cat food only increases the risk for developing diabetes, which has become epidemic in US cats. Consider dry cat food to be "cat candy". 

*** i.e. dry cat food

REFERENCES

1.  Panciera D, et al. Epizootiologic patterns of diabetes mellitus in cats. JAmer Vet Med Assoc 1990; 197: 1504-1508.

2.  Rand JS. Management of feline diabetes. Aust Vet Practit 1997;27:68-75.

3.  O'Brien TD, Butler PC, Westermark P, Johnson KH. Islet amyloid polypeptide: A review of its biology and potential roles in the pathogenesis of diabetes mellitus. Vet Pathol 1993 ;30:3 17-332.

4.  Lutz TA, Rand JS. A review of new developments in type 2 diabetes mellitus in human beings and cats. Brit VetJ 1993;149:527-536.

5.  Crenshaw KL, Peterson ME. Pretreatment clinical and laboratory evaluation of cats with diabetes mellitus: 104 cases (1992-1994) JAmer Vet MedAssoc 1996;209:943-949.

6.  Whitely NT, Drobatz KJ, Panciera DL. Insulin overdose in dogs and cats :28 cases (1986-1993). J Amer Vet Med Assoc 1997;21 1(3):326-330.

7.  Cuddon P. Diabetic neuropathy. Proc Amer Coll Vet Int Med. Chicago. 1999;650-653.

8.  Nelson RW, Scott-Moncrieff C, DeVries 5, et al: Dietary insoluble fiber and glycemic control of diabetic cats (abstract). J Vet Intern Med 8:165, 1994.

9.  Ballard FJ. Glucose utilization in mammalian liver. Comp Biochem and Physiol 1965; 14:437-443.

10. Kettlehut IC, Foss MC, Migliorini RH. Glucose homeostasis in a carnivorous animal (cat) and in rats fed a high-protein diet. Amer JPhysiol 1978;239:R115-R121.

11. Kitamura T, Yasuda J, Hashimoto A. Acute insulin response to intravenous arginine in nonobese healthy cats. J Vet Intern Med 1999;13(6):549-556.

12. Martin GJW, Rand JS. Lack of correlation between food ingestion and blood glucose in diabetic cats. Proc ₁₅th Ann Amer Coll Vet Int Med, 1997;670.

13. Unger RH, Foster DW. Diabetes mellitus. In Williams Textbook of Endocrinology, Wilson and Foster (eds). Philadelphia. WB Saunders. 1998, pp⁹⁷³-¹⁰⁶⁰.

14. Gougeon R, Jones JHP, Styhler K, Marliss EB, Morias JA. Effects of oral hypoglycemic agents and diet on protein metabolism in type 2 diabetes. Diabet Care 2000;23:1-8.

15. Mazzaferro EM, Greco DS, Turner AS. Treatment of feline diabetes mellitus with a high protein diet and acarbose. (abstract) J Vet Intern Mcd, 2000: 14(3):345.

16. Bennett N, Greco DS, Peterson ME. Comparsion of a high fiber vs low carbohydrate diet for the treatment of diabetes mellitus in cats. (abstract) J Vet Intern Med, 200; 1 5(3):3 81

17. Frank (3, Anderson W, Pazak H, Hodgkins E, et al. Use of a high protein diet in the management of feline diabetes mellitus. Vet Therapeut 2001 ;2(3):238-246.Author Information
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Deborah S. Greco, DVM, PhD, Diplomate ACVIM
Associate Professor, Small Animal Medicine, Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University
Fort Collins, CO, USA