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  • Disciplina: Alimentazione
  • Specie: Cane e Gatto

Diabetes mellitus is undoubtedly one of the most frequent endocrine disorders in the dog and cat. Diabetes is a disease characterised by hyperglycaemia resulting from insulin deficiency and/or resistance; it is the consequence of absolute or relative insulin deficiency, caused, in turn, by an inefficiency of the beta cells of the endocrine pancreas. The clinical manifestations are mainly linked to the effects of the resulting hyperglycaemia. In most cases, subjects with diabetes mellitus require life-long therapy; however, an accurate therapeutic management of the diabetic patient allows to maintain a good quality of life.

 

AETIOLOGY AND PATHOGENESIS


In veterinary medicine, no internationally accepted criteria exist for the classification of diabetes; this said, the disease is commonly divided into:

  • diabetes mellitus type 1: formerly called "insulin-dependent diabetes"; the most common form of diabetes in the dog;
  • diabetes mellitus type 2: formerly called "non-insulin-dependent diabetes"; the most common form of diabetes in the cat (Hoenig, 2002).

In type 1 diabetes there is destruction of beta cells in the pancreas. The underlying mechanism is still unknown but in the dog, genetic predisposition, environmental factors and immune-mediated mechanisms seem to play a dominant role in the pathogenesis and development of the disease. Type 1 diabetes is therefore characterised by the destruction of beta cells with progressive and absolute insulin deficiency.

In the cat, type 2 diabetes is instead related to a form of insulin resistance in the tissues, typically associated with obesity (Appleton et al., 2001). In such cases insulin is not deficient, it is less effective at tissue level.

 

CLINICAL SYMPTOMS


The four classic symptoms of diabetes mellitus are polyuria, polydipsia, polyphagia and weight loss. Insulin deficiency determines a decreased use of glucose, amino acids and fatty acids, an increased hepatic glycogenolysis and gluconeogenesis and, consequently, a state of hyperglycaemia.

Polyuria and polydipsia (Pu/Pd): the increased levels of circulating glucose widely exceed the capacity of renal tubular cells to absorb the glucose present in the glomerular ultra-filtrate, hence the loss of glucose in the urine. Glycosuria is usually established when blood glucose exceeds 180-200 mg/dl in dogs and 200-300 mg/dl in cats. Osmotic diuresis is therefore present, which causes polyuria and consequent compensatory polydipsia.

Polyphagia and weight loss: the inability of peripheral tissue cells to use glucose causes progressive weight loss. The interaction between the hypothalamic satiety centre and the hunger centre is responsible for the amount of food that the subject eats. The hunger centre is constantly functional, but it can be temporarily inhibited by the satiety centre after the ingestion of food. Glucose enters into the cells of the satiety centre only in the presence of insulin; in the presence of diabetes mellitus, glucose is therefore not able to activate the satiety centre and consequently to inhibit the hunger centre. Notwithstanding the state of hyperglycaemia, subjects with diabetes mellitus are therefore polyphagic.

 

THERAPY


The goal of treatment in diabetic patients is to achieve blood glucose control by means of a proper dietary intervention combined with the administration of insulin and appropriate physical exercise.

As regards the dietary management of diabetic patients, it is necessary to take into account not only the nutritional characteristics of the diet but also the amount and mode of administration of the food given.

 

NUTRITIONAL PROPERTIES OF THE DIET


Water. High water intake is very often the first symptom noticed by the owner in the animal which develops diabetes mellitus. In view of the polyuria and polydipsia which characterise the clinical picture it is therefore essential for the animal to always have access to fresh water.

Sources of digestible carbohydrates. The selection of the starch source to be included in the diabetic patient's diet is of extreme importance, as it has a direct impact on postprandial glycaemia. It is first necessary to remember that the diabetic cat, being a strictly carnivorous animal, should receive diets containing less starch than those tolerated by a diabetic dog. In fact, in cats, even in healthy ones, the activity of hepatic enzymes responsible for the oxidation of glucose as well as of those which allow its conversion to glycogen is lower than in the dog (Zoran, 2002). Not surprisingly, when a cat is fed with a high-starch diet the postprandial rise in blood glucose levels lasts significantly longer than what can be observed in dogs or in humans, reflecting a lower efficiency of carbohydrate metabolism in the feline species (Farrow et al., 2012).

Among the different sources of starch usable in the diet of dogs and cats suffering from diabetes mellitus, those rich in soluble fibre should be preferred, such as some cereals (barley, oats and rye) and some legumes (peas, lentils, beans, etc.). In fact, when soluble fibres come into contact with the liquid medium found in the stomach and in the small intestine they tend to form a gel, which increases the viscosity of intestinal chyme and slows down the digestive process; this reduces the risk of a sharp post-prandial blood glucose increase. The use of highly-glycaemic foods should instead be avoided, or at least limited; these include rice, wheat, corn and potatoes (although whole wheat and rice have a lower glycaemic index; Foster-Powell et al., 2002). In a study on overweight cats, Appleton et al. (2004) observed that the administration of a diet based on sorghum and corn allowed a better control of blood glucose compared to a rice-based diet containing the same amount of starch. In other studies it was observed that the highest postprandial blood-glucose levels were caused by diets containing corn, compared to diets in which the source of starch was represented by sorghum, peas or lentils, both in cats (de-Oliveira et al., 2008) and in dogs (Carciofi et al., 2008).

The total amount of starch in the diet has also clearly an impact on blood sugar and must therefore be limited, especially in the cat, whose carnivorous nature complicates the management of glucose originated from the digestion of starch (Hewson-Hughes et al., 2011). Precisely in the cat, it seems appropriate to resort to the use of high-protein diets characterised by low levels (less than 20% of the dry matter of the diet) or the complete absence of starch (preferably from sources with a low glycaemic index) in order to improve the glycaemic control (Bennett et al., 2006; Kirk, 2006; Zoran and Rand, 2013). Although the pathogenesis of diabetes mellitus in dogs is different, a similar approach is believed to be beneficial also in this animal species (Nelson et al., 1998).

Finally, in no case should the diet contain significant amounts of sugars (the content of which is often high in semi-moist diets and snacks for dogs and cats).

Fibre. It has already been mentioned that the use of fibre-rich starch sources can be useful in the control of post-prandial glycaemia (Nelson et al, 2000; Bennett et al, 2006). For this reason, diets of diabetic patients should contain higher levels of fibre compared to a standard maintenance diet. Among other things, the addition of fibre reduces the energy density of the diet and may promote weight loss in the presence of obesity, a condition that, as previously mentioned, is very common in diabetic cats.

Protein. For the reasons already mentioned concerning the need to limit carbohydrates, diets for diabetic dogs and cats should be rich in protein. In particular, in the cat, diets very rich in protein and poor in starch (or even with no starch) stimulate hepatic gluconeogenesis, with a constant input of glucose into the blood, eliminating the blood glucose peaks that typically follow meals rich in carbohydrates with a high glycaemic index. In addition, in overweight cats, diets rich in protein and low in digestible carbohydrates can help to control the cat’s body weight.

Lipids. With regard to fats, the dyslipidaemias that often characterise diabetes in the dog and cat advise not to exceed with the lipid content in the diet. Among the employable lipid sources, fish oil is often suggested, as the omega-3 fatty acids it contains are useful in the treatment of lipid disorders that characterise diabetes and they appear to improve blood sugar control in the cat, through a reduction of insulin resistance (Wilkins et al., 2004). Paradoxically, however, in human medicine, the consumption of high amounts of fish oil has been correlated with an increased incidence of type 2 diabetes mellitus (Zhang et al., 2013); this evidence, though still rather weak, suggests caution in the supplementation of fish oil in the diet of diabetic dogs and cats (Lenox and Bauer, 2013).

Minerals and vitamins. As regards mineral macro-elements, and the electrolytes Na, K and Cl in particular, the diet should contain them in adequate amounts as the polyuria present in the animal increases their losses via the kidneys. Naturally, should the diabetes be associated with renal failure, the levels of phosphorus and sodium chloride in the diet should be limited (the same holds true for the protein content of the diet). Similarly, the diet must contain adequate levels of trace minerals and vitamins. In particular, in healthy cats, chromium supplementation apparently improves the metabolism of carbohydrates (Appleton et al., 2002).

Other nutrients. Although no specific studies have ever been conducted in the cat, there is evidence that in type 2 diabetic patients the supplementation of the diet with particular molecules, such as quercetin (Kim et al., 2011) and other plant polyphenols (Bahadoran et al., 2013) can have a positive effect on the metabolism of carbohydrates and lipids.

 

DIETARY MANAGEMENT


Once the most appropriate diet has been chosen it is then necessary to determine the amount of food and the number of meals that the animal will receive daily. As previously mentioned, in cats, type 2 diabetes is often associated with a condition of obesity; there is evidence of the fact that, often, if the animal is brought back to its own normal weight, the insulin-resistance regresses until resolution of the clinical picture (Bennett et al., 2006; Reusch et al., 2006). In such cases, therefore, the amount of food must be calculated so as to favour weight loss, through restriction of the energy supply (the cat should receive about 20% less energy than the metabolisable energy corresponding to the maintenance requirement for the desired ideal weight). Conversely, in other cases it may also be possible for the patient to be underweight (especially when the disease is not under control): in such cases the goal is to favour weight gain, by increasing the daily amount of food (and avoiding, in such cases, diets excessively rich in fibre that would make body weight recovery difficult).

The number and the timing of the meals will be decided in function of insulin administration, in order to maximize its effectiveness. Ideally, since the amount of food influences postprandial blood sugar levels, diabetic patients should have many small meals throughout the day. It is however evident that this type of approach is complicated by the fact that at each meal exogenous insulin must be administered: consequently, two daily meals are generally administered, with at least 8-10 hours between the morning and the evening meal.

Physical exercise is another factor that plays a very important role in blood sugar control, as it promotes both body weight reduction and a possible condition of insulin resistance.

 

CONCLUSIONS


Diabetes mellitus is a rather frequent disease in both the dog and the cat; its management cannot ignore the correct dietary management of the patient. In the cat, in particular, the disease is often the consequence of a state of insulin resistance secondary to obesity; overweight correction is a possible approach for the remission of the disease.

 

REFERENCES


1.    Appleton DJ, Rand JS, Priest J, et al. 2004. Dietary carbohydrate source affects glucose concentrations, insulin secretion, and food intake in overweight cats. Nutrition Research 24, 447-467.

2.    Appleton DJ, Rand JS, Sunvold GD. 2001. Insulin sensitivity decreases with obesity, and lean cats with low insulin sensitivity are at greatest risk of glucose intolerance with weight gain. Journal of Feline Medicine and Surgery 3, 211-228.

3.    Appleton DJ, Rand JS, Sunvold GD, Priest J. 2002. Dietary chromium tripicolinate supplementation reduces glucose concentrations and improves glucose tolerance in normal-weight cats. Journal of Feline Medicine and Surgery 4, 13-25.

4.    Bahadoran Z, Mirmiran P, Azizi F. 2013. Dietary polyphenols as potential nutraceuticals in management of diabetes: a review. Journal of Diabetes and Metabolic Disorders 12, 1.

5.    Bennett N, Greco DS, Peterson ME, et al. 2006. Comparison of a low carbohydrate–low fiber diet and a moderate carbohydrate–high fiber diet in the management of feline diabetes mellitus. Journal of Feline Medicine & Surgery 8, 73-84.

6.    Carciofi AC, Takakura FS, De‐Oliveira LD, et al. 2008. Effects of six carbohydrate sources on dog diet digestibility and post‐prandial glucose and insulin response. Journal of Animal Physiology and Animal Nutrition 92, 326-336.

7.    De-Oliveira LD, Carciofi AC, Oliveira MCC, et al. 2008. Effects of six carbohydrate sources on diet digestibility and postprandial glucose and insulin responses in cats. Journal of Animal Science 86, 2237-2246.

8.    Farrow H, Rand JS, Morton JM, Sunvold G. 2012. Postprandial glycaemia in cats fed a moderate carbohydrate meal persists for a median of 12 hours - Female cats have higher peak glucose concentrations. Journal of Feline Medicine and Surgery 14, 706-715.

9.    Foster-Powell K, Holt SH, Brand-Miller JC. 2002. International table of glycemic index and glycemic load values: 2002. The American Journal of Clinical Nutrition 76, 5-56.

10.Hewson-Hughes AK, Gilham MS, Upton S, et al. 2011. The effect of dietary starch level on postprandial glucose and insulin concentrations in cats and dogs. British Journal of Nutrition 106 (S1), S105-S109.

11.Hoenig M. 2002. Comparative aspects of diabetes mellitus in dogs and cats. Molecular and Cellular Endocrinology 197, 221-229.

12.Kim JH, Kang MJ, Choi HN, et al. 2011. Quercetin attenuates fasting and postprandial hyperglycemia in animal models of diabetes mellitus. Nutrition Research and Practice 5, 107-111.

13.Kirk CA. 2006. Feline diabetes mellitus: Low carbohydrates versus high fiber? Veterinary Clinics of North America: Small Animal Practice 36, 1297-1306.

14.Lenox CE, Bauer JE. 2013. Potential Adverse Effects of Omega‐3 Fatty Acids in Dogs and Cats. Journal of Veterinary Internal Medicine 27, 217-226.

15.Nelson RW, Duesberg CA, Ford SL, et al. 1998. Effect of dietary insoluble fiber on control of glycemia in dogs with naturally acquired diabetes mellitus. Journal of the American Veterinary Medical Association 212, 380-386.

16.Nelson RW, Scott-Moncrieff JC, Feldman EC, et al. 2000. Effect of dietary insoluble fiber on control of glycemia in cats with naturally acquired diabetes mellitus. Journal of the American Veterinary Medical Association 216, 1082-1088.

17.Reusch CE, Tschour F, Kley S, et al. 2006. Diabetes mellitus in the cat: A review. Schweizer Archiv für Tierheilkunde 148, 130-138.

18.Wilkins C, Long RC Jr, Waldron M, et al. 2004. Assessment of the influence of fatty acids on indices of insulin sensitivity and myocellular lipid content by use of magnetic resonance spectroscopy in cats. American Journal of Veterinary Research 65, 1090-1099.

19.Zhang M, Picard-Deland E, Marette A. 2013. Fish and marine omega-3 polyunsatured fatty acid consumption and incidence of type 2 diabetes: a systematic review and meta-analysis. International Journal of Endocrinology, 2013.

20.Zoran DL. 2002. The carnivore connection to nutrition in cats. Journal of the American Veterinary Medical Association 221, 1559-1567.

21.Zoran DL, Rand JS. 2013. The role of diet in the prevention and management of feline diabetes. Veterinary Clinics of North America: Small Animal Practice 43, 233-243.