Abstract
Leonardo da Vinei onee said, “The smallest feline is a masterpiece”. And, for those of us who marvel at the wonder that is the cat, there can be no doubt that is true. But, it is also true that the cat is unique in almost every aspeet of their existence, from behavior to biochem istry. It is those differences that bring us to this topic: the nutritional peculiarities of the feline. In particular, this review will not only consider their metabolic and nutritional peculiarities, but more importantly, we will review how these differenees lead to disease (hepatic lipidosis, diabetes, possibly IBD), disability (obesity), and possibly, improper nutritional management of our sick feline patients
Feline Nutrition
(ats are obligate carnivores. This statement is news to no one, and yet the importanee of that statement to the dai y lives of cats is stunning. While cats ean use earbohydrates (CHD) as a source of metabolic energy, they have no requirement for them (nor do dogs for that matter), and their metabolic machinery is not ideally suited to use them in large doses. More importantly, because cats evolved eonsuming prey (e.g. high protein, low to moderate fat, minimal carbohydrate), they are metabolically adapted for higher protein metabolism and lower CHD utilization. What does that mean metabolically and nutritionally? There are a number of speeific metabolic and biochemical differences in feline physiology that are important. For those who are interested in the speeific details of these metabolic and physiologic differenees in the nutritional biochemistry of cats, the reader is referred two recent reviews of this subject12
“Because cats naturally eat high-protein, low carbohydrate foods, continuous adivity of amino acid catabolicenzymes provides a continuoussourceof carbonskeletons for glucoseor energyptoduaion and nitrogen for synthesis of dispensible amino acidsand other nitrogenouscompounds. This constant degradation of amino acidsresults in continuous shuttling of amino acids through either gluconeogenicenzymes or energy-producing pathwayssuch as the tricarboxylic acid (TeA) cye/e. Gluconeogenic enzymes convertglucogenicamino acids, lectic acid, propionic acid and glycerol to glucoseand, thereby, sustain blood glucose concentration. However, continuousprotein catabolism Iimits the cet's ability to conserve protein, leading to an obligate nitrogen lossand a higher dietary protein requirement than omnivores.
compared to the postabsorptive phase in omnivores. Dietaryamino acidsare potent secretagogues of insulin in cats;consequently, gluconeogenicactivity is important in maintaining blood glucoselevels in the face of high insulin concentrations and low intakes of dietary carbohydrate. After energy, amino acid, nitrogen and glucoseneeds havebeen met, surpIusprotein (in the form of amino acids) is metabolized for energyor stored as fat. In view of the limited capacity to store protein within the body, this is an important means of energyconservation during protein surplus” (from Kirk, CA, Debraekeleer, J, Armstrong, PJ: Normal Cats.: Small Animal Clinical Nutrition (4th ed), p298.)
Unique Nutritional Features of Cats (And Why Anorexia is So Detrimental)
Cats have an obligate need for protein and amino aeids in their daily diet beeause they are unable to down regulate their urea cycle or transaminases (protein conversion to energy) as other speeies can in times of starvation
Cats utilize protein for energy, even in the face of large amounts of CHD in the diet (there is no “down-regulation” or protein sparing when CHD are plentiful in the diet as with other speeies).
Because of these metabolic differenees, cats requirement for protein (0/0 of diet) is much higher (290/0), than dogs (120/0) or humans (80/0)
Taurine, arginine, methionine, cysteine, and possibly carnitine requirements for cats are greater than dogs or other noncarnivores.
Arachidonic aeid is also an essential fatty aeid in cats (it is not in dogs), and is found only in fats from animal tissue.
Cats require vitamin A and D to be present in the aetive form in their diet as they are unable to synthesize adequate amounts from other dietary precursors (e.g. carotenoids or vitamin D precursors in skin).
Cats have an inereased need for many B vitamins in their diet (e.g. thiamin, pyridoxine, niadn, pantothenic aeid) as they have greater metabolic needs for these vitamins and cannot synthesize or get them from other sources.
Salivary amylase is absent in cats, and they have greatly reduced levels of intestinai and pancreatic amylases (< 10%) - so CHO digestion is much less effieient.
Cats have fewer disaccharidases and other brush border enzymes in their small intestine designed to digest and absorb starches.
The small intestine of cats is mueh shorter than that of an equally sized omnivore - longer Gl traets are necessaryfor handling of complex carbohydrates (in herbivores and omnivores).
Cats have greatly reduced aetivities of hepatic enzymes (e.g. glucokinase) designed to convert a post prandial glucose load to glycogen and thus a glueose load takes longer to process (4-16 hr).
There are no fruetokinases in cats - they are unable to utilize fruetose and other simple sugars.
To summarize the major differences, cats have obligate and daily needs for additional protein, speeific requirements for eertain amino aeids (e.g. taurine, arginine), increased requirements for many B vitamins, and a mare Iimited ability to digest, absorb and metabolize carbohydrates.
Feline Obesity
While figures vary, reeent studies indicate that 25-40% of cats in the United States are overweight or obese, There are a large number of faetors that contribute to this problem, ineluding sex (intaet vs. neutered, male vs. female), age, aetivity (indoor vs. outdoor), and feeding style (meal feeding vs free choice). In a reeent paper studying the effects of neutering on hormones and obesity, two very important findings were uneavered: 1) after neutering a rapid increase in IGF-l and prolaetin occurs that is dosely followed by an increase in body weight, and 2) dysregulation of glueose metabolism (in assoeiation with increases in leptin levels that are significant enough to cause insulin resistance). Thus, to prevent the deleterious effeets of these hormonal changes, prevention of obesity by redueing food intake and careful monitaring of body weight becomes essential. Further, because “it is much harder to take it off, than it is to put it on” - it is important to eontrol weight and diet from the onset (in kittens). Another faetor that is increasingly being considered, both in the development of and treatment of obesity, is the role of CHO in the feline diet. Because of their metabolic requirement to utilize protein as an energy source, CHO in the diet that are not immediately used for energy (e.g. via exereise or other utilization for energy in addition to the protein they util ize for energy) will be stored as fat. Traditional weight loss plans inelude feeding an energy restrieted (e.g. low fat, high CHO, high fiber) diet. However, while these diets may result in weight loss, they do so to the detriment of lean body mass (because cats continue to use gluconeogenesis from protein for energy production even in the face of plenty of available CHD). Successtui weight loss requires loss ot adipose tissue as weil as maintenance of lean body mass, as lean body mass is the driver of basal energy metabolism (loss of lean body mass is a major contributor to weight regain as appetite is not reduced and satiety not reached). Several reeent studies have evaluated use of a high protein, low CHO diet (protein 45% or higher) for weight loss in cats, and in those studies, all cats lost weight, but maintained lean body mass. Importantly, high protein, low carbohydrate diets not only result in sustained weight loss in these cats, but also in normalization of appetite (redueed urge to eat constantly because they are satiated). Because dry foods must be extruded (Le. made into a biseuit), CHO are required in the cooking process, and thus, the best commereial diets for achieving a high protein, low CHO profile are canned (e.g. kitten or growth) foods. However, it must be stated that high protein, low CHO diets are not “magical” - their profile is ideal for cats, but the number of calories consumed is the critical key to appropriate weight redudion and control. High protein/low CHO dry foods are generally very calorically dense (rn/d has 485 kcal/cup, DM has 580 kcal/cup, Ennava ENO has 540 kcal/cup, etc), and can be diffieult to feed in appropriate amounts to achieve target calories. On the other hand, canned foods have lower calories/unit (rn/d canned has 165 kcal/can, DM has 180 kcal/can, etc). An important eonsideration is that most cats need to eat no more than their resting energy requirement to stay at the ir ideal body weight. However, in cats for which weight loss is needed, a reduction of 60-80% of RER willlikely be necessary to achieve weight loss. What does this mean? The veterinarian must counsel cat owners both on the type of food and the amount of food they feed the ir cats
Feline Diabetes Mellitus
Approximately 85-90% of all diabetie cats fall into the category of Type II diabetes (obese, adult onset diabetes, that maybe transient or insulin dependent). This is in eontrast to the disease in dogs, where the overwhelming majority of cases are insulin dependent diabetes. Dietary reeommendations for years (whiehwere extrapolated from human and canine reeommendations) have been to feed theseaffeeted cats with diets high in complex CHO (e.g. high fiber diets). However, reeent studies have shown that high protein, 10wCHO dietsareextremely beneficial in the management of diabetes in cats, resulting in a greater than 50% reduetion in the amount of insulin in 8 of 9 cats in one study. In anotherstudy, completecessation of the insulin requirement oceurred in a third of the cats. Other studies have recently shown that, contrary to what is observed in dogs, fiber containing dietsdo not alter glueose toleranee (an important reason for feedinghigh fiber diets in canine diabeties). Finally, feedinghigh CHO diets to eats resulted in development of hyperinsulinemia, even in cats with a normal body weight. In studies of normal cats eatingeither 250/0 or 500/0 of ealories from CHO, blood blueose concentrations were approximately 25% higherthan normal from 4-18 hoursafter eatingthe high CHO diet In diabetie cats, the effeet on beta eeli funetion is exaeerbated beeause of the prolanged period of hyperglyeemia after eating, whieh may lastfor 24 hoursand lead to glucose toxicity. Chronic hyperinsulinemia (either due to insulin resistanee from obesity, drugs, or other causes) or due to diet influences, leads to beta eeli apoptosis. In other words, a high CHD diet fed long term contributes to beta eeli death. Anothercause of beta eeli damage and death is deposition of amyloid in the islets. Amyloid is a precipitate of amylin, whieh is co-secreted with insulin. (ats with hyperinsulinemia seerete greater amountsof amylin and thus are at inereased riskfor amyloiddeposition and beta eeli death. Further, hyperinsulinemia is a metabolie state resulting in decreased utilization of fats for energy, and thus, the tendency toward weight gain, and in some cats, can lead to beta eeli exhaustion. In addition to the benefits listedabove of high protein/low CHD diets, there is a reduction in post prandial hyperglycemia (fewer CHO in diet to lead to a smaller post prandial surge) and, this results in a concurrent reduetion in hyperglycemia induced glueose toxicity, a lower insulin requirement (exogenous or endogenous) and fewer calories to contributeto obesity.
Feline Hepatic Lipidosis
Idiopathichepatic lipidosis (IHL) is a weil reeognized cause of hepatic failure in cats, especially in cats that are obese or undergoing stressed starvation. However, reeent studies suggest IHLis the result of a combination of faetors: excessive peripherallipid mobilization (due to high eateeholamine release from stress or iIIness), and subsequent development of nutritional deficiencies that compromisethe formatian of lipoproteins and the mobilization of hepatic triglyeerides. The individual nutrientsthat maybe involved includetaurine, carnitine, arginine, threonine, citrulline, choiineand eobalamin. Further studies are required to elucidate which, if any, of these nutrientsmaybe important in the development of the lipid and lipoprotein derangements that charaeterize IHL. In addition to the metabolie derangements, cats with IHLalsoappear to have decreased liver coneentrations of glutathione, and thus maybe at greater risk of oxidantdamage to hepatocytes. Thekeyto treatmentof IHLremains feeding affected cats, usually through a feedingtube (esophagostomy or PEG tube) until their metabolism normalizes. Feeding a high quality, moderate to high protein diet for 2-6 weeks, or until the cat begins to eat on its own again, is the most important aspect of treatment This cannotbe over-stated: the keyto treatment is for the cat to receive adequate protein and fat calories via tube feedingto correct the nutritional imbalance that hasbeencreated. However, other supportive measures that maybe included in the therapyare control of vomiting, reduetion of gastritis by judicioususeof histamine-z blocking drugs, carnitine supplementation (250 mg/cat/day) to improve lipid metabolism, and antioxidant therapy. Supplementation of B vitamins is suggested to improve appetiteand cellular metabolism, and in somecats with severe liverfailure, addedvitamin Eand K maybe necessary as weil.
Juvenile Feline Diarrhea and Inflammatory Bowel Disease
There are multiple faetors to consider in the development of diarrhea in kittens, but dietarycauses are important. Whileit hasbeen extremely difficult to charaeterize species and numbersof baeteria in the Gl traet, most researehers believe that eats have much higherconcentrations of baeteria in their small intestine, eompared to dogs and people. Thereason for the increased intestinai microflora in cats is not known, but along with their shorteroverall intestinallength (eompared to dogs), the presence of inereased numbers of bacteria mayserve to enhanee digestion of proteinsand fats, both of whieh are higherin normal feline diets.
Conversely, diets higherin CHD andfiber (especially solublefibers) maypredispose eats to bacterial overgrowth, changes in bacterial flora numbersor speeies, or result in developmentof intolerance or allergy due to development of increased inflammation and immune responsiveness. This problem may becomeprominent when kittensare switched from milk to dry food or from canned kitten foods to dry food (because of the high CHO in dry foods). Alterations in bacterial populations are believed to be important in human IBO, and may be important in kittens as weil. Thus, in young cats with diarrhea, or in cats with intermittent vomiting or diarrhea that may be aresult of dietaryintolerance, feeding diets that are low in CHO may resolve the problem. In kittenswith severe diarrhea, antibacterial therapy along with the diet changes may be needed. Theusefulness of probiotic therapy in cats for bacterial population control is unknown, primarily because the appropriate probioticsfor cats are unknown. Feline inflammatorybowel disease (IBO) is an idiopathic, inflammatorydisease of the intestinai tract for which dietaryand immunosuppressive/anti-inflammatory therapyseems to control, but for which we stiil haveno c1ear understanding of its cause or perpetuation. A wide variety of possible causes have also been investigated in humanswith IBO, but current research is focused on the role of bacteria in the developmentand progression of the aberrant immune response that occurs. This hypothesis may also be important in the pathogenesis of feline IBOasweil, espeeially owing to the fact that cats otten respond when combinations of metronidazole and steroids are usedtogether. Further supportive evidence for a speeific role of bacteria in the development of feline IBOis lacking, but several aspects of feline digestion and feline diets are suggestive of a possible role for microbes in the disease (seeabove). Oiets higher in CHOand fiber (espeeially solublefibers) may predispose cats to changes in baeterial flora numbers or speeies that result in development of a local immune response, which if uncorreeted, or if perpetuated by immune mechanisms, may lead to development of IBO. It is the alterations in bacterial populations or speeies that is believed to lead to the abnormal intestinai inflammatory response in humanswith IBO, and mayalso be important in feline IBOas weil. Oietary therapy may be appropriate for prevention of feline IBO, but oncethe disease hasbeen initiated, diets may not be suffieient to control the excessive or aberrant immune response. In fact, increased protein mayresult in an increased exposure of the gut immune system to these proteins resulting in further sensitization and inflammation. Nevertheless, in cats with intermittent vomiting or diarrhea, feeding diets high in protein (espeeially novel protein) and low in CHO (canned) maybe important to resolution or control of the problem.