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Diets/Nutrition for Cats Claudia A. Kirk, DVM University of Tennessee Carbohydrates and the Nutritional Management of Feline Diabetes (part II) Diabetes mellitus can be classified into multiple subtypes however the majority of feline diabetics are either Type I or Type II (non-insulin dependent diabetes mellitus: NIDDM in people) (1). In the cat, Type II appears to predominate despite the need for exogenous insulin therapy. Over 80% of cats are type-II, with the remaining thought to be secondary to other conditions like pancreatitis or acromegaly. Type II diabetes has been referred to as a relative insulin deficiency since the amount of insulin actually secreted may be increased, decreased or normal but it is always inadequate relative to serum glucose levels. Cats with type- 2 DM require either oral hypoglycemic drugs or exogenous insulin coupled together with nutritional management. (2) The goals of nutritional management in diabetes mellitus is to 1) blunt postprandial hyperglycemia, 2) control body weight, 3) support altered nutrient needs, 4) improve peripheral insulin sensitivity, 5) avoid diabetic complications such as hypoglycemia, ketosis, neurophathies, etc. and 6) coordinate peak nutrient uptake with insulin activity. Taken together, the diet composition and feeding plan should optimize glycemic control. Etiopathogenesis of Type II Diabetes Type II (Non-Insulin Dependent Diabetes Mellitus) - The deposition of islet amylin and progressive -cell destruction is characteristic of Type II in both people and cats. (3,4) Amylin is formed from islet amyloid polypeptide (IAPP), a peptide co-secreted with insulin. In people, chronic -cell stimulation and increased IAPP release occurs following high simple carbohydrate intake and peripheral insulin resistance. Increased pancreatic amyloid deposition is associated with impaired glucose tolerance (3,4). Obesity is the main driving force in the development of Type II in people. This same phenomenon appears to occur in cats (3,4), possibly because as true carnivores, metabolic adaptations have reduced their tolerance to dietary carbohydrates. This phenomenon has been referred to as the "carnivore connection". During the Ice Ages when man consumed a meat-based low carbohydrate diet, metabolic adaptations limited insulin effect to sustain blood glucose levels. Cats, adapted to a meat-based diet, have also evolved to maintain blood glucose in the face of low carbohydrate intake. Cat adaptations result in constant hepatic glucose production from amino acids (gluconeogenesis) and delay in carbohydrate utilization (low glucokinase activity). Unfortunately factors, such as prolonged elevation of plasma glucose, can result in factors that lead to diabetes. Chronic hypersecretion of insulin is thought to lead to beta-cell exhaustion, chronic hyperglycemia causes hydropic degeneration of the feline -cell ("glucose toxicity"); both leading to decrease pancreatic insulin secretion in cats (5). Recent studies have described large proportions of diabetic cats whereby nutritional management and pharmacologic therapy have resulted in resolution of the diabetic state (6, 7, 8, 9). These transient diabetics presumably have regained -cell function upon reversal of glucose toxicity and/or improved peripheral insulin resistance. The rate of transient diabetes appears to be increasing with the advent of new diet strategies and insulin therapy. Whereas transient diabetes was reported to occur in 10-25% of feline diabetics, upwards of 50-70% of cats with diabetes < 2 yrs in duration are transient. (12). Diabetes mellitus affects cats of any age and gender but is diagnosed more commonly in neutered males greater than 6 years of age, the same population most at-risk for obesity (10,11). (Table 1) In the cat, obesity has been shown to result in abnormal glucose tolerance and peripheral insulin resistance (12,13,14), factors which are known to precede the development of Type II DM in cats and people. The risk of developing diabetes mellitus increases by 4 fold in obese cats (11). Of important note, diabetes in dogs is related to beta-cell destruction (Type 1 DM) and is not associated with obesity. KEY NUTRITIONAL FACTORS
Diet composition, form and feeding methodology can have a significant impact on diabetic regulation. When choosing a food to manage the diabetic, concentrations of key nutrients that may alter regulation should be considered. Energy - Cat with diabetes mellitus often present with a history of significant weight loss yet are overweight or obese (10). Before making recommendations for daily energy requirements (DER) it is important to emphasize that the clinical response to nutritional management of the diabetic cat is highly dependent on satisfactory medical management. As previously discuss, fiber fortified foods designed for weight control (3.5 kcal/g ME) are appropriate for weight reduction and glycemic control. Good results can be achieved with appropriate compliance. In underweight cats or those with poor tolerance to dietary fiber, higher energy foods are more appropriate (4.0-4.5 kcal/g ME). In these cats, the low carbohydrate foods, with their reduced fiber and increased fat and calorie content are good alternatives. Protein - Diabetic animals occasionally may have increased loss of amino acids in urine attributable to inappropriate or inadequate hormonal signals and glomerulonephropathies. More commonly, loss of lean body mass is due to inadequate insulin concentrations with poor cellular amino acid uptake and increased protein metabolism via hepatic gluconeogenesis. Diabetic cats require high quality protein of good biologic value. Protein content of the food should be > 30% dm of the food and > 85% digestible. Newer low-carbohydrate high-protein foods supply relatively similar protein levels as high-fiber formulas when determined as a percent of metabolic energy (ME) intake. (Table 3) In the face of limited dietary carbohydrates, higher protein levels are theoretically required in order to support increased hepatic gluconeogenesis and normal blood glucose production. Failure to maintain blood glucose due to high glucose demands and insufficient hepatic gluconeogenesis has only been reported only during gestation and lactation in the feline (15). In adult cats, the increased protein requirements reported for cats already account for sustained gluconeogenis and increased protein metabolism. Thus, the absolute protein requirement for the adult diabetic cat is unlikely to be significantly higher than adult maintenance requirements (16) and would certainly be below the average protein content of most commercial feline foods. Nontheless, when lowering the overall carbohydrate content of a diet, fat, protein or both must increase to account for the difference. Since, fat (especially saturated fat) is known to increase insulin resistance and decrease glucose tolerance,(10) it is logical to replace carbohydrates with protein as opposed to fat. The total amount of protein is only modestly increased in newer low carbohydrate foods, Nevertheless, there are certain conditions where this increased protein may be contraindicated. Cats with concurrent renal disease typically experience increased blood urea nitrogen when switched to a higher protein diet. It has been suggested that increase GFR in response to higher protein, or alleviation of a diabetic nephropathy actually improved renal function. In my experience, cats having blood urea nitrogen values above 45 mg/dl while eating low carbohydrate foods demonstrate better attitude and appetite when switched to a lower protein renal therapeutic diet. To continue limiting carbohydrate utilization, adding acarbose therapy (12.5 mg/BID with meal) to the new diet has sustained the benefit of low carbohydrate intake. Using low carbohydrate diets in cats with pancreatitis is also contraindicated according to some product guides. Because CCK is maximally secreted by proteins, amino acids, and fat, the use of moderate protein, low fat and high carbohydrate foods have been recommended. This is an area of great uncertainty. Many cats with chronic pancreatitis are well maintained on recovery-type diets (high protein, fat and low carbohydrates) however, cats with acute/active pancreatitis should be fed bland intestinal therapeutic foods with a larger portion of the calories obtained from carbohydrates. Finally, cats with sever liver disease and hepatoencephalopathy, or at reasonable risk of hyperammonemia should not be fed these high protein foods. Carbohydrates - The ideal composition, and quantity, of carbohydrates in foods for management of diabetes mellitus in people and cats is controversial. Diets containing up to 85% carbohydrate have been recommended in people with the bulk containing highly complex carbohydrates and soluble fibers (17). Significantly lower levels of carbohydrates (< 10-20% dry matter) have recommended for diabetic cats due to their nutritional peculiarities as an obligate carnivore (18, 19). The optimal level of soluble carbohydrate for feline diabetes has not been defined. Recent studies have demonstrated a improved glycemic control to both healthy and diabetic cats fed low carbohydrate foods (< 15% dm) (7,8,9). By limiting dietary carbohydrates, blood glucose is maintained primarily from hepatic gluconeogensis, which releases glucose into the circulation at a slow steady rate. Fluctuations in blood glucose concentrations related to postprandial glucose absorption is avoided (8). When feeding very low-carbohydrate canned foods with our without acarbose (alpha-amylase inhibitor), blood glucose and serum fructosamine concentrations and exogenous insulin requirements were observed to decline (7). More interestingly, Mazzaferro (7) reported over 60% of cats fed low-carbohydrate foods reverted to a non-diabetic state. The proposed mechanism of diabetes reversal is improved glycemic control, lower insulin requirement and reversal of sustained hyperglycemia thereby reversing glucotoxicity and allowing recovery of peripheral insulin sensitivity. Newer studies comparing low-carbohydrate foods to a high-fiber, high-carbohydrate food in cats with naturally occurring diabetes mellitus also found a large proportion of cats reverted to a non-insulin dependent state within 4 months of diet change. (9). About 68% of cats in the low-carbohydrate group and 41% of cats fed high fiber foods were able to discontinue insulin. Calculated odds ratios indicate that cats fed a low-carbohydrate food are 3 times more likely to discontinue insulin and revert to a non-diabetic state. For cats that required ongoing exogenous insulin therapy, glycemic control and insulin dose was not significantly different between groups. The responders (improved glucose control and clinical signs) and non-responders were evident in both food groups but with no clear biochemical or physical marker identified as response predictors. Is there a "Best" carbohydrate source? Carbohydrates sources suggested to have lower glycemic index in the cat include corn, sorghum, oats, and barley. Highly processed rice (fine ground and fully gelatinized by cooking) is 100% digestible and readily absorbed. Although studies have suggested that diabetic cats fed free choice have negligible postprandial glucose elevation, delayed intestinal glucose absorption is considered beneficial. Ketosis and low carbohydrate foods - As previously discussed low carbohydrate foods can improve weight loss and increase blood ketone levels. Despite possible concerns over diet-induced ketone production and the development of ketoacidosis, diet-mediated ketosis is minimal compared to that seen with poor diabetic regulation. (Table 2) In non-ketotic cats, the improved glycemic control and peripheral insulin activity appears to negate complications that might be associated with the slight increased ketone production. By experience, providing adequate insulin therapy is key to correcting ketosis and low carbohydrate foods have not been observed to worsen ketosis. Fiber - Fiber aids in glycemic control by promoting slow and sustained GI absorption of glucose following meals. Some studies have found improved insulin activity and reduce peripheral insulin resistance following fiber supplementation (20). In cats, support for feeding fiber-supplemented foods come from clinical experience and a study demonstrating moderate fiber intake improved glycemic control in diabetic cats (21). Cats fed fiber supplemented foods (12% w/w cellulose) exhibited lower postprandial serum glucose and mean glucose concentrations compared to cats fed similar foods containing starch (21). Although several studies in rodents and people indicate soluble fiber is most desirable, evidence of a clear benefit of soluble over insoluble fiber is lacking in the cat. The soluble fiber may be partially fermented to short chain fatty acids and then used as energy for enterocytes or absorbed into the blood for utilization by the animal. Recent studies do suggest, moderate levels of fiber suffice when feeding low carbohydrate foods (< 8%), particularly when of mixed fiber source. Although an ideal fiber content and source has not been established, it is appears that the inclusion of moderate amounts of mixed fiber (approximately 5-12% of DM) aids glycemic control and weight management of the diabetic cat. Transition metals/trace minerals - Certain transition metals (chromium and vanadium) are purported to improve peripheral insulin sensitivity and glucose tolerance. Experimental evidence suggests low doses of oral vanadium improve glycemic control (22). However, poor food intake and gastrointestinal side-effects limit its use. Chromium is a component of "glucose tolerance factor" that aids in insulin activity and glucose uptake and utilization. Studies demonstrating a beneficial effect of chromium supplementation in cats have been conflicting (23, 24). Appleton reported lower glucose levels, glucose half-life and glucose AUC following IV glucose injections in healthy cats supplemented with 300 ppb or 600 ppb chromium as chromium tripicolinate (23). Cohn et al. conducted similar studies with daily supplementation of 100 mcg of chromium (24). No difference in glucose tolerance, insulin concentrations or glucose disposal was observed in normal and obese cats. Further studies are required before widespread chromium supplementation to the diabetic cat can be recommended. Antioxidants - Many of the secondary complications associated with diabetes (diabetic nephropathy, cataracts, vascular fragility, retinopathy and neuropathy) are likely related to Oxidative by products. The benefit of antioxidant vitamins in feline diabetes has not been evaluated. A single study has suggested increased vitamin E intake is associated with a decrease in glucose tolerance in healthy cats (25) but has not been noted to cause overt increases in blood glucose values in other studies (26; personal observations). Alpha-lipoic acid acts both as a potent antioxidant and improves glucose uptake at the level of the GLUT receptor in animal models and people. Unfortunately, unpublished reports suggest cats experience salivation and ataxia at doses of 30 mg/kg BID (Hill A., personal communication). Doses of 1-5 mg/kg/day with a maximum dose of 25 mg/day/cat have been used empirically by some practitioners (27). Improvement in glycemic control has not been documented in the cat. Carnitine - Carnitine supplementation has been shown to have a beneficial effect in reducing lipid accumulation in cats undergoing rapid weight loss (28). In skeletal muscle, the importance of the function of the carnitine system in the control and regulation of fuel partitioning not only relates to the metabolism of fatty acids and the capacity for fatty acid utilization, but also to systemic fat balance and insulin resistance (29). Feeding Plan It is important to emphasize that the efficacy of dietary treatment depends on diet selection, feeding method, daily activity and use of anti-diabetic drugs or insulin. In all cases large variations in activity or diet may alter glycemic control. Food changes or weight loss may result in an adjustment of insulin dose by up to 20%. Food choice - Both high-fiber low-fat and low-carbohydrate high-protein formulas for the management of diabetes are commercially available. Low carbohydrate foods are available from each of the major therapeutic food manufacturer (Hill's m/d, Purina DM, and Royal Canin DS 44) along with moderate- to high-fiber alternatives. These are good choices as they are palatable, low in protein and fortified with vitamins and minerals that may be beneficial in diabetes mellitus. In addition, the products are consistent in formula and calorie content allowing for predictable dietary intake, needed for optimal diabetic regulation. For cats reluctant to eat therapeutic foods, several gourmet-type and growth-formula canned foods are available in the grocery chains and have similarly low carbohydrate levels. A quick check of the ingredient label will indicate these products contain: animal meats, vitamins, minerals and gums (but no grains or flours). Owners must be cautioned that it is ONLY the canned forms of these products that are low carbohydrates and formulas can vary between flavors so label reading is a must. Studies are limited as to which food profile (high-fiber vs low-carbohydrate) provides optimal glycemic control. Feeding a low-carbohydrate foods clearly increases the reversion rate of clinical diabetes to a non-insulin dependent state (transient diabetes) by 3-fold compared to cats fed a high-fiber foods (8,9). Nonetheless, transient diabetes occurs when feeding both food profiles (high-fiber or low-carbohydrate) and diabetic control is not significantly different between foods in cats that remain insulin-dependent (9). It appears that there is individual variability in response to low-carbohydrate vs high-fiber therapeutic foods. Like the response to weight control therapy, there are no obvious clinical or biochemical indicators that predict the optimal food profile for an individual diabetic cat. Current recommendations for newly diagnosed cats are to start with a low-carbohydrate food and good insulin control (typically twice daily glargine or lente insulin). This practice has resulted in the highest rate of diabetic remission (transient diabetes) in cats to date. However, cats well regulated on moderate-fiber foods, or where higher protein levels are contraindicated, should continue the current diet. Cats on chronic insulin therapy were equally well controlled on either the low carbohydrate or higher fiber diet (9). Until further studies are available, the clinician is left using diet history, personal preference and individual food trial to determine the best food choice. References upon request. Table 1. Comparison of risk factors for obesity and diabetes mellitus in the cat
Table 2. Ketone production in the cat
Table 3. Nutrient comparisons for selected therapeutic foods designed to manage feline diabetes mellitus (% DM (g/100 kcal)).
Clinical Aspects of Obesity and Low Carbohydrates Obesity is the most common form of malnutrition in dogs and cats in the United States (1). A 1974 report noted the prevalence of obesity in cats was only 6-12 % (2). More recently, two national studies using body condition scores to establish weight categories reported approximately 30- 35% of dogs and cats visiting private veterinary practices are overweight to obese. (1, 3) And, nearly 50% of the pets between the ages of 5 and 10 were overweight or obese. Despite the fact that veterinarians physically assessed this large proportion of cats as overweight or obese, obesity was diagnosed in only 1.6% of this population. Why are we, as veterinarians, reluctant to diagnose and treat obesity in our small animal patients? The answer is multi-fold but 3 key factors are important: 1) the impact of obesity on the health and well-being of cats has not immediate; 2) the long-term success of our current obesity treatment programs has been disappointing; and 3) perceived negative social interaction with the client. Many veterinarians are concerned their advice will seem judgmental or imply owner incompetence. Ironically, owners tended to score their cats heavier than did the veterinarians in one study. (Fig. 1) One wonders if these veterinarians politeness clouded their objectivity during examination or if owners are actually more critical of their pets' condition. Defining Obesity Obesity has been defined in both functional and quantitative terms. Functionally, obesity can be defined as the state when body fat has accumulated to a level that impairs health or normal function. This may be obvious in the grossly obese patient with concurrent disease. However, it is not easily determined in patients where the risk for obesity-related disease is increased but the disease itself is not yet evident. Quantitatively, obesity is generally defined as exceeding ideal body weight by 15-20% or more (> 30% body fat). This may be easier to identify than the functional definition, but not much. Because breed, genetic, and gender differences result in wide variations in body size and type, establishing an ideal weight can be equally challenging. Diagnosis Determining the level or percent of body fat is the first step in the accurate diagnosis of obesity and is fundamental to monitoring progress of a weight loss program. A variety of techniques have been employed to assess body composition in the living animal. A review of the various techniques reveals they are imprecise, prohibitively expensive, or overly complex for use in a practice setting (4). Body condition scoring (BCS) is a practical tool available to the practitioner to semi-quantify body fat. This method is practical, fast, cost-effective, and reasonably accurate in the diagnosis of obesity. We use a 5 point scale which provides a reasonable differentiation of body condition but is easy to remember and use (Table 1). Body condition scoring has been validated using both traditional methods as well as Dual Energy X-Ray Absorptiometry (DXA) (4, 5). (Table1) It is important to note there are other scales used to classify body condition: 1-3, 1-6, and 1-9. All methods have essentially the same goal, to quantitatively assess the fat composition of an animal. (Table 2) The choice of which method or scale to use is largely personal preference but it should provide sufficient discrimination to generate meaningful values. That is: 1) to identify animals with a body fat content that places the cat at risk for disease or physical dysfunction and 2) to monitor changes in body fat over time. For both goals a systematic approach is required and a scale of at lease 5 points should be considered. Clinical Impact of Feline Obesity Diseases that have been associated with obesity in dogs and cats include diabetes, hypertension, neoplasias, impaired immune response, pancreatitis, hepatic lipidosis, urolithiasis, musculoskeletal problems, respiratory and cardiovascular disease, dermatopathies, anesthetic and surgical complications, and heat and exercise intolerance. (6) The degree to which each of these contributes to morbidity and the early mortality of obese pets is unknown. However, it is interesting to note that recent studies have observed the prevalence of obesity in geriatric cat populations is substantially diminished from that of middle-aged pets (1, 7). (Fig 2) This begs the question: Is this decline in obesity the result of early mortality in obese cats or does weight loss occur with advancing age? It appears a combination of both is at work. As cats age they are at risk of developing diseases which may result in loss of both fat and lean body tissue. In addition, there is a 2.8 fold increase in mortality in obese middle-aged (8-12 yr.) cats compared to optimum weight cats (8). Within this age group, cats with optimal body condition had an 83% probability of survival, compared to obese cats with only 53% probability of survival and chechectic cats with 43% survival. Obesity is considered an inflammatory disease. Fat cells, or adipocytes, secrete proinflammatory mediators (TNF , IL6, acylation stimulatoing protein, adiponectin, and leptin). Not only do these peptides directly stimulate inflammatory cells, they alter metabolism to increase insulin resistance, oxidative stress, and chronic disease. Inflammatory cytokines are higher in obese dogs and cats compared to lean animals and likely contribute to disease risk associated with obesity. Risk Factors for Obesity One of the least addressed strategies for obesity management is prevention. Veterinarians should identify risk factors within the animal and environment that are associated with obesity. (Table 3) Risk factors such as age, gender, breed and indoor environment cannot be eliminated but should serve as markers for additional monitoring. Others such as high fat diet and inactivity can be addressed early on. Neutering results in a significant risk for obesity, particularly in male cats and female dogs (3). Limited exercise with indoor housing may be addressed with owner-induced play in both dogs and cats. Effect of Neutering - Neutering cats has been shown to reduce the daily energy requirement (DER) of adult cats by 24 %-33% compared intact control cats. (9,10) The decrease in DER does not appear to be influenced by age at neutering. (9) Reduced energy requirements have also been noted in neutered dogs. The reduction in energy requirement is most likely attributable to a reduction in basal metabolic rate as obvious changes in behavior or activity following neutering were not observed. (10) The mechanism of reduction in basal metabolism following neutering is unclear. Suggestions include; a potential reduction in lean body mass following the removal of reproductive hormones (9), or changes in thermogenic activity within the liver. (10) Because reduction in DER without reduction in food intake will lead to obesity, it is imperative nutritional counseling is provided to owners at the time their pet is neutered. Others have found a simple increase in food intake is the culprit. The role of altered feedback inhibition of androgens on leptin has been suggested but not proven. Regardless, the advice remains the same: owners need to control food intake and monitor BCS after neutering and be prepared to reduce intake at the first sign of weight gain. Traditional Weight Loss Management As with any disease, successful obesity treatment requires a clear understanding of the etiology. Unlike most diseases, the cause of obesity is simple. Caloric intake is greater than caloric expenditure and the balance of excess energy is stored as adipose tissue. Obesity treatment in small animal nutrition consists of restricting calories, increasing exercise, and modification of feeding practices (owner behavior). Various theoretical calculations of the daily caloric requirement of the pet at its current or, more appropriately, ideal body weight have been described (11). Once the theoretical requirement is calculated, the amount of food is then restricted to obtain 60-80% of this caloric requirement. From this 20 to 40% daily caloric deficit a rate of weight loss can then be determine. These calculations (described elsewhere) are straightforward, and computerized programs are available to aid in the calculation. If the cause for obesity is simple caloric excess, and the treatment only requires caloric restriction, then why do some animals fail to loose weight? Reasons for Failure Appetite and Satiety - One of the main driving forces in weight maintenance is appetite and satiety. Most people and animals will maintain there adult weight within a fairly narrow range over many years. The reason is both appetite and satiety have long-term and short-term regulators with tremendous redundancy. This redundancy of regulation is why appetite control is probably the biggest stumbling block to successful weight control. Individual Set Point - Animals and people seem to have an innate set point for body weight or, more appropriately, body fat. This set point is determined, in part, by the number of fat cells within the body but also by factors, such as genetic makeup, which are less well understood. The amount of body fat is now thought to be controlled in rats and people by a peptide, leptin, secreted directly from the fat cell. (12) And similar relationships are observed in dogs and cats. This represents a form of negative feedback. When fat stores are low leptin is low. Low hypothalamic leptin results in increased Neuropeptide Y which stimulates appetite. This continues until fat stores are replenished and leptin is released at levels sufficient to inhibit secretion of NPY. This is the purported mechanisms of the lipostatic theory of food intake (12). We can reduce a pet's caloric intake by feeding smaller quantities or reducing the energy content of a diet. The animal will successfully lose weight. However, without continued food or caloric restriction the pet will increase its food consumption until the body weight returns. A host of peripheral and central peptides influence satiety (Table 6) with the advantage seemingly in favor of appetite support and weight maintenance. Non-compliance - Non-compliance is a common reason for failure of weight loss therapy. Non-compliance by the pet occurs because it is striving to maintain its set-point. Owner compliance is often poor due to social/psychological factors important to a particular client-pet relationship and also due to begging behavior of the unsatisfied pet. A study by Kienzle found that owners of obese pets were not more attached to their pets than owners of lean pets. (13) However, the human -pet relationship was considered more "humanistic". Pets slept with owners, shared food and were generally indulged as fellow-people. Feeding was of crucial importance and there was a lack of discipline toward feeding. (13) These issues must be recognized and addressed for successful weight loss to occur. We commonly use licensed social workers to help clients manage interpersonal issues that sabotage weight loss plans for their pet. Disease factors - Certain diseases, such as hypothyroidism or hyperadrenocorticism, alter metabolism such that weight loss is slow or difficult in dogs. In cats, acromegaly and innate insulin resistance may play a role in metabolic rate. Obesity research is stacking up against a true "thrifty gene" as a metabolic basis for obesity. While genetics certainly influences the risk for obesity, reports of specific gene mutations (i.e. melanocortin 4 receptor) that result in hyperphagia and obesity (14) are the exception in people, as well as pets. Obesity still comes down to energy intake exceeds energy output and few cases are related to concurrent disease. Inaccurate estimation of ideal body weight- Inaccurate estimation of ideal body weight can occur unless some assessment of body condition is coupled with the weight measurement. Weight alone gives no indication of body composition. Because it is the lean body mass that is metabolically active, failure to estimate an ideal weight based upon ideal lean mass can result in a gross overestimation of energy requirement. Be tough! Accurate energy calculation depends on accurate assessment of ideal weight. Inaccurate estimation of energy requirement- Inaccurate estimation of energy requirement and food portion is often an unrecognized cause of failure. Caloric recommendations that do not result in weight loss negatively influence both owner and veterinarian enthusiasm and compliance. Inaccurate estimation occurs due to a wide variation in individual caloric need (see Fig. 2), food measurement errors, or incorrect daily activity estimations. Formulas used for estimating the daily metabolic energy requirement generally comes from populations of normal pets or lab animals. Few studies have focused on the average energy expenditure of obese pets. For example, adult cats are reported to need 70 kcal/kg to 90 kcal/kg but actual intakes ranged from 39-66 kcal/kg in a group of inactive cats. (16) Thus, a cat eating 39 kcal/day offered a 30% reduction from 70 kcal/kg (49kcal/kg) would likely gain not loose weight! Tips for Successful Weight Management Successful weight loss requires that each of the reasons for failure be appropriately addressed. Successful weight maintenance requires a lifelong commitment. Individual Set Point - During caloric restriction animals defend their energy stores, i.e. body fat, by a variety of mechanisms. The two major mechanisms are decreased energy use and increased hunger. The goal is to diminish the effect of these mechanisms. To overcome the adjustment of energy expenditure that occurs with small decrements in caloric intake, substantial reductions in intake should be maintained for sustained periods of time. At the same time, excessive energy restriction resulting in excessively fast weight loss may predispose the patient to rapid return or overshoot of its fat set point. In fact, previously obese people need 10-15% less energy than normal weight people of the same size. This seems to be true in the dog and is likely true in the cat. Long-term, if control of food intake is not maintained weight cycling may occur. Appropriate caloric restriction should result in loss of 1- 2% of body weight per week, however 0.5- 0.8% seems more typical in cats. If you are not achieving adequate weight loss don't hesitate to reduce food intake by 10% per week until successful. Body weight should be monitored frequently during and after weight loss to assess adequacy of caloric restriction and prevent return to the set point while the body establishes a new set point. To directly influence the patient's ability to decrease its energy need, increased activity should be prescribed. It has been shown that a simple 10 min. play session per day is as effective as diet in the cat. We use 30 min of daily walks or water treadmill to enhance weight loss in dogs. Non-compliance - Compliance can be enhanced by altering the external and internal factors that influence the desire to eat. The external factors are psychological, social and food related (palatability and feeding method). Most of the internal factors relate to the food itself and its presence in the GI tract. Chemical neural and mechanical satiety signals influence the desire to eat and other behaviors, like begging. Despite conflicting data, increasing fiber in the diet is one effective means of decreasing voluntary food intake and the desire to eat, particularly in dogs. Dogs tend to be bulk feeders and here is where fiber can help. Anecdotally, feeding a single flavor of high moisture content canned foods seems to help in cats. Dividing the daily food allotment into multiple meals and appropriately timing these meals can influence hunger and the perception of hunger, as well as waste a few calories via the thermic effect of food. Client education and assistance in working through the behavioral problems that may come from food seeking behavior is one of the most important aspects of successful management. We recheck patients every two weeks until adequate rates of weight loss are achieved. Rule out / treat other diseases - Most weight loss failures are not due to concurrent disease, however, it is important to not overlook this possibility. However, the role of insulin resistance and the propensity for lipogenesis is related to the development of obesity and diabetes. Dietary factures that reduce insulin resistance (low carbohydrate foods) are considered beneficial in preventing obesity and treating diabetes. Accurately estimate ideal body weight - Weight and body condition score can be used together to more accurately determine what ideal body weight should be. Most pets with a BCS of 4 are 10 to 20% above their ideal weight. Patients with BCS of 5 are more than 20% above ideal, most will fall in the range of 20 to 40% overweight. Morbidly obese patients can be more than 30% overweight (i.e. greater than 45% body fat). Better estimation of ideal weight helps in setting goals, but more importantly, allows better estimation of energy requirement. Accurately estimate energy requirement - Because most overweight patients are also very inactive, maintenance energy requirements (MER) may be very close to RER (.8 - 1.2 x RER) (16). RER can be calculated using the following formulas: RER = 70 x WtKg0.75. MER is calculated from the RER multiplied and activity factor. This factor is about 1.2 for a normal lean housecats. Restricting 30% for cats results in the following calculations for weight loss, for cats 0.8 x RER. In dogs, the factor for weight loss is 1.0 to 1.2 times RER. These calculations should be considered a starting point and will not work in all animals. If compliance is good but expected results are not achieved, the amount fed should be reduced by 10%/week until a reasonable rate of loss is accomplished. A better approach is to actually determine the individual patient's MER by the use of a food diary and restrict 20%. Clinical strategies for obesity treatment The choices for weight loss include 1) reduction in overall food intake (e.g. psychological counseling, pharmacological therapy, and surgery); 2) caloric control (e.g. reduced calorie foods, fat blockers, and starch blockers) or 3) metabolic control (e.g. exercise, metabolic shift, and/or futile cycling). Of these therapies reduced calorie diets have been the standard to achieve negative energy balance and weight loss in cats. Calorie Control - Reducing caloric intake is the cornerstone of obesity treatment in small animal nutrition. This has been accomplished by using low calorie foods and modification of feeding practices (owner behavior). Traditional weight loss formulas consist of lower fat and calories compared to standard cat foods. Strategies for reducing calories in commercial foods include adding water to canned diets to dilute calories, the addition of insoluble dietary fiber, and lowered fat concentrations. Many weight loss formulas contain between 10-15% dietary fiber. (17) Fiber effectively provides diet bulk, dilutes calories, and promotes a sense of satiety. The effect of fiber on long-term satiety is unknown. Short-term studies have demonstrated reduced food intake and presumed satiety in diets containing 12% (dm) fiber in dogs and cats (Jewell et al., unpublished data on file). Not all cats tolerate fiber-enhanced foods without complication. Increase stool volume, food refusal, constipation, dry skin and unacceptable begging behavior have been associated with weight-reduction foods and protocols. The benefit of typical commercial weight loss diets are the enhanced nutrient supplementation of protein, minerals and vitamins added in amounts that compensate for the reduction in food and caloric intake. A further advantage of weight reducing formulas is the measured volume of food is often similar to the previous diet. This promotes owner compliance by reducing the owner's visual recognition of food restriction. Case examples will be discussed. Low carbohydrate diets and metabolic control New alternatives in feline obesity management have capitalized upon the concept of "metabolic control" of low carbohydrate foods similar to the well known Atkin's Diet (18). By providing foods very low in carbohydrates but surfeit in protein and fat, the metabolic drive shifts from glucose oxidation to fat metabolism as the animal's primary energy source. Low carbohydrate intake results lower plasma glucose concentrations and limited insulin secretion from the pancreas. Purported benefits of a low-carbohydrate and high-protein diet include: appetite control, increased calorie loss via futile cycling and ketone loss, improved insulin sensitivity, and a shift from glucose oxidation and lipogenesis to lipolysis and weight loss (18). Carbohydrates and Metabolic shift - The red blood cell, kidney medulla, and central nervous system all have an absolute requirement for preformed glucose from the blood. The typical feline diet provides abundant glucose to meet essential needs. Once this "essential glucose pool" is filled, excess energy supplied as glucose is readily converted to triglyceride and stored as fat in adypocytes. (Fig. 3). When a high-carbohydrate diet is consumed, blood glucose rises, insulin is increased, lipoprotein lipase activity increases and a greater portion of glucose enters the adipose cells where it is converted to fatty acids and stored as fat. Conversely, when fed a low carbohydrate food, blood glucose and insulin levels are low and storage of fat becomes more difficult. (Fig. 4) This metabolic shift from fat storage (lipogenesis) to fat loss (lipolysis) is due to several alterations in substrate and hormone availability. With low carbohydrate intake, the conversion of glucose to ?-glycerol phosphate (?-GP) in the adipocyte is reduced. As ?-GP is required for triglyceride formation, lipogenesis is limited. More importantly, low insulin concentrations together with relative increases in glucagon increases cAMP in the adipose cells. High intracellular cAMP activates hormone sensitive lipase (HSL), the enzyme responsible for lypolysis. (Fig. 5) Subsequently, within the adypocyte the rate of triglyceride hydrolysis to free fatty acids (FFAs) increases. FFAs are released into blood bound to albumin (Non-esterified fatty acids, NEFA) where they serve as a preferred energy source to other tissues. In the liver, NEFA's readily undergo ?-oxidation and production of ketone bodies. Muscles, heart and to some extent the central nervous system uses ketones and NEFAs in preference to glucose. Simply stated, when lipids and proteins and are consumed in the absence of carbohydrates, insulin levels remain low. The metabolic response is similar to those observed during starvation. High levels of NEFAs and low insulin indicate a starvation state (high glucose and insulin signal a fed state). These signals alter enzyme activities in the intermediary pathways to conserve glucose, limit gluconeogeneis from amino acids (to conserve body proteins) and mobilize fats. Ideally, these diets are moderate to low in fat. The lipotoxicity theory of insulin resistance suggest excess fat, NEFAs and ketones may alter hepatic insulin sensitivity; promoting insulin resistance. This appears to have credence in dogs, but less so in cats. Markers of Metabolic shift (lipogenesis to lipolysis) - The hallmark of effective metabolic shift is increased ketone body (acetoacetate, acetone and ?-hydroxybutyrate, BHBA) production as measured in the blood and urine. Increased fat metabolism in cats favors the production of BHBA and lesser increases in acetoacetate or acetone compared to humans where ketogenesis generates high levels of acetoacetate and acetone. Recall that urine reagent strips designed to detect ketones react only with acetoacetate and acetone (19). Thus, these urine strips are not useful for monitoring benign dietary ketosis in cats, as in people. Only when ketone concentrations are significantly elevated (as with uncontrolled diabetes mellitus) will urine test positive for ketones in the cat. Ketosis that occurs during low carbohydrate feeding is relatively mild compared to ketosis that accompanies uncontrolled diabetes mellitus, pregnancy toxemia of ewes or ketosis of lactating cattle. Levels of BHB increase from approximately 0.1 mmol/L in the fed state to upwards of 3.0 mmol/L when fed a low-carbohydrate food (Schoenherr W, Hill's data on file). At these levels, metabolic complications associated with ketosis are not observed. This is in contrast to diabetes mellitus where BHB levels typically exceed 15 mmol/l and are associated with metabolic acidosis and electrolyte imbalances. Satiety - Higher protein and low carbohydrate intake in helps promote satiety by two proposed mechanisms. 1) Protein and fat stimulate increased release of CCK from the gut. CCK acts peripherally to delay gastric emptying, which can prolong a feeling of fullness. CCK also acts centrally at the hypothalamus, to stimulate satiety (20). 2) Ketosis is known to provide a sense of well-being, as well as stimulate satiety, in humans and animals. Increased CNS concentrations of BHB increase the relative neuronal uptake of glutamate and thereby stimulate production of GABA in the forebrain (21). GABA inhibits eating and promotes a sense of well-being via its modulation of dopamine activity (22). Other studies support a direct satiety effect of BHB mediated via vagal afferent neurons (23). Safety and clinical efficacy - Dietary carbohydrate is not essential in the diet of most animals. Cats, as true carnivores, are particularly adapted to foods high in protein and fat. Thus, a diet void of carbohydrates poses few nutritional dilemmas for the healthy feline. More important considerations are the efficacy of such foods for weight loss and weight management programs. Recent reports in human nutrition have confirmed increased compliance and total weight loss in people using low-carbohydrate diet programs compared to typical food plans promoted by the American Heart Association (24). Food trials in healthy obese cats have demonstrated similar findings. In studies, reported by Schoenherr (Hill's data on file) found that obese cats lost slightly greater fat mass and total body weight when fed a low carbohydrate food compared to standard weight loss formulas. While, studies have demonstrated weight loss in overweight and obese cats with unrestricted feeding (25), our experience indicates food restriction is required in most cats. To date, no detrimental effects were observed upon physical examination, complete blood count or blood chemistry evaluations. As expected, low normal blood glucose concentrations have been consistently observed in cats fed the low carbohydrate foods. Furthermore, behavioral scores, as assessed by animal technicians masked to the food type, were indicative of reduced food seeking activities (Kirk, unpublished data). Is there a best carbohydrate source? In humans, glycemic index (GI) has been used to quantify the impact of certain carbohydrates on glucose availability and relationship to insulin resistance, obesity, and diabetic control. Simple sugars and readily digested starches typically have high GI, while complex carbohydrates like whole grains and vegetables are low GI foods. Data is limited in dogs and cats. Processed rice was found to be high GI in dogs, while corn, barley and sorghum were low. Cats readily digest and absorb carbohydrates in pet foods, approximating 100% digestibility. Utilization is slow due to carnivorous adaptations resulting in low activity of hepatic enzymes that clear large glucose loads and the constant hepatic production of glucose from amino acids. Thus, it appears low levels of carbohydrates are more effective that type of carbohydrate in regulating insulin resistance in cats. Choosing the best weight loss strategy -Clinical studies comparing low carbohydrate and high fiber foods for feline weight loss are limited. While rate of weight loss does not appear to be consistently reduced by low carbohydrate feeding, the proportion of fat loss and lean mass retention is improved in both dogs and cats. (28, 29, 30) Clinical experience and studies in diabetic cats (26,27) support a beneficial effect in >68% of the cats eating commercial low carbohydrate foods, while the other subset appears to respond more favorably to high-fiber low-fat foods. Unfortunately, there are no phenotypic or biochemical markers that indicate which diet would be best suited to an individual cat. The decision to utilize low-carbohydrate strategies vs. high-fiber is currently based upon the clinician's preference, concurrent patient disease, response to previous therapies and patient preference. References
Figure 1: Prevalence of overweight cats among cats without serious illness by age 
From: Scarlett JM, Donoghue S, Saidla J, Wills J. Overweight cats: prevalence and risk factors. Intl J Obesity 1994; 16 (S1):S22-S28. Figure 2: Comparison of energy requirement to calculated requirements in cats 
Figure 3. Nutrient utilization on standard dry feline foods CANNOT DUPLICATE. Figure 4. Nutrient utilization on low-carbohydrate expanded dry foods CANNOT DUPLICATE. Figure 5. The role of insulin and hormone sensitive lipase in lipid metabolism 
Table 1: Body condition scoring using a 5 point scale
Table 2: Relationship of 5 point BCS Scale to approximate body fat and ideal weight
Table 3: Risk Factors Associated with Obesity in Cats
Table 4: Clinical disorders associated with overweight and obesity in Cats (1, 2)
Table 5: Examples of peptides that modulate food intake
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