Feline Obesity: Disease Associations and Management
World Small Animal Veterinary Association World Congress Proceedings, 2011
P. Jane Armstrong, DVM, MS, MBA, DACVIM (SAIM)
University of Minnesota, St. Paul, MN, USA


Concurrent with the epidemic of obesity in humans and pets, there has been a revolution in our understanding of the functions of adipose tissue.1,2 Fat has long been recognized as serving the roles of energy storage, thermal insulation, and structural support for abdominal organs. Fat is now recognized as the most abundant source of hormones in the body, making it the largest endocrine organ. Adipose tissue releases a diverse group of proteins, collectively called adipokines. Adipokines are secreted by adipocytes and by adipose-resident macrophages and fibrocytes. To date, over 100 adipokines have been identified, most of which have increased circulating levels in obese individuals and a very limited number (such as adiponectin and tumor necrosis factor-α) have decreased levels in obesity. They exert their effects in the central nervous system and peripherally in tissues such as skeletal muscle and the liver. Because of changes in adipokine levels, obesity is characterized by chronic, low-grade inflammation.3 Recognizing that adipose tissue is not inert has helped understand the complex relationship between obesity and some of the diseases associated with it.

Assessing Obesity in Cats

Various reports document the prevalence of feline obesity.3 In the USA, 35% of adult cats were overweight (19–29%) or obese (6–8%).4 Of cats aged 10–11 years, 45% were overweight or obese.4 A recent survey in Scotland found an obesity or overweight prevalence of 39%.5

Risk Factors for Obesity in Cats

1.  Genetics: Mixed breed (DSH, DLH, DMH) and Manx cats were found more likely to be obese than most purebred cats.

2.  Gender/neuter status: Male cats are predisposed to being obese. Neutering further increases the risk.

3.  Age: Risk increases with increasing age.

4.  Activity: Reduced activity increases risk for weight gain. This is presumed to be why apartment dwelling is associated with feline obesity.

5.  Food and feeding: Highly palatable foods, high fat foods, free choice feeding, feeding 2 or 3 times a day, and excessive treats have all been associated with obesity.

Disease Associations with Obesity in Cats

Obesity can alternatively be defined as a disease in which excess body fat accumulates such that health may be adversely affected. Obesity has major adverse health implications for cats. Some disease associations with obesity overlap with those documented in dogs and some parallel the health problems observed in humans with metabolic syndrome. In cats, obesity is a strong risk factor for the development of diabetes as it results in insulin resistance and hyperinsulinemia. Other conditions associated with obesity are hepatic lipidosis, lameness, neoplasia, and diseases of the oral cavity, urinary tract, gastrointestinal tract and skin.3,4 Obesity makes clinical procedures, such as collecting blood and urine and placing intravenous catheters, more difficult.

Life expectancy has not been evaluated in cats in relation to body condition. Based on data from multiple other species, however, it is likely that obesity in cats is associated with reduced life expectancy. Descriptive population data show that mean body condition score (BCS) declines in aging cats. It is unknown, however, if this occurs due to disproportionate loss of a segment of the population due to premature death of obese cats, or due to a decline in body condition in geriatric cats due to concurrent disease or other factors.

Obesity Management

Preventing obesity should be a high priority in primary care practice. The BCS and muscle condition score should be assessed at each visit.6 BCS can be used to estimate percent body fat (%BF) based on data that has been collected on colony and pet cats.7,8 As a rule of thumb, %BF increases about 5% for each unit increase on the 9-point BCS scale (10% for each unit change in BCS on a 5-point scale).7,8 A %BF of 20–30% is often considered optimal, but a study in pet cats found the mean %BF of cats with a BCS of 5/9 was 31.2.8 A cat with a BCS of 5/5 or 9/9 will have at least 40% BF, and maybe even considerably higher.

Conventional options for weight management are caloric restriction, exercise and behavioral modification. Feeding a specific measured amount of a food formulated for weight loss remains the mainstay of obesity management in cats. Microsomal triglyceride transfer protein inhibitors, which are an option for weight loss programs in dogs, are neither licensed for, nor safe to use in, cats.

Weight loss diets are protein enhanced not because weight loss is more rapid, but because the amount of lean tissue lost is minimized. Micronutrients are supplemented, relative to energy content, in order to reduce the chance of deficiency states arising during weight loss. Since evidence emerged suggesting that L-carnitine supplementation during weight loss helps maintain lean body mass in cats9, many weight loss diets are formulated with an enhanced L-carnitine level.

Human studies have shown that absorption of macronutrients is lower after consumption of high-protein foods than after consumption of foods with high-carbohydrate or high-fat content. Supplementing dietary protein appears to improve satiety in dogs (but not cats). In cats, given that protein content is a major determinant of palatability and voluntary food intake, the best effect on satiety occurs with fiber supplementation and modest increase in protein content.10 High protein diets allow a higher energy intake during weight loss in cats, reducing the intensity of energy restriction.11 Protein intake also seemed to have a longer-term effect such that weight maintenance required more energy than when a lower protein diet was fed.11 This longer-term effect is particularly desirable as resting metabolic rate, and therefore caloric needs, are typically lower after weight loss than would be predicted. One report showed energy intake of 50–55 kcal/kg body weight in cats at stable, obese weights and just under 25 kcal/kg in the same cats at stable, lean weights.12

Selection of a weight loss diet with a protein level of 40–60% dry matter (10–18 g/kcal) and a fat level of 8–20% dry matter (2.5–5.0 g/100 kcal) is recommended.12 For weight loss, the cat can be fed 80% of current caloric intake based on a 3-day food diary. Alternatively, weight loss occurs when cats are fed 50–75% of maintenance energy requirements (MER) at ideal body weight. Several formulas can be used to calculate MER.13,14 One formula is MER = 85 x(BWkg)0.75 Start by feeding 75% of ideal weight MER13 for two weeks. Further energy restriction to between 45–60% of the MER of the target body weight is usually needed to achieve optimal weight loss. Weight loss of about 1% per week will limit loss of lean tissue to about 10%.15

Three dietary strategies were evaluated in a recent study: a novel dry high fiber ration in pre-measured pouches, ready-prepared portions of dry and moist food, and a commercial dry high fiber food fed with a measuring cup.10 Mean weight loss did not differ over 20 weeks of study, but owners' subjective score of their cat's hunger was highest with the last strategy. Owner satisfaction was lowest with this strategy, with more owners regarding food allowance as insufficient.10

Concurrent with energy restriction, the owner should be encouraged to increase the level of their cat's activity in gradual steps and make it a regular feature of the cat's life. Some successful methods are increasing play behavior, encouraging the cat to exercise itself (e.g., a cat tree) and increasing activity by using food treats (e.g., hollow toys that contain small amounts of kibbles). Most owners appreciate a treat allowance of 20–25 kcal/day.


1.  Radin MJ, et al. Adipokines: a review of biological and analytical principles and an update in dogs, cats, and horses. Vet Clin Pathol 2009;38:136–156.

2.  Lusby Al, et al. 2009. The role of adipokines in obesity and insulin resistance in cats. J Am Vet Med Assoc 235,518–522.

3.  German AJ, et al. Obesity, its associated disorders and the role of inflammatory cytokines in companion animals. Vet J 2010;185:4–9.

4.  Lund EM, et al. Prevalence and risk factors for obesity in adult cats from private US veterinary practices. Int J Res Vet Med 2005;3:88–96.

5.  Courcier EA, et al. Prevalence and risk factors for feline obesity in a fist opinion practice in Glasgow, Scotland. J Feline Med Surg 2010;12:746–753.

6.  Fleeman L, et al. WSAVA nutritional assessment guidelines. J Feline Med Surg 2011;13:516–525.

7.  Laflamme DP. Development and validation of a body condition scoring tool for cats: a clinical tool. Feline Pract 1997;25:13–18.

8.  Bjørnvad CR, et al. Evaluation of a 9-point body condition scoring system in physically inactive pet cats. Am J Vet Res 2011;72:433–437.

9.  Center SA, et al. Influence of L-carnitine on metabolic rate, fatty acid oxidation, body condition, and weight loss in obese cats. Abstract, Annual ACVIM Forum. 2007.

10. Bissot T, et al. Novel dietary strategies can improve the outcome of weight loss programmes in obese client-owned cats. J Feline Med Surg 2010;12:104–112.

11. Vasconcellos RS, et al. Protein intake during weight loss influences the energy required for weight loss and maintenance in cats. J Nutr 2009;139:855–860.

12. Hoenig M, et al. Insulin sensitivity, fat distribution, and adipocytokine response to different diets in lean and obese cats before and after weight loss. Am J Physiol Regul Integr Comp Physiol 2007;191:R227–R234.

13. Remillard R. Overweightedness/obesity–feline. In: Nestle Purina PetCare Handbook of Canine and Feline Clinical Nutrition. Nestle Purina PetCare Company, St Louis, MO. 2010:36–37.

14. Toll PW, Yamka RM, Schoenherr WD, Hand MS. Obesity. In: Small Animal Clinical Nutrition, 5th ed. Hand MS et al (eds). Mark Morris Institute, Topeka KS. 2010:501–540.

15. Butterwick RF, et al. The effect of different levels of energy restriction on body weight and composition in obese cats. J Vet Intern Med 1995;9:138–142.


Speaker Information
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P. Jane Armstrong, DVM, MS, MBA, DACVIM (SAIM)
University of Minnesota
St. Paul, MN, USA

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