![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Department of Veterinary Clinical Sciences, University of Liverpool, Small Animal Hospital, Liverpool, L7 7EX, UK
4 To whom correspondence should be addressed. E-mail: ajgerman{at}liv.ac.uk.
 |
ABSTRACT |
|---|
 TOP ABSTRACT LITERATURE CITED |
|---|
KEY WORDS: • overweight • nutrition • canine • feline • adipose tissue
Obesity is defined as an accumulation of excessive amounts of adipose tissue in the body (1). In humans, the application of this definition is based upon epidemiologic data, which demonstrate increased morbidity and mortality risk with increasing body fat mass. Criteria have been established for what constitutes "overweight" and what constitutes "obesity"; such criteria are usually based on measures of adiposity such as the BMI [weight (kg) divided by height2 (m)]; Caucasians, for example, are defined as overweight when BMI is >25 kg/m2, and obese when BMI exceeds 30. In contrast, one report classified cats and dogs as overweight when their body weight is >15% above their "optimal body weight," and as obese when their body weight exceeds 30% of optimal (1). However, these criteria have not been confirmed with rigorous epidemiologic studies, and limited data exist on the nature of an optimal body weight.
Obesity is an escalating global problem in humans (2), and current estimates suggest that almost two-thirds of adults in the United States are overweight or obese (3). Studies from various parts of the world have estimated the incidence of obesity in the dog population to be between 22 and 40% (4). The most recently published data come from a large study in Australia in which 33.5% of dogs were classed as overweight, whereas 7.6% were judged to be obese (4). The incidence of feline obesity is similar (1,5,6). Most investigators agree that, as in humans, the incidence in the pet population is increasing.
Measurement of obesity in companion animals
All measures of adiposity involve defining body composition, or the "relative amounts of the various biological components of the body." The main conceptual division of importance is between fat mass (FM,5 the triglyceride component in adipose tissue) and lean body mass (LBM) (7). Various techniques are available to measure body composition (Table 1), and these differ in applicability to research, referral veterinary practice, and first-opinion practice. Whatever method is used, investigators should be aware of both its precision and accuracy. The accuracy of a test is defined as the closeness with which a measurement of the variable represents its true value, whereas precision is the ability to yield the same estimated result on repeated analysis (irrespective of accuracy). Ideally, a test that is both accurate and precise should be used; however, many tests for body composition are precise but not accurate, whereas some lack both precision and accuracy. Other important aspects of a test are cost, ease of use, acceptance by veterinarians and clients, and invasiveness. Currently, there is no method that cannot be criticized; therefore, the perfect tool for analysis does not yet exist.
|
Morphometry. This is defined as the measurement of "form"; in relation to body composition analysis, it refers to a variety of measured parameters that are used to estimate body composition. The 3 main approaches are measurement of skinfold thickness, dimensional evaluations (in which various measures of stature are combined with weight), and body condition scores.
Dimensional evaluations.
Such evaluations are usually performed by tape measure, and a number were reported in dogs and cats. Measurements of "length" (e.g., head, thorax, and limb) are correlated with lean body components (8), whereas measurements of girth were shown to correlate with both LBM (8) and FM (9). Segmental limb measures and (likely) truncal length are thought to be better measures of stature and thus correlate best with LBM. By combining >1 measure (usually 1 that correlates with FM, and 1 correlating with LBM), equations can be generated to predict different body components. The best example of such a measure is the feline BMI (9), where:
 |
Here, the ribcage measurement is the circumference measured at the 9th rib, and LIM stands for the "limb index measurement," which is the distance between the patella and calcaneus of the left hindlimb. All measurements are made in centimeters, and measurements are made with the cat in a standing position, with the legs perpendicular to the ground and the head upright.
Such techniques do provide a more objective measure of body composition than body condition scoring (see below), but problems exist when similar schemes are extrapolated to the many breeds of dog. Despite this, a BMI has been suggested for dogs (10).
Body condition scoring. This is a subjective, semiquantitative method of evaluating body composition. A number of schemes were devised, with a 9-point scheme being the most widely accepted (11,12). All systems assess visual and palpable characteristics that correlate subcutaneous fat, abdominal fat, and superficial musculature (e.g., ribcage, dorsal spinous processes, and waist). A new 7-point algorithm-based approach, specifically designed to be used by owners to assess their own pets, was developed recently. A recent study demonstrated good correlation between the system and body fat measurements made by DXA and excellent agreement among experienced operators (13). Most importantly, good agreement was found between measurements by the experienced operators and the owners, suggesting that the method is reliable when used without prior training.
Causes of obesity
Although some diseases (e.g., hypothyroidism and hyperadrenocortism in dogs), pharmaceuticals (e.g., drug-induced polyphagia caused by glucocorticoids and anticonvulsant drugs), and rare genetic defects (in humans) can cause obesity, the main reason for the development of obesity is having a positive mismatch between energy intake and energy expenditure. Therefore, either excessive dietary intake or inadequate energy utilization can lead to a state of positive energy balance; numerous factors may be involved, including genetics, the amount of physical activity, and the energy content of the diet (1).
The effect of genetics is illustrated by recognized breed associations in both dogs (e.g., Labrador Retriever, Cairn Terrier, Cavalier King Charles Spaniel, Scottish Terrier, Cocker Spaniel) and cats (e.g., Domestic Shorthair) (14,15).
Neutering is an important risk factor for obesity in both species; many studies suggested that this is due to a decrease in metabolic rate after neutering (16–19). However, increased FM is usually present in neutered animals; when energy expenditure is expressed on a lean mass basis, no difference in metabolic rate is noted between neutered and entire individuals (20–23). Alternative explanations for the effect of neutering on obesity is an alteration in feeding behavior leading to increased food intake (17,18,21–25), and decreased activity without a corresponding decrease in energy intake (26,27). Gender itself is also a predisposing factor in some canine studies, with females overrepresented (14,28). Other recognized associations in dogs include indoor lifestyle and middle age (4,14,15). In cats, middle age and apartment dwelling are possible risk factors (6).
Dietary factors can also lead to the development of obesity in both species. For instance, obesity in dogs is associated with the number of meals and snacks fed, the feeding of table scraps, and the dog's presence when its owners prepared or ate their own meal (29). Interestingly, the type of diet fed (prepared pet food vs. homemade) does not appear to predispose to obesity (14,15,29). However, the price of the pet food does have a notable effect, i.e., obese dogs are more likely to have been fed inexpensive rather than more expensive foods. Further, obese cats more commonly have a free choice of food intake (30).
Behavioral factors also play a part in the development of obesity. For cats, possible factors involved in the development of obesity include anxiety, depression, failure to establish a normal feeding behavior, and failure to develop control of satiety (31). The human-animal relationship is also of importance and was shown to be more intense in the owners of obese cats (30). Further, misinterpretation of feline behavior on the part of the owner is also of importance; in this regard, many owners misread signals about the behavior of their cat associated wth eating. In contrast to humans and dogs for whom eating is a social function, cats do not have any inherent need for social interaction during feeding times. When the cat initiates contact, owners often assume that they are hungry and are asking for food when they are not (31). Nevertheless, if food is provided at such times, the cat soon learns that initiating contact results in a food reward. For dogs, owner factors that are of importance include the duration that the owner observed the dog eating (more likely to be longer in obese dogs), interest in pet nutrition, obesity of the owner, health consciousness of the owner (both for their pet and themselves), and lower income (29).
The pathological importance of obesity
In humans, obesity is important because it increases mortality risk and can predispose to a variety of diseases. Obese humans, on average, do not live as long, and are more likely to suffer from diseases such as type II diabetes mellitus (DM), hypertension, coronary heart disease, certain cancers (e.g., breast, ovarian, prostate), osteoarthritis, respiratory disease, and reproductive disorders. Similarly, obesity has detrimental effects on the health and longevity of dogs and cats (Table 2), although data are more limited. Problems to which obese companion animals may be predisposed include orthopedic disease, DM, abnormalities in circulating lipid profiles, cardiorespiratory disease, urinary disorders, reproductive disorders, neoplasia (mammary tumors, transitional cell carcinoma), dermatological diseases, and anesthetic complications. Human obesity is associated with an increased risk of type II DM, cancer, cardiac disease, hypertension, and decreased longevity (32). Some studies do suggest an increase in morbidity in sick patients with poorer body condition (33,34).
|
Longevity. Dietary restriction can increase longevity in other species (37–39), and a recent prospective study confirmed a similar effect in dogs (40–45). Labrador retrievers (24 pairs, 48 in total) participated in the study, and 1 dog in each pair was randomly assigned to 1 of 2 groups (43). The dogs in one group consumed food ad libitum, whereas the dogs in the other group were fed 75% of the amount consumed by their counterparts. In the energy-restricted group, the body condition score was closer to "optimal" (e.g., group mean 4.5/9) than in the ad libitum feeding group (e.g., group mean 6.8/9). Although causes of death did not differ between the 2 groups, the lifespan was increased in the energy-restricted group (e.g., median 13 y with energy restriction vs. 11.2 y with ad libitum consumption) (45). Additional beneficial effects of feed restriction (and thus maintenance of body condition) included a reduced risk of hip dysplasia and osteoarthritis, and improved glucose tolerance (40–45).
Diseases associated with obesity
Endocrine and metabolic diseases. Hormonal diseases with a reported association with obesity include DM, hypothyroidism, hyperadrenocorticism, and insulinoma (1). Some conditions predispose to obesity, whereas others arise more commonly in animals that are obese. Acromegaly can lead to a generalized increase in tissue mass, and is thus a differential diagnosis for obesity. However, in this condition, lean tissue and bone mineral are likely to be deposited in addition to adipose tissue.
Insulin resistance, DM, and the metabolic syndrome Insulin secreted by pancreatic ß cells controls the uptake and use of glucose in peripheral tissues. In humans, tissues become less sensitive to insulin (i.e., become "insulin resistant") with excessive energy intake (46), and plasma concentrations of insulin increase in direct proportion to increasing BMI in both men and women (47). Thus, obesity, particularly abdominal obesity, is a major determinant of insulin resistance and hyperinsulinemia (48). Cats most often suffer from DM, which resembles "type II" DM in humans; therefore, obesity is a major risk factor in this species (49). Indeed, it was proven experimentally that diabetic cats have significantly lower sensitivity to insulin than cats without DM (50). In contrast, dogs more commonly suffer from DM resembling human type I DM. Obesity causes insulin resistance (45), and obesity is a risk factor for DM in this species (51). However, because type II DM is uncommon in dogs, obesity rarely leads to overt clinical signs of DM (52).
In humans, the metabolic syndrome was originally termed "syndrome of insulin resistance"; in fact, it is a group of risk factors associated with both insulin resistance and cardiovascular disease (53). The main characteristics of metabolic syndrome are as follows: 1) fasting plasma glucose > 110 mg/dL (6.10 mmol/L); 2) visceral obesity (e.g., waist circumference > 90 cm in women and > 102 cm in men; 3) Hypertension e.g., blood pressure > 130/85 mm Hg; and 4) low concentrations of HDL cholesterol (HDL-C; <40 mg/dL in men, < 50 mg/dL in women).
Additional features may include systemic inflammation, prothrombotic state, and increased oxidant stress (54). Further, in 
20% of cases of metabolic syndrome, there is concurrent pancreatic ß-cell dysfunction leading to DM (53). Some of these criteria were applied to dogs, and this species is often used as a model for human metabolic syndrome (55).
Hypothyroidism and thyroid function Although hypothyroidism is commonly cited as an underlying cause for obesity, such cases are the exception rather than the rule. The prevalence of hypothyroidism in dogs is estimated at 0.2%, with less than half of these dogs reported to be obese (56). In contrast, the proportion of dogs that are obese is much greater (25–40%) (4). Hypothyroidism is extremely rare in cats. Thus, although hypothyroidism should always be considered, it is rarely the reason for obesity. Obesity itself has a subtle, but likely clinically insignificant effect on thyroid function (57); obese dogs had higher concentrations of both total thyroxine (T4) and total triiodothyronine (T3) than nonobese controls, although such concentrations remained within the reference range and other parameters [e.g., free T4, canine thyroid-stimulating hormone (cTSH), TSH stimulation test] did not differ. Further, weight loss caused significant decreases in total T3 and cTSH. Thus, although obesity and subsequent weight restriction may have some effects on energy balance and thyroid homeostasis, such changes are unlikely to affect the interpretation of thyroid function tests.
Hyperlipidemia and dyslipidemia. Limited data exist for dogs with naturally occurring obesity, and most information was derived from experimental studies. Published data suggest that lipid alterations can occur in obese dogs, with increases in cholesterol, triglycerides, and phospholipids all noted, albeit often not exceeding the upper limit of the reference range (58–60). Making laboratory dogs obese by feeding a hyperenergetic diet was shown to increase plasma nonesterified fatty acid and triglyceride concentrations by increasing concentrations of VLDL and HDL, while decreasing those of HDL-C (59). Such changes were associated with insulin resistance and, interestingly, were also described in insulin-resistant humans. Whether lipid alterations account for the increased incidence of pancreatitis in obese dogs requires further studies (61). Thus, additional work is warranted to assess further the significance of lipid abnormalities in dogs.
Orthopedic disorders. Obesity is a major risk factor for orthopedic diseases in companion animals, especially dogs. An increased incidence of both traumatic and degenerative orthopedic disorders was reported (14,62). One study reported body weight to be a predisposing factor in humeral condylar fractures, cranial cruciate ligament rupture, and intervertebral disc disease in cocker spaniels (63). A recent study in boxers reported a link between neutering and hip dysplasia (64); although the effect of obesity was not assessed directly in that study, this association was attributed to an increased incidence of obesity in neutered dogs. Further, a number of studies highlighted the association between obesity and the development of osteoarthritis (41,42), whereas weight reduction can lead to a substantial improvement in the degree of lameness in dogs with hip osteoarthritis (65).
Cardiorespiratory disease and hypertension. Obesity can have a profound effect on respiratory system function. Most notably, obesity is an important risk factor for the development of tracheal collapse in small dogs (66). Obesity can exacerbate heatstroke in dogs; other respiratory diseases that can be exacerbated by obesity include laryngeal paralysis and brachycephalic airway obstruction syndrome. Obesity can also affect cardiac function; increased body weight can result in effects on cardiac rhythm and increased left ventricular volume, blood pressure, and plasma volume. The effect of obesity on hypertension is controversial in dogs. One study suggested that obesity was significantly associated with hypertension, but its effect was only minor (67). In contrast, many experimental studies utilized the obese dog as a model for the pathogenesis of hypertension and insulin resistance (68). Obesity may also be associated with portal vein thrombosis (69) and myocardial hypoxia (70).
Urinary tract and reproductive disorders. There is evidence from experimental dogs that the onset of obesity is associated with histologic changes in the kidney, most notably an increase in Bowman's space (as a result of expansion of the Bowman's capsule), increased mesangial matrix, thickening of glomerular and tubular basement membranes, and an increased number of dividing cells per glomerulus (71). Functional changes were noted in the same study and included increases in plasma renin concentrations, insulin concentrations, mean arterial pressure, and plasma renal flow. As a consequence, the authors speculated that these changes, if prolonged, could predispose to more severe glomerular and renal injury. An association between obesity and some cases of urethral sphincter mechanism incompetence (USMI) was reported. Obesity is not the only risk factor, with ovariohysterectomy (and consequent lack of sex hormones) itself also playing a major role. Nevertheless, the effect of obesity is clear in some dogs that become incontinent only when they become obese. Further, weight reduction in overweight dogs with USMI can often be all that is required for continence to be restored. The mechanisms that predispose obese animals to USMI are not known, although it was suggested that the effect is purely mechanical, e.g., increased retroperitoneal fat leading to caudal displacement of the bladder (72). The risk of developing calcium oxalate urolithiasis is also reported to be increased in obese dogs (73). Finally, obese animals are reported to suffer from an increased risk of dystocia, likely related to excess adipose tissue in and around the birth canal (14,74,75).
Neoplasia. In humans, obesity predisposes to a number of different types of cancer; the International Agency for Research on Cancer found a significant link between obesity and cancers of the female breast (postmenopausal), colon/rectum, kidney (renal cell), and esophagus (47). It is estimated that, if this link is entirely causal, 1 in 7 cancer deaths in both men and women in the United States might be the direct result of being overweight or obese (47). Breast cancer is the most common form of cancer among women (76), and obesity was shown consistently to increase rates of breast cancer in postmenopausal women by 30–50% (48). An association between mammary carcinoma and obesity was also reported in some (74) but not all (77,78) canine reports. Overweight dogs were also reported to have an increased risk of developing transitional cell carcinoma of the bladder (79).
Miscellaneous disorders. Obese animals were reported to be at increased risk of certain dermatologic disorders. Diffuse scale is commonly observed (especially in cats), most likely due to a reduced ability to groom efficiently. Animals that are severely obese can develop pressure sores. Decreased immune function has also been documented, with obese dogs showing less resistance to the development of infections (80,81).
Treatment of obesity
In humans, current therapeutic options for obesity include dietary management, exercise, psychological and behavioral modification, drug therapy, and surgery. Many of these options are available for companion animals, although it is not ethically justifiable to consider surgical approaches. Further, to date, there are no pharmaceutical compounds licensed for weight loss in dogs and cats. Dietary therapy forms the cornerstone to weight management in dogs and cats, but increasing exercise and behavioral management comprise useful adjuncts.
Dietary management. It is recommended that the weight reduction protocol be tailored toward the individual patient. Although total energy restriction (starvation) successfully leads to weight loss, it has the disadvantages of causing excessive protein (and thus lean body mass) loss and requiring hospitalization for proper monitoring (1). Therefore, it is preferable to use purpose-formulated weight reduction diets, which generally are restricted in fat and energy, while being supplemented in protein and micronutrients. Protein supplementation is important because the amount of lean tissue lost is minimized even though the weight loss is not more rapid (82,83). Supplementation of micronutrients ensures that deficiency states do not arise (84,85).
Additional dietary factors that may be of benefit for weight loss include L-carnitine supplementation (to maintain lean mass), conjugated linoleic acid (CLA), and the use of high-fiber diets (to provide satiety).
L-Carnitine is an amino acid that is synthesized de novo in the liver and kidneys from lysine and methionine in the presence of ascorbate. Dietary supplementation of L-carnitine improves nitrogen retention, increasing lean mass and reducing fat mass (86). Incorporation of L-carnitine at a level of 50–300 ppm, in weight reduction diets, was shown to reduce lean tissue loss during weight loss (86,87). Possible mechanisms for this protective effect on lean tissue include enhancing fatty acid oxidation and energy availability for protein synthesis during times of need.
CLA is a family of fatty acid isomers derived from linoleic acid. Various studies in experimental animals suggested that it has an antiadipogenic effect; proposed mechanisms include inhibition of stearoyl-CoA desaturase activity, which limits the synthesis of monounsaturated fatty acids for triglyceride synthesis, and suppression of elongation and desaturation of fatty acids into long-chain fatty acids (86). At present, data on the use of CLA as an antiobesity agent in humans and cats are conflicting, with the most recent data suggesting the lack of a significant effect (88,89). Therefore, more information is required before its use can be recommended. There is also controversy concerning the effect of fiber satiety; some reports suggested that feeding up to 12–16% of dry matter as dietary fiber has no effect (90–92), whereas other work demonstrated appetite suppression when 21% of the diet was consumed as dietary fiber (93).
Lifestyle management. Increasing physical activity is a useful adjunct to dietary therapy; when used in combination with dietary therapy, it promotes fat loss (94) and may assist in lean tissue preservation (95). There is also some evidence that exercise may help prevent the rapid regain in weight that can occur after successful weight loss (94). The exact program must be tailored to the individual and take into account any concurrent medical concerns. Suitable exercise strategies in dogs include lead walking, swimming, hydrotherapy, and treadmills. Exercise in cats can be encouraged by increasing play activity, using cat toys (e.g., fishing rod toys), motorized units, and feeding toys. Cats can also be encouraged to "work" for their food by moving the food bowl between rooms before feeding, or by the use of feeding toys.
Monitoring of weight loss. In addition to the above strategies, it is essential that the whole weight reduction regimen be supervised. This is labor intensive, requires some degree of expertise and training in owner counseling, and often requires a dedicated member of staff. Nevertheless, in the author's opinion, correct monitoring is the single most important component of the weight loss strategy. A recent study demonstrated that weight loss is more successful if an organized strategy is followed with regular weigh-in sessions (96). It is essential to continue to monitor body weight after the ideal weight has been achieved to ensure that weight that was lost is not regained; as with humans, a rebound effect was demonstrated after weight loss in dogs (97).
Summary
Obesity is a growing concern in companion animals, and the increasing incidence appears to be mirroring the trend observed in humans. The main medical concern of obesity relates to the many disease associations that accompany the adiposity. There is a need to increase awareness within the veterinary profession that obesity in companion animals is a serious medical concern.
|
ACKNOWLEDGMENTS |
|---|
|
FOOTNOTES |
|---|
2 Author disclosure: Expenses for the author to travel to the symposium and honoraria were paid by WALTHAM.
3 Supported by grants from the Waltham Centre for Pet Nutrition, Royal Canin, and BBSRC. A.J. German's lectureship is currently funded by Royal Canin.
5 Abbreviations used: CLA; conjugated linoleic acid; cTSH, canine thyroid-stimulating hormone; DM, diabetes mellitus; DXA, dual-energy X-ray absorptiometry; FM, fat mass; HDL-C, HDL cholesterol; LBM, lean body mass; LIM, limb index measurement; T3, triiodothyronine; T4, thyroxine; USMI, urethral sphincter mechanism incompetence.
|
LITERATURE CITED |
|---|
|
TOPABSTRACTLITERATURE CITED |
|---|
1. Burkholder WJ, Toll PW. Obesity. In: Hand MS, Thatcher CD, Reimillard RL, Roudebush P, Morris ML, Novotny BJ, editors. Small animal clinical nutrition, 4th edition. Topeka, KS: Mark Morris Institute. 2000; p. 401–30.
2. Kopelman PG. Obesity as a medical problem. Nature. 2000;404:635–43.[Medline]
3. Flegal KM, Carroll MD, Ogden CL, Johnson CL. Prevalence and trends in obesity among US adults, 1999–2000. J Am Med Assoc. 2002:288:1723–1727.
4. McGreevy PD, Thomson PC, Pride C, Fawcett A, Grassi T, Jones B. Prevalence of obesity in dogs examined by Australian veterinary practices and the risk factors involved. Vet Rec. 2005;156:695–707.[Abstract]
5. Armstrong PJ, Lund EM. Changes in body composition and energy balance with aging. Vet Clin Nutr. 1996;3:83–7.
6. Scarlett JM, Donoghue S, Saidla J, Wills J. Overweight cats: prevalence and risk factors. Int J Obes Relat Metab Disord. 1994;18:S22–8.
7. Burkholder WJ. Precision and practicality of methods assessing body composition of dogs and cats. Comp Cont Educ Pract. 2001;23:1–10.
8. Stanton CA, Hama DW, Johnson DE, Fettman MJ. Bioelectrical impedance and zoometry for body composition analysis in domestic cats. Am J Vet Res. 1992;53:251–7.[Medline]
9. Hawthorne A, Butterwick RB. Predicting the body composition of cats: development of a zoometric measurement for estimation of percentage body fat in cats [abstract]. J Vet Intern Med. 2000;14:365.
10. Pendergrass PB, Bartley CM, Nagy F, Ream LJ, Stuhlman R. A rapid method for determining normal weights of medium-to-large mongrel dogs. J Small Anim Pract. 1983;24:269–76.
11. Laflamme DP. Development and validation of a body condition score system for dogs. Canine Pract. 1997;22:10–5.
12. Laflamme DP. Development and validation of a body condition score system for cats: a clinical tool. Feline Pract. 1997:25:13–18.
13. German AJ, Holden SL, Moxham G, Holmes K, Hackett R, Rawlings J. A simple, reliable tool for owners to assess the body condition of their dog or cat. J Nutr. 2006:136:2031S–3S.
14. Edney AT, Smith PM. Study of obesity in dogs visiting veterinary practices in the United Kingdom. Vet Rec. 1986;118:391–6.[Abstract]
15. Mason E. Obesity in pet dogs. Vet Rec. 1970;86:612–6.[Medline]
16. Root MV, Johnston SD, Olson PN. Effect of prepuberal and postpuberal gonadectomy on heat production measured by indirect calorimetry in male and female domestic cats. Am J Vet Res. 1996;57:371–4.[Medline]
17. Harper EJ, Stack DM, Watson TDG, Moxham G. Effect of feeding regimens on body weight, composition and condition score in cats following ovariohysterectomy. J Small Anim Pract. 2001;42:433–8.[Medline]
18. Flynn MF, Hardie EM, Armstrong PJ. Effect of ovariohysterectomy on maintenance energy requirements in cats. J Am Vet Med Assoc. 1996;209:1572–81.[Medline]
19. Hoenig M, Ferguson DC. Effects of neutering on hormonal concentrations and energy requirements in cats. Am J Vet Med Res. 2002;63:634–9.
20. Fettman MJ, Stanton CA, Banks LL. Effects of neutering on body weight, metabolic rate and glucose tolerance in domestic cats. Res Vet Sci. 1997;62:131–6.[Medline]
21. Kanchuk ML, Backus RC, Calvert CC, Morris JG, Rogers QR. Weight gain in gonadectomized normal and lipoprotein lipase-deficient male domestic cats results from increased food intake and not decreased energy expenditure. J Nutr. 2003;133:1866–74.
22. Martin L, Siliart B, Dumon H, Backus R, Biourge V, Nguyen P. Leptin, body fat content and energy expenditure in intact and gonadectomized adult cats: a preliminary study. J Anim Physiol Anim Nutr (Berl). 2001;85:195–9.[Medline]
23. Nguyen PG, Dumon HJ, Siliart BS, Backus R, Biourge V. Effects of dietary fat and energy on body weight and composition after gonadectomy in cats. Am J Vet Res. 2004;65:1708–13.[Medline]
24. Goggin JM, Schryver HF, Hintz HF. The effect of ad libitum feeding and caloric dilution on the domestic cat's ability to maintain energy balance. Feline Pract. 1993:21:7–11.
25. Houpt KA, Hintz HF. Obesity in dogs. Canine Pract. 1978;5:54–8.
26. Hart BL, Barrett RE. Effects of castration on fighting, roaming and urine spraying in adult male cats. J Am Vet Med Assoc. 1973;163:290–2.[Medline]
27. Houpt KA, Coren B, Hintz HF, Hildernrandt JE. Effect of sex and reproductive status on sucrose preference, food intake, and body weight of dogs. J Am Vet Med Assoc. 1979;174:1083–5.[Medline]
28. Krook L, Larsson S, Rooney JR. The interrelationship of diabetes mellitus, obesity, and pyometra in the dog. Am J Vet Res. 1960;21:120–4.[Medline]
29. Kienzle E, Bergler R, Mandernach A. Comparison of the feeding behaviour of the man-animal relationship in owners of normal and obese dogs. J Nutr. 1998;128:2779S–82.
30. Kienzle E, Berger R, Ziegler D, Unshelm J. The human-animal relationship and overfeeding in cats [abstract]. Compendium on Continuing Education for the Practicing Veterinarian. 2000;23:73.
31. Heath S. Behaviour problems and welfare. In: Rochlitz I, editor. The welfare of cats. Animal welfare, Vol. 3. London: Springer, 2005; p. 91–118.
32. Kolonin MG, Saha PK, Chan L, Pasquani R, Arap W. Reversal of obesity by targeted ablation of adipose tissue. Nat Med. 2004;10:625–32.[Medline]
33. Doria-Rose VP, Scarlett JM. Mortality rates and causes of death among emaciated cats. J Am Vet Med Assoc. 2000;216:347–51.[Medline]
34. Scarlett JM, Donoghue S. Associations between body condition and disease in cats. J Am Vet Med Assoc. 1998;212:1725–31.[Medline]
35. Clutton RE. The medical implications of canine obesity and their relevance to anaesthesia. Br Vet J. 1988;144:21–8.[Medline]
36. Van Goethem BE, Rosenweldt KW. Kirpensteijn J. Monopolar versus bipolar electrocoagulation in canine laparoscopic ovariectomy: a nonrandomized prospective, clinical trial. Vet Surg. 2003;32:464–70.[Medline]
37. Weindruch R, Walford RL. The retardation of aging and disease by dietary restriction. Springfield (IL): Charles C. Thomas Publishers; 1988.
38. McCay CM, Crowell MF, Maynard LA. The effect of retarded growth upon the length of life span and upon the ultimate body size. J Nutr. 1935;10:63–79.
39. Lane MA, Black A, Ingram DK, Roth GS. Calorie restriction in non-human primates: implications for age-related disease risk. Anti-Aging Med. 1998;1:315–26.
40. Kealy RD, Olsson SE, Monti KL, Lawler DF, Biery DN, Helms RW, Lust G, Smith GK.. Effects of limited food consumption on the incidence of hip dysplasia in growing dogs. J Am Vet Med Assoc. 1992;201:857–63.[Medline]
41. Kealy RD, Lawler DF, Ballam JM, Lust G, Smith GK, Biery DN, Olsson SE. Five-year longitudinal study on limited food consumption and development of osteoarthritis in coxofemoral joints of dogs. J Am Vet Med Assoc. 1997;210:222–5.[Medline]
42. Kealy RD, Lawler DF, Ballam JM, Lust G, Biery DN, Smith GK, Mantz SL. Evaluation of the effect of limited food consumption on radiographic evidence of osteoarthritis in dogs. J Am Vet Med Assoc. 2000;217:1678–80.[Medline]
43. Kealy RD, Lawler DF, Ballam JM, Mantz SL, Biery DN, Greeley EH, Lust G, Segre M, Smith GK, Stowe HD. Effects of diet restriction on life span and age-related changes in dogs. J Am Vet Med Assoc. 2002;220:1315–20.[Medline]
44. Larson BT, Lawler DF, Spitznagel EL, Kealy RD. Improved glucose tolerance with lifetime restriction favorably affects disease and survival in dogs. J Nutr. 2003;133:2887–92.
45. Lawler DF, Evans RH, Larson BT, Spitznagel EL, Ellersieck MR, Kealy RD. Influence of lifetime food restriction on causes, time, and predictors of death in dogs. J Am Vet Med Assoc. 2005;226:225–31.[Medline]
46. Pittas AG, Joseph NA, Greenberg AS. Adipocytokines and insulin resistance. J Clin Endocrinol Metab. 2004;89:447–52.
47. Calle EE. Thun MJ Obesity and cancer. Oncogene. 2004;23:6365–78.[Medline]
48. Arner P. The adipocyte in insulin resistance: key molecules and the impact of the thiazolidinediones. Trends Endocrinol Metab. 2003;14:137–45.[Medline]
49. Nelson RW, Himsel CA, Feldman EC, Bottoms GD. Glucose tolerance and insulin response in normal weight and obese cats. Am J Vet Res. 1990;51:1357–62.[Medline]
50. Feldhahn JR, Rand JS, Martin G. Insulin sensitivity in normal and diabetic cats. J Feline Med Surg. 1999;1:107–15.[Medline]
51. Klinkenberg H, Sallander MH, Hedhammar Å, Feeding, exercise, and weight identified as risk factors in canine diabetes mellitus. J. Nutr. 2006;136:1985S–8S.
52. Rand JS, Fleeman LM, Farrow HA. Canine and feline diabetes mellitus: nature or nurture? J Nutr. 2004;134:2072S–80.
53. Vega GL. Obesity and the metabolic syndrome. Minerva Endocrinol. 2004;29:47–54.[Medline]
54. Hawkins MA. Markers of increased cardiovascular risk: are we measuring the most appropriate parameters? Obes Res. 2004;12:107S–14S.[Medline]
55. Kim SP, Ellmerer M, Van Citters GW, Bergman RN. Primacy of hepatic insulin resistance in the development of the metabolic syndrome induced by an isocaloric moderate-fat diet in the dog. Diabetes. 2003;52:2453–60.
56. Scott-Moncrief JCR, Guptill-Yoran L. Hypothyroidism. In: Ettinger, SJ, Feldman EC editors. Textbook of veterinary internal medicine. 5th edition. Philadelphia: WB Saunders; 2000. p. 1419–28.
57. Daminet S, Jeusette I, Duchateau L, Diez M, VandeMaele I, DeRick A. Evaluation of thyroid function in obese dogs and in dogs undergoing a weight loss protocol. J Am Vet Med Assoc Ser A Physiol Pathol Clin Med. 2003;50:213–8.
58. Chikamune T, Katamoto H, Nomura K, Ohashi F. Serum lipid and lipoprotein concentration in obese dogs. J Vet Med Sci. 1995;57:595–8.[Medline]
59. Bailhache E, Ouguerram K, Gayet C, Krempf M, Siliart B, Magot T, Nguyen P. An insulin-resistant hypertriglyceridaemic normotensive obese dog model: assessment of insulin resistance by the euglycaemic hyperinsulinaemic clamp in combination with the stable isotope technique. J Anim Physiol Anim Nutr (Berl). 2003;87:86–95.[Medline]
60. Diez M, Michaux C, Jeusette I, Baldwin P, Istasse L, Biourge V. Evolution of blood parameters during weight loss in experimental obese Beagle dogs. J Anim Physiol Anim Nutr (Berl). 2004;88:166–71.[Medline]
61. Hess RS, Kass PH, Shofer FS, Van Winkle TJ, Washabau RJ. Evaluation of risk factors for fatal acute pancreatitis in dogs. J Am Vet Med Assoc. 1999;214:46–51.[Medline]
62. Smith GK, Mayhew PD, Kapatkin AS, McKelvie PJ, Shofer FS, Gregor TP. Evaluation of risk factors for degenerative joint disease associated with hip dysplasia in German Shepherd Dogs, Golden Retrievers, Labrador Retrievers, and Rottweilers. J Am Vet Med Assoc. 2001;219:1719–24.[Medline]
63. Brown DC, Cozemius MG, Shofer FS. Body weight as a predisposing factor for humeral condylar fractures, cranial cruciate rupture and intervertebral disc disease in Cocker Spaniels. Vet Comp Orthop Traumatol. 1996;9:75–8.
64. van Hagen MA, Ducro BJ, van den Broek J, Knol BW. Incidence, risk factors, and hereditability estimates of hind limb lameness caused by hip dysplasia in a birth cohort of boxers. Am J Vet Res. 2005;66:307–12.[Medline]
65. Impellizeri JA, Tetrick MA, Muir P. Effect of weight reduction on clinical signs of lameness in dogs with hip osteoarthritis. J Am Vet Med Assoc. 2000;216:1089–91.[Medline]
66. White RAS, Williams JM. Tracheal collapse in the dog—is there really a role for surgery? A survey of 100 cases. J Small Anim Pract. 1994;35:191–6.
67. Bodey AR, Mitchell AR. Epidemiological study of blood pressure in domestic dogs. J Small Anim Pract. 1996;37:116–25.[Medline]
68. Truett AA, Borne AT, Monteiro MP, West DB. Composition of dietary fat affects blood pressure and insulin responses to dietary obesity in the dog. Obes Res. 1998;6:137–46.[Medline]
69. Van Winkle TJ, Bruce E. Thrombosis of the portal vein in eleven dogs. Vet Pathol. 1993;30:28–35.[Abstract]
70. Baba E, Arakawa A. Myocardial hypoxia in an obese beagle. Vet Med Sm Anim Clin. 1984;79:788–91.
71. Henegar JR, Bigler SA, Henegar LK, Tyag S, Hall JE. Functional and structural changes in the kidney in the early stages of obesity. J Am Soc Nephrol. 2001;12:1211–7.
72. Holt PE. Studies on the control of urinary continence in the bitch [PhD thesis]. Bristol (UK): University of Bristol; 1987.
73. Lekcharoensuk C, Lulich JP, Osborne CA, Pusoonothornthum R, Allen TA, Koehler LA, Urlich LK, Carpenter KA, Swanson LL. Patient and environmental factors associated with calcium oxalate urolithiasis in dogs. J Am Vet Med Assoc. 2000;217:515–9.[Medline]
74. Sonnenschein EG, Glickman LT, Goldschmidt MH, McKee LJ. Body conformation, diet, and risk of breast cancer in pet dogs: a case-control study. Am J Epidemiol. 1991;133:694–703.
75. Glickman LT, Sonnenschein EG, Glickman NW, Donoghue S, Goldschmidt MH. Pattern of diet and obesity in female adult pet dogs. Vet Clin Nutr. 1995;2:6–13.
76. Spencer E, Key T. Obesity and cancers of the endometrium and breast. Prog. Obes Res. 2003;9:668–71.
77. Perez Alenza MD, Rutteman GR, Pena L, Beynen AC, Cuesta P. Relation between habitual diet and canine mammary tumors in a case-control study. J Vet Intern Med. 1998;12:132–9.[Medline]
78. Perez Alenza MD, Pena L, del Castillo N, Nieto AI. Factors influencing the incidence and prognosis of canine mammary tumours. J Small Anim Pract. 2000;41:287–91.[Medline]
79. Glickman LT, Schofer FS, McKee LJ, Reif JS, Goldschmidt MH. Epidemiologic study of insecticide exposure, obesity, risk of bladder cancer in household dogs. J Toxicol Environ Health. 1989;28:407–14.[Medline]
80. Williams GD, Newberne PM. Decreased resistance to Salmonella infection in obese dogs [abstract]. Fed Proc. 1971;30:572.
81. Fiser RH, Beisel WR, Rollins JB. Decreased resistance against infectious canine hepatitis in dogs fed a high-fat ration. Am J Vet Res. 1972;33:713–19.[Medline]
82. Diez M, Nguyen P, Jeusette I, Devois C, Istasse L, Biourge V. Weight loss in obese dogs: evaluation of a high-protein, low-carbohydrate diet. J Nutr. 2002;132:1685S–7.
83. Blanchard G, Nguyen P, Gayet C, Leriche I, Siliart B, Paragon BM. Rapid weight loss with a high-protein low-energy diet allows the recovery of ideal body composition and insulin sensitivity in obese dogs. J Nutr. 2004;134:2148S–50.
84. Fisler JS. Cardiac effects of starvation and semi-starvation diets: safety and mechanisms of action. Am J Clin Nutr. 1992;56:230S–4.
85. Weinsier RL, Wadden TA, Ritenbaugh C, Harrison GG, Johnson FS, Wilmore JH. Recommended therapeutic guidelines for professional weight control programs. Am J Clin Nutr. 1984;40:865–72.
86. MacIntosh MK. Nutrients and compounds affecting body composition and metabolism. Compendium on Continuing Education for the Practicing Veterinarian. 2001;23:18–28.
87. Heo K, Odle J, Han IK, Cho W, Seo S, van Heugten E, Pilkington DH. Dietary L-carnitine improves nitrogen utilization in growing pigs fed low-energy, fat-containing diets. J Nutr. 2000;130:1809–14.
88. Desroches S, Chouinard PY, Galibois I, Corneau L, Delisle J, Lamarche B, Couture P, Bergeron N. Lack of effect of dietary conjugated linoleic acids naturally incorporated into butter on the lipid profile and body composition of overweight and obese men. Am J Clin Nutr. 2005;82:309–19.
89. Leray V, Dumon H, Martin L, Siliart B, Sergheraert R, Biourge V, Nguyen P. No effect of conjugated linoleic acid or garcinia cambogia on fat-free mass and energy expenditure in normal cats. J Nutr. 2006;136:1982S–4S.
90. Fahey GC, Merchen NR, Corbin JE, Hamilton AK, Serbe KA, Lewis SM, Hirakawa DA. Dietary fiber for dogs: I. Effect of graded levels of dietary beet pulp on nutrient intake, digestibility, metabolizable energy and digesta mean retention time. J Anim Sci. 1990;68:4221–8.[Abstract]
91. Fahey GC, Merchen NR, Corbin JE, Hamilton AK, Serbe KA, Hirakawa DA. Dietary fiber for dogs: II. Iso-total dietary fiber (TDF) additions of divergent fiber sources to dog diets and effects of nutrient intake, digestibility, metabolizable energy and digesta mean retention time. J Anim Sci. 1990;68:4229–35.[Abstract]
92. Butterwick RF, Markwell PJ. Effect of level and source of dietary fiber on food intake in the dog. J Nutr. 1994;124:2695S–700S.
93. Jewell DE, Toll PW. Effect of fiber on food intake in dogs. Vet Clin Nutr. 1996;3:115–8.
94. Van Dale D, Sarris WHM. Repetitive weight loss and weight reduction, resting metabolic rate, and lipolytic activity before and after exercise and/or diet treatment. Am J Clin Nutr. 1989;49:409–16.
95. Phinney SD. Exercise during and after very low calorie dieting. Am J Clin Nutr. 1992;56:190S–4.
96. Yaissle JE, Holloway C, Buffington CAT. Evaluation of owner education as a component of obesity treatment programs for dogs. J Am Vet Med Assoc. 2004;224:1932–5.[Medline]
97. Laflamme DP, Kuhlman G. The effect of weight loss regimen on subsequent weight maintenance in dogs. Nutr Res. 1995;15:1019–28.
This article has been cited by other articles:
|
|
 |
|
  C. Villaverde, J. J. Ramsey, A. S. Green, D. K. Asami, S. Yoo, and A. J. Fascetti Energy Restriction Results in a Mass-Adjusted Decrease in Energy Expenditure in Cats That Is Maintained after Weight Regain J. Nutr., May 1, 2008; 138(5): 856 - 860. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. P.M. Veiga, C. A. Price, S. T. de Oliveira, A. P. dos Santos, R. Campos, P. R. Barbosa, and F. H.D. Gonzalez Association of canine obesity with reduced serum levels of C-reactive protein J Vet Diagn Invest, March 1, 2008; 20(2): 224 - 228. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Trayhurn, C. Bing, and I. S. Wood Adipose Tissue and Adipokines--Energy Regulation from the Human Perspective J. Nutr., July 1, 2006; 136(7): 1935S - 1939S. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
