1. No category

COMPANION ANIMALS SYMPOSIUM: Obesity in dogs and cats: What is wrong
with being fat?
D. P. Laflamme
J ANIM SCI 2012, 90:1653-1662.
doi: 10.2527/jas.2011-4571 originally published online October 7, 2011
The online version of this article, along with updated information and services, is located on
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http://www.journalofanimalscience.org/content/90/5/1653
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COMPANION ANIMALS SYMPOSIUM:
Obesity in dogs and cats: What is wrong with being fat?1
D. P. Laflamme2
Nestle Purina PetCare Research, Checkerboard Square–2S, St. Louis, MO 63164
ABSTRACT: Few diseases in modern pets are diet
induced. One possible exception to this is obesity,
which is ultimately caused by consuming more calories than needed by the dog or cat. Although fat is the
most concentrated and efficiently stored source of calories, and protein least so, an excess of calories from
any source will contribute to adiposity. Obesity is an
excess of body fat sufficient to result in impairment
of health or body function. In people, this is generally
recognized as 20 to 25% above ideal BW. This degree
of excess is important in dogs as well. A lifelong study
in dogs showed that even moderately overweight
dogs were at greater risk for earlier morbidity; these
dogs required medication for chronic health problems
sooner than their lean-fed siblings. The average difference in BW between groups was approximately 25%.
Obese cats also face increased health risks, including
an increased risk of arthritis, diabetes mellitus, hepatic
lipidosis, and early mortality. The risk for development of diabetes increases about 2-fold in overweight
cats and about 4-fold in obese cats. Altered adipokine
secretion appears to be an important mechanism for
the link between excess BW and many diseases. Once
considered to be physiologically inert, adipose tissue
is an active producer of hormones, such as leptin and
resistin, and cytokines, including many inflammatory
cytokines such as tumor necrosis factor-α, IL-1β and
IL-6, and C-reactive protein. The persistent, low-grade
inflammation secondary to obesity is thought to play a
causal role in chronic diseases such as osteoarthritis,
cardiovascular disease, diabetes mellitus, and others.
For example, tumor necrosis factor-α alters insulin sensitivity by blocking activation of insulin receptors. In
addition, obesity is associated with increased oxidative
stress, which also may contribute to obesity-related
diseases. Management of obesity involves nutritional modification as well as behavioral modification.
Increased protein intake combined with reduced calorie intake facilitates loss of body fat while minimizing
loss of lean body mass. Limiting treats to 10% of calorie intake and increasing exercise both aid in successful
BW management.
Keywords: adipokine, canine, diabetes, feline, insulin resistance, obesity
© American Society of Animal Science. All rights reserved.
INTRODUCTION
The last published survey of obesity involving a
large number of dogs and cats was conducted well over
a decade ago. At that time, about 1 in 3 adult dogs and
1Based on a presentation at the Companion Animals Symposium
titled “Living Beyond 20: Discoveries in Geriatric Companion Animal
Biology” at the Joint Annual Meeting, July 10 to 14, 2011, New Orleans,
Louisiana. The symposium was sponsored, in part, by Hill’s Science
Diet (Topeka, KS), Proctor & Gamble (Cincinnati, OH), and Purina
(St. Louis, MO) with publication sponsored by the Journal of Animal
Science and the American Society of Animal Science.
2Corresponding author: [email protected]
Received August 9, 2011.
Accepted October 1, 2011.
J. Anim. Sci. 2012.90:1653–1662
doi:10.2527/jas2011-4571
cats seen by veterinarians were overweight or obese
(Lund et al., 2005, 2006). The prevalence was even
greater among middle-aged dogs and cats; almost 50%
of dogs and cats between 5 and 10 yr of age are overweight or obese.
Just what is obesity? It is defined by excess body
fat sufficient to cause or contribute to disease. How
much excess fat is needed to increase risk of disease,
and how does adiposity increase the risk for disease?
Whereas few data on the prevalence of obesity have
been generated in the last decade, considerable new information is being generated regarding the pathophysiology and management of obesity. The objective of
this paper is to review the role of obesity in pet health
as well as to address the management of pet obesity.
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Laflamme
OBESITY AS A CAUSE OF DISEASE
Obesity is an excess of body fat sufficient to result
in impairment of health or body function (Laflamme,
2006). In people, this is generally recognized as a BW
20 to 25% above ideal. This degree of excess BW appears to be important in dogs and cats as well. A lifelong
study in dogs showed that even moderately overweight
dogs were at greater risk for earlier morbidity, and the
median lifespan was reduced (Kealy et al., 2002).
In that study, one group of Labrador retrievers was
fed 25% less food than their sibling pair-mates throughout life (Kealy et al., 2002). The average adult BCS for
the lean-fed and control dogs were 4.6 ± 0.2 and 6.7 ± 0.2,
respectively, based on a 9-point BCS system (Laflamme,
1997b). Thus, the control dogs were moderately overweight (typical of many pets) and weighed about 26%
more, on average, than the lean-fed group. This difference in body condition was sufficient to affect median
life span, which was about 15% greater for the lean-fed
dogs. In addition, the heavier dogs required medication
for osteoarthritis, or other chronic health problems, an
average of 3.0 or 2.1 yr, respectively, sooner than their
lean-fed siblings (Kealy et al., 2002).
Insulin resistance, or reduced sensitivity to insulin,
has been well documented to increase in overweight
and obese dogs (Larson et al., 2003; Gayet et al., 2004;
Verkest et al., 2011a). One study showed that this alteration in insulin resistance occurs with increased body fat,
independent of BW change (Kim et al., 2003). Dogs fed
a high-fat diet (i.e., 44% of calories from fat) increased
visceral body fat 2-fold over baseline with a minimal
(i.e., 5%) increase in BW. Concurrent with this, the investigators documented an increase in fasting insulin
and hepatic insulin resistance (Kim et al., 2003). With
this in mind, it is important to assess body condition in
clinical patients, rather than just BW. Body weight does
not take into account differences in body composition,
whereas it is reasonably well estimated using a BCS system (Laflamme, 1997a,b; Mawby et al., 2004; German
et al., 2006).
Obese cats also face increased health risks, including an increased risk of diabetes mellitus, hepatic lipidosis, urinary tract diseases, lameness, and dermatopathies
(Scarlett and Donoghue, 1998; Lund et al., 2005). The
risk for development of diabetes increases about 2-fold
in overweight cats and about 4-fold in obese cats. Even
moderate increases in BW can cause significant changes
in insulin sensitivity (Fettman et al., 1998; Hoenig et al.,
2007). According to Hoenig et al. (2007), each kilogram
increase in adult cat BW contributes to a 30% decrease
in insulin sensitivity. And, like dogs, cats fed a highfat diet are at greater risk for increasing their body fat
(Nguyen et al., 2004; Backus et al., 2007).
Pathophysiology of Obesity
Adipose tissue is composed primarily of adipocytes
and preadipocytes, as well as supporting cells such as
endothelial cells, fibroblasts, macrophages, and leukocytes (Wozniak et al., 2009; Balistreri et al., 2010).
Adipose tissue serves as a reservoir of fatty acids that are
used as an energy source during the postprandial fasting
state. Adipose tissue uses very little energy, so contributes little to basal energy expenditure. At one time, its
primary role in disease was thought to be the effect of
increased weight bearing, causing stress on joints, and
increasing the workload on the heart. However, ongoing
research has indicated another mechanism for the link
between excess BW and numerous diseases. Adipose
tissue is an active producer of hormones, cytokines, and
other cell-signaling substances, collectively called adipokines (Kershaw and Flier, 2004; Trayhurn and Wood,
2005), which may contribute to obesity-related diseases.
The discovery of the hormone, leptin, in 1994, led
to the recognition of the extensive secretory function
of adipose tissue (Trayhurn and Wood, 2005). That first
adipokine was followed by the identification of many
others, with over 100 cytokines, chemokines, hormones,
and other biologically active mediators identified to date
(Kershaw and Flier, 2004; Trayhurn and Wood, 2005;
Wozniak et al., 2009; Balistreri et al., 2010). Although
the physiological functions served are not yet known for
all adipokines, many can be grouped as involved in energy balance or metabolism, pro- or anti-inflammatory
regulation, or promoters of insulin resistance (Table 1).
Adipokines are secreted from both the adipocytes and
the associated cells, including macrophages.
Some adipokines can have systemic endocrine or
inflammatory effects, whereas others have paracrine
functions, affecting only those tissues in close proximity
(Wozniak et al., 2009; Balistreri et al., 2010). The effects
of various adipokines can vary, depending on animal
species and source within the body (Radin et al., 2009;
Wozniak et al., 2009; Verkest et al., 2011b). Adipokines
from visceral fat can differ in effect from those secreted
from intramuscular, perivascular, or epicardial adipose
tissue (Wozniak et al., 2009).
Adipose Tissue Is a Major Endocrine Organ
Among the best studied hormones produced by
adipose tissue are leptin and adiponectin (Kershaw and
Flier, 2004; Trayhurn and Wood, 2005; Hoenig et al.,
2007). Leptin secretion increases as adiposity increases in dogs and cats, as well as other species (Hoenig et
al., 2007; Grant et al., 2011; Verkest et al., 2011a). The
primary functions that have been identified for this hormone include appetite and energy regulation, as well as
immune and neuroendocrine functions (Wynne et al.,
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Obesity in Pets
2005). Leptin can stimulate diet-induced thermogenesis,
increasing energy expenditure to help balance the effects of excessive calorie intake (Trayhurn et al., 2006).
Leptin triggers the hypothalamus to decrease appetite
and reduce food intake, which occurs in normally responsive individuals. Unfortunately, many obese people
appear to be resistant to the effects of leptin (Wynne et
al., 2005). With leptin resistance, the obese individual
does not have normal feedback to downregulate food intake nor increase metabolic energy expenditure. Whether
or not this is also true in dogs or cats has not been shown.
Adiponectin, which functions to enhance insulin
sensitivity and stimulate basal energy expenditure, decreases with increasing adiposity and insulin resistance
in most species (Kershaw and Flier, 2004; Wynne et al.,
2005; Shoelson et al., 2006; Belsito et al., 2009; Eirmann
et al., 2009; Radin et al., 2009). The effects of adiponectin differ depending on the target organ, but include antidiabetic, anti-inflammatory, and antiatherogenic effects
(Kershaw and Flier, 2004). There do, however, appear
to be some species differences. One difference shown
in cats is the source of adiponectin. In humans, subcutaneous fat produces the greatest amount of adiponectin,
whereas in cats, visceral fat appears to be the predominant source (Lusby et al., 2009; Zini et al., 2009)
Adiponectin circulates as either low molecular weight
or high molecular weight (HMW) multimers. In humans,
decreased concentrations of circulating total or HMW
adiponectin concentrations are not only associated with
insulin resistance, but predict progression to type 2 diabetes or metabolic syndrome (Li et al., 2009; Hirose et al.,
2010). Recently, 3 studies (German et al., 2009; Verkest et
al., 2011a; Wakshlag et al., 2011a) failed to find an effect
of obesity on adiponectin concentrations in dogs despite
significant effects of obesity on insulin resistance. Among
lean subjects, lean dogs had HMW adiponectin concentrations 3 to 4 times greater than lean humans. Unlike in
humans, there was no decrease in HMW adiponectin in
obese dogs (Verkest et al., 2011b) and no change after BW
loss (Wakshlag et al., 2011a). Because dogs do not naturally develop type 2 diabetes, it was proposed that this
species difference in adiponectin may be a protective factor against this condition in dogs (Verkest et al., 2011b).
Additional research on this potentially important species
difference is warranted.
Obesity Is an Inflammatory Condition
In addition to various hormones and metabolically
active proteins, several adipokines are inflammatory mediators, contributing to chronic inflammation in obesity.
Some of the inflammatory cytokines released in greater
amounts from adipose tissue in obese subjects include
tumor necrosis factor-α, IL-1β and IL-6, C-reactive pro-
Table 1. Key adipokines and their physiological roles1
Energy balance,
metabolism
Leptin
Adiponectin
Resistin
Adipsin
Apelin
Visfatin
Vaspin
Omentin
Proinflammatory
Leptin
Resistin
TNF-α2
IL-1
IL-6
IL-8
MCP-12
PAI-12
Angiotensinogen
CRP2
SAA2
IFNβ2
IP-102
Antiinflammatory
Adiponectin
IL-1Rα2
IL-4
IL-10
TGFβ2
Insulin
resistance
Resistin
RBP-42
LCN-22
IL-6
TNF-α2
1Adapted
from Wozniak et al. (2009), Balistreri et al. (2010), and Singla
et al. (2010).
2TNF = tumor necrosis factor; MCP = monocyte chemoattractant protein;
PAI = plasminogen activator inhibitor; CRP = C-reactive protein; SAA =
serum amyloid A; IFN = interferon; IP = interferon-gamma inducible protein;
IL-1Rα = IL-1 receptor antagonist; TGF = transforming growth factor; RBP
= retinol binding protein; LCN = lipocalin.
tein (CRP), and others (Miller et al., 1998; Gayet et al.,
2004; Trayhurn and Wood, 2005; Shoelson et al., 2006;
Hoenig et al., 2007; Tanner et al., 2007; Wozniak, et
al., 2009; Balistreri et al., 2010; Verkest et al., 2011a;
Wakshlag et al., 2011a). Among its various effects, tumor
necrosis factor-α has direct endocrine effects that influence energy metabolism (Kershaw and Flier, 2004), and
it promotes inflammation and causes insulin resistance
by blocking activation of insulin receptors (Plomgaard
et al., 2005). Interleukin-1β, IL-6, and CRP also contribute to insulin resistance, via different pathways, as well
as promoting inflammation (Wellen and Hotamisligil,
2003). In addition, adipose tissue produces monocyte
chemoattractant protein-1, which attracts macrophages.
Thus, adipose tissue in obese individuals is characterized
by an increased population of activated macrophages,
which further contribute to inflammation and release of
cytokines (Wellen and Hotamisligil, 2003, 2005; Xu et
al., 2003; Kasuga, 2006; Shoelson et al., 2006; Balistreri
et al., 2010; Singla et al., 2010).
The inflammation in obesity extends beyond the
adipose tissue. The liver is affected, either via fatty infiltration directly or from adipose-derived inflammatory
mediators (Shoelson et al., 2006). This results in activation of inflammatory signaling pathways in the liver,
including Kupffer cell activation. Unlike adipose tissue,
where macrophages are numerically sparse but increase
in obesity, Kupffer cells make up 5% of the total cells in
the liver. Activation of these macrophage-type cells contributes to further production of inflammatory mediators
and recruitment of other immune cells, and may play a
role in hepatic insulin resistance (Shoelson et al., 2006).
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Laflamme
The persistent, low-grade inflammation secondary to
obesity is thought to play a causal role in chronic diseases, such as osteoarthritis and diabetes mellitus (Coppack,
2001; Wellen and Hotamisligil, 2005; Shoelson et al.,
2006; Trayhurn et al., 2006). In addition, obesity is associated with increased oxidative stress, which also
contributes to obesity-related diseases (Urakawa et al.,
2003; Furukawa et al., 2004; Tanner et al., 2007).
Obesity Increases Oxidative Stress
Oxidative stress is an imbalance between the amount
of pro-oxidants and antioxidants normally present in the
body. Under physiological conditions, the pro-oxidant
reactive oxygen species (ROS) are balanced by an elaborate antioxidant defense system. However, under conditions of increased ROS or reduced antioxidant capacity, there is an increase in ROS activity, causing oxidative stress. Oxidative stress can cause cellular injury and
tissue damage (Furukawa et al., 2004).
Oxidative stress has been established as another
cause of insulin resistance in obesity (Kyselová et al.,
2002; Urakawa et al., 2003; Subauste and Burant, 2007).
Increased intracellular free fatty acids, which contribute to oxidative stress, lead to reduced translocation of
GLUT4 (an insulin-sensitive glucose transporter), resulting in insulin resistance (Rudich et al., 1998; Ceriello
and Motz, 2004). This is consistent with the observation
that GLUT4 expression decreases early in the development of obesity, at least in cats (Brennan et al., 2004).
The FFA or ROS also cause an increase in pro-inflammatory adipokines (Urakawa et al., 2003; Furukawa et al.,
2004; Subauste and Burant, 2007). The inflammatory
cytokines can independently cause insulin resistance, as
previously noted. In addition, ROS in adipose tissue decreases adiponectin gene expression, further contributing to insulin resistance (Furukawa et al., 2004).
Regardless of mechanism, the association between obesity and markers of oxidative stress has
been confirmed in multiple species, including cats and
dogs (Urakawa et al., 2003; Ceriello and Motz, 2004;
Furukawa et al., 2004; Shoelson et al., 2006; Kim et al.,
2007; Tanner et al., 2007; Grant et al., 2011). Oxidative
stress appears to be an important link between obesity,
insulin resistance, and multiple health problems.
Insulin Resistance Contributes
to More than Diabetes Mellitus
An important effect of the dysregulated adipokines
and oxidative stress in obesity is to increase insulin resistance, which is central to many of the adverse effects
of obesity. Insulin resistance reflects the inability of tissues to respond normally to insulin, causing a compensatory secretion of more insulin from the pancreas. Insulin
resistance and the resulting hyperinsulinemia is thought
to contribute to the development of numerous diseases,
such as cardiovascular disease; breast, prostate, or colon
cancer; kidney disease; liver disease; and others (Reaven,
1988; Bruning et al., 1992; Varthakavi et al., 2002; Hsing
et al., 2003; Komninou et al., 2003; Vrbíková et al., 2004;
Kasuga, 2006; Utzschneider and Kahn, 2006; WhaleyConnell et al., 2006; Cubbon et al., 2007; Knight and Imig,
2007; Méndez-Sánchez et al., 2007; Ota et al., 2007). With
the exception of diabetes, most of these links have not
yet been confirmed in veterinary species. However, many
are just newly recognized in humans, perhaps because of
the dramatic increase in hyperinsulinemia in the human
population (Li et al., 2006). Certainly, insulin resistance
is a common feature of obesity in both dogs and cats
(Mattheeuws et al., 1984; Fettman et al., 1998; Gayet et
al., 2004; Hoenig et al., 2007; Verkest et al., 2011a). In
cats, insulin sensitivity decreases by about 30% for each
kilogram of BW gain (Hoenig et al., 2007), and feline obesity is associated with up to an 4-fold increased risk for
development of diabetes mellitus (Scarlett and Donoghue,
1998; Lund et al., 2005).
In addition to disease associations, reduced insulin
sensitivity has been associated with decreased lifespan
(Larson et al., 2003; Taguchi et al., 2007). Larson et
al. (2003) reported that decreased insulin sensitivity in
moderately overweight dogs was associated with a 15%
decrease in median life span, compared with siblings
undergoing lifelong, mild food restriction. The effects
of insulin resistance in some conditions appear to be independent of, but made worse by, obesity (McLaughlin
et al., 2004).
Insulin resistance not only contributes to secondary diseases, it can also contribute to ongoing obesity
via disruptions in energy homeostasis. Insulin plays a
dominant role in energy homeostasis and appetite via
receptors in the brain (Kasuga, 2006), and insulin resistance in obesity affects insulin receptors in the brain
as well (Anthony et al., 2006). In all mammals, there
is an increase in energy expenditure after consumption
of a meal, termed diet-induced thermogenesis. Insulin
facilitates this increase in normal individuals (Schwartz
et al., 1992). However, diet-induced thermogenesis is
decreased in many obese subjects, and the decrease is
correlated with degree of insulin-resistance (Segal et al.,
1992; Watanabe et al., 2006). Normally, insulin crosses
the blood-brain barrier and functions in the hypothalamus as an appetite suppressor (Wynne et al., 2005). With
insulin resistance, this effect is inhibited. Instead, insulin resistance with hyperinsulinemia promotes increased
eating and decreased fat oxidation, as well as decreased
diet-induced thermogenesis (Velasquez-Mieyer et al.,
2003; Kasuga, 2006; Watanabe et al., 2006). These effects can make reversing obesity more difficult.
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Obesity in Pets
Insulin sensitivity can be improved via several independent mechanisms including BW loss, fermentable
dietary fibers, exercise, and pharmaceutical agents including metformin, thiazolidinediones, and angiotensin-converting enzyme inhibitors (Wang et al., 2004;
Respondek et al., 2008; Li et al., 2010). In addition,
eliminating the obesity-related oxidative stress and inflammation that promote insulin resistance may help reverse this condition.
MANAGEMENT OF OBESITY
There are many factors that play a role in creating
obesity. Prevention of obesity relies on understanding
contributing or associated risk factors, and managing
them appropriately. Important risk factors for obesity in
pets include neutering and inactivity. Neutering can reduce maintenance energy requirements (MER) by 25 to
35%, as well as increase spontaneous food intake (Root,
1995; Fettman et al., 1997; Jeusette et al., 2004; Belsito et
al., 2009). Fortunately, controlling food intake can reduce
the development of obesity in neutered pets (Harper et
al., 2001). Feeding high-fat diets contributes to increased
body fat, especially when fed ad libitum (Kim et al., 2003;
Nguyen et al., 2004; Backus et al., 2007). As noted above,
obesity is associated with significant health risks; thus,
diagnosing and managing obesity is an important part of
health care management of dogs and cats.
The first step in an effective obesity management
program is recognition of the problem. Perhaps the most
practical methods for veterinary- or owner-assessment of
obesity are a combination of BW and BCS. According
to studies using a 9-point system (Laflamme, 1997a,b;
Mawby et al., 2004), each unit increase in BCS above
ideal (BCS = 5) is approximately equivalent to 10 to 15%
over ideal BW. Therefore, a dog or cat with BCS equaling
7 is about 20 to 30% over ideal BW. By recording both BW
and BCS, ideal BW can be reasonably estimated. Animals
that are becoming obese can be recognized sooner and
managed more easily. An illustrated BCS system can provide a useful tool for pet owner education regarding obesity prevention and management.
Once obesity is recognized, it is important to develop a management plan that fits the needs of both patient and owner. This must consider owner ability and
willingness to control calories and enhance exercise for
their pet. In addition to an appropriate diet for calorie
restriction, other keys to success are flexibility in design
and regular follow-up.
Dietary Factors: Energy and Macronutrients
Body weight loss depends, above all, on creating
a negative energy balance. Of utmost importance is
recognition that individual animals can differ greatly
1657
in their MER (Laflamme et al., 1997; Butterwick and
Hawthorne, 1998), and the degree of calorie intake that
induces significant BW loss in 1 dog or cat may cause
BW gain in another. Adjustments in calorie allowance
made on a regular basis, for example, every month, will
help address these individual differences as well as the
reductions in MER that occur during BW loss.
Use of an appropriate diet for BW loss is important,
and there are several criteria to consider. Although it is
ultimately calorie restriction that induces BW loss, it
is important to avoid excessive restriction of essential
nutrients. Therefore, a low-calorie product with an increased nutrient-to-calorie ratio should be considered.
Further, an important goal for BW loss is to promote fat
loss while minimizing loss of lean body mass (LBM),
which may be influenced by dietary composition.
Dietary protein is especially important in BW loss
diets. Consumption of low-calorie diets with increased
protein significantly increases fat loss and reduces the
loss of LBM in dogs and cats (Hannah and Laflamme,
1998; Diez et al., 2002; Bierer and Bui, 2004; Laflamme
and Hannah, 2005; Vasconcellos et al., 2009), as well as
humans (Farnsworth et al., 2003; Layman et al., 2003;
Leidy et al., 2007a,b), undergoing BW loss. Among overweight cats, increasing dietary protein from 35 to 45%
of energy resulted in more than 10% greater fat loss despite almost identical total BW loss and rate of BW loss
between groups of cats (Laflamme and Hannah, 2005). A
similar pattern was observed in dogs, with greater fat loss
in those fed the greater protein diets during calorie restriction (Hannah and Laflamme, 1998). Most importantly,
absolute loss of LBM during BW loss was cut in half by
increasing dietary protein in both cats and dogs (Hannah
and Laflamme, 1998; Laflamme and Hannah, 2005).
Protein has a significant diet-induced thermogenesis
effect, meaning that postprandial ME expenditure is increased more when protein is consumed, compared with
carbohydrates or fats (Nair et al., 1983; Karst et al., 1984;
Swaminathan et al., 1985; Hoenig et al., 2007; Leidy et
al., 2007b). At least a portion of this thermic effect is due
to increased protein turnover and protein synthesis, which
is stimulated by protein intake. Protein synthesis expends
energy at a rate of 4 mol ATP (i.e., approximately equivalent to 80 kcal) used per mole of AA incorporated into
protein (Wolfe, 2006). The thermic effect of protein results in a small but significant increase in total daily energy expenditure (Mikkelsen et al., 2000; Wei et al., 2011).
Metabolic adaptation to calorie restriction includes a
reduction in resting energy expenditure, which can slow
BW loss and may contribute to BW rebound (Laflamme
and Kuhlman, 1995; Agus et al., 2000; Villaverde et al.,
2007). The thermic effect provided by a high-protein diet
(Vasconcellos et al., 2009; Wei et al., 2011) can help offset this reduction. In humans, isocaloric consumption of
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Laflamme
higher protein diets limited the decrease in resting energy
expenditure by 50 to 75% (Agus et al., 2000; Torbay et al.,
2002). In a small study, dogs fed a higher protein diet were
able to consume more calories but lose the same amount
of BW, compared with those fed a lower protein diet
(Jeusette et al., 2006). Likewise, cats fed a high-protein
diet during BW loss achieved the same rate of BW loss
despite almost 10% greater calorie intake (Vasconcellos
et al., 2009). In human subjects, increased dietary protein
provides a satiety effect as well as an enhanced ability
to sustain BW maintenance after BW loss (Crovetti et
al., 1998; Westerterp-Plantenga et al., 2004; Leidy et al.,
2007a,b). This same BW maintenance benefit appears to
occur in cats; cats that had been fed a high-protein diet
during BW loss were able to consume about 12% more
calories in the post-loss BW maintenance period without
BW gain (Vasconcellos et al., 2009).
In addition to the thermic and metabolic effects
of protein, higher protein diets reduce oxidative stress
compared with lower protein diets or diets limited in
sulfur AA (Petzke et al., 2000; Machín et al., 2004;
Blouet et al., 2007). In obese cats undergoing BW loss,
the use of a high-protein, low-fat diet resulted in significant improvements in markers of oxidative stress
compared with cats fed a lower protein product (Tanner
et al., 2006). Likewise, in that study, the higher protein
diet resulted in a greater reduction in the inflammatory
cytokines, CRP and IL-6. Thus, a higher protein diet can
help reduce the oxidative stress and chronic inflammation associated with obesity.
Dietary fiber is an important consideration for BW
loss diets. The low digestibility of dietary fiber means
that it provides little dietary energy. When dietary fiber
replaces fat or digestible carbohydrates, the caloric density of the food is reduced. In addition, dietary fiber provides a satiety effect that may be of value in BW management (Jackson et al., 1997; Jewell et al., 2000; Bosch
et al., 2009). Dietary fiber, especially fermentable fibers,
may reduce the insulin resistance that is common in
obese subjects (Respondek et al., 2008; Li et al., 2010).
Other Nutrients and Nutraceuticals
Many nutraceuticals and herbal compounds have
been evaluated for use in BW loss diets. A few have demonstrated benefits that may be of some help in BW management. Recently, studies have evaluated soy isoflavones
for use in BW management diets (Pan, 2006; Cave et al.,
2007; Pan et al., 2008). Studies in dogs, published thus far
only in abstract form, showed loss of fat was enhanced in
dogs fed the low-calorie diet containing soy isoflavones;
these dogs were more likely to achieve their target body
fat compared with those fed a similar diet without isoflavones (Pan, 2006). In addition, markers of oxidative
damage were significantly reduced in dogs consuming
the isoflavone-containing diet (Pan et al., 2008).
Soy isoflavones can reduce the BW gain or increase
in body fat normally associated with castration or spaying.
Dietary soy isoflavones reduced BW gain by 50% in overfed, neutered female and male dogs (Pan, 2006). In male and
female cats, supplemental isoflavones were able to reduce
the increase in body fat after neutering, compared with control cats, despite no effect on food intake or total BW (Cave,
et al., 2007). In addition, LBM increased in the cats treated
with isoflavones. These effects indicate a beneficial metabolic repartitioning associated with the soy isoflavones, which
may help reduce BW rebound in animals after BW loss.
Diacylglycerols (DAG) are lipids that contain 2
fatty acids per glycerol molecule, unlike the traditional
triglycerides that contain 3 fatty acids per glycerol. The
fatty acids from DAG are metabolized differently and
tend to be oxidized readily (Bauer et al., 2006). Studies
in mice, rats, humans, and dogs indicate that DAG may
be of benefit in BW management (Umeda et al., 2006).
Overweight dogs fed a diet containing 7% DAG lost
2.3% of their starting BW over 6 wk, whereas the control dogs consuming the same amount of calories maintained BW (Umeda et al., 2006). In addition, dogs fed
DAG had significantly reduced serum triglycerides
compared with control diets (Bauer et al., 2006).
Carnitine is one of the most studied nutraceuticals
for BW management. Most studies have shown little
benefit (Dyck, 2000; Villani et al., 2000; Brandsch and
Eder, 2002; Aoki et al., 2004). Center et al. (2000) reported a significant increase in rate of BW loss in cats
supplemented with carnitine compared with a control
group (24 vs. 20%, respectively, over an 18-wk period).
Carnitine is produced endogenously from the AA lysine and methionine, so supplementation is likely to be
of greatest benefit when the intake of dietary protein or
other precursors is insufficient to promote adequate endogenous production. In semi-starved cats (Armstrong
et al., 1992) and rats (Feng et al., 2001) undergoing
very rapid BW loss, L-carnitine reduced hepatic fat accumulation in cats, and enhanced lipid metabolism and
reduced ketogenesis in rats. In humans, severe calorie
restriction resulted in reduced urinary and plasma carnitine, an effect that was attenuated by increased dietary
protein during BW loss (Davis et al., 1990). No peerreviewed studies regarding the use of carnitine for BW
management in dogs have been published. In a recent
abstract, Pan et al. (2008) noted that carnitine appeared
to inhibit the beneficial effects of soy isoflavones, which
otherwise reduce fat or BW or both gain in overfed dogs.
Management: Client and Behavioral Factors
In addition to diet, feeding management and exercise are critically important to successful BW manage-
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1659
Obesity in Pets
ment. The creation of a treat allowance equal to 10% of
the daily calories allows owners to continue this pleasurable activity while also achieving appropriate energy
balance. Owners may benefit from a menu of low-calorie foods or commercial treats that would be appropriate
to use within the allowed calories.
Increasing exercise aids in BW management by
expending calories and preserving LBM. Wakshlag et
al. (2011b) reported that increased activity in the form
of both structured and unstructured activities allowed
dogs to consume about 20% more calories yet achieve a
similar rate of BW loss, compared with less active dogs.
Interactive exercise provides an alternative activity for
pet and owner to enjoy together, rather than food-related
activities. Activity in cats may be enhanced by interactive play, such as with a toy on a string or a laser light.
Food toys provide another option. These are plastic balls
or other shapes with holes that dispense kibble or treats
as the cat or dog plays with the toy.
Gradual BW loss in dogs, as in people, is more likely to allow long-term maintenance of the reduced BW
(Laflamme and Kuhlman, 1995). Body weight rebound
can be minimized by providing controlled food intake
and adjusting the calories fed to just meet the needs of
the pet for BW maintenance. Owners already accustomed to measuring food and monitoring the BW of
their pet should be encouraged to apply these behavior
modifications to long-term BW management.
Pharmaceutical Management of Obesity
Two new drugs, mitratapide (Yarvitan, Boehringer
Ingelheim, Stockholm, Sweden) and dirlotapide (Slentrol,
Pfizer Animal Health, Kalamazoo, MI), both microsomal
transfer protein inhibitors, were introduced in 2007 to aid in
canine BW management (Wren et al., 2007b; Dobenecker
et al., 2009). Their primary mode of action is to inhibit food
intake. The drugs interfere with enzymes involved in fat
absorption from the intestines, resulting in both a slight decrease in fat absorption and a physiologic release of satiety
factors that inhibit food intake (Wren et al., 2007a). Both
drugs are associated with mild side effects that include
vomiting, diarrhea, and increased liver enzymes (Wren et
al., 2007b; Dobenecker et al., 2009).
Reduced food intake during drug-induced BW loss
results in restriction of essential nutrients as well as calories, unless a therapeutic BW loss diet with an increased
nutrient to energy ratio is fed. On the other hand, due
to the side effects from these drugs, a new food should
not be introduced at the same time as the drug. In most
cases, ongoing control of food intake will be essential
to continue BW loss or maintain ideal BW once drug
therapy is completed.
SUMMARY AND CONCLUSIONS
Obesity is a common problem affecting almost 50%
of dogs and cats between 5 and 10 yr of age. Obesity is
an excess of body fat sufficient to result in impairment
of health or body function, often estimated to begin at
20 to 25% above ideal BW. Adipose tissue in obese subjects secretes several adipokines, including inflammatory cytokines. Obesity is an inflammatory condition and
is associated with increased oxidative stress as well as
insulin resistance. These factors appear to play a causative role in several chronic health problems, including
diabetes mellitus and osteoarthritis. Successful management of obesity in pets begins with recognition of the
problem. Body weight management programs should be
tailored to meet the needs of both pet and owner. Treats
and exercise are important components of most BW
management programs, as well as controlled feeding of
low-calorie foods. Increased dietary protein provides a
unique advantage by stimulating metabolism, promoting
fat loss, and helping preserve LBM during BW loss.
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Errata
The following articles were published with the incorrect DOI. The correct DOI numbers are listed below for each article. The DOI
numbers have been corrected in the online version of the articles.
“Administration of estradiol, trenbolone acetate, and trenbolone acetate/estradiol implants alters adipogenic and myogenic gene expression in bovine skeletal muscle” (J. Anim. Sci 90:1421–1427). Correct DOI is as follows: doi:10.2527/jas2010-3496.
“Phosphorus requirements for 60 to 100 kg pigs selected for high lean deposition under different thermal environments” (J. Anim. Sci
90:1499–1505). Correct DOI is as follows: doi:10.2527/jas2010-3623.
“Effect of the administration program of two beta-adrenergic agonists on growth performance, carcass, and meat characteristics of
feedlot ram lambs” (J. Anim. Sci 90:1521–1531). Correct DOI is as follows: doi:10.2527/jas2010-3513.
“Influence of a rumen-protected conjugated linoleic acid mixture on carcass traits and meat quality in young Simmental heifers” (J.
Anim. Sci 90:1532–1540). Correct DOI is as follows: doi:10.2527/jas2010-3617.
doi:10.2527/jas2011-4571
“Obesity in dogs and cats: What is wrong with being fat?” (J. Anim. Sci. 90:1653–1662). There is an incorrect statement saying that
obesity increases the risk for diabetes in cats 8 fold. This is stated in both the text on page 5, and in the abstract. The text and abstract
should read that obesity increases the risk for diabetes in cats 4 fold, rather than 8 fold. The author regrets the error.
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