Fighting Pet Obesity – Part 1: Causes in Small Animals

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Fighting pet obesity – part 1: causes in small animals

Author : Marge Chandler

Categories : Practical, RVNs

Date : May 24, 2017

It is a common perception obese people overeat and under-exercise by choice, and that obese pets are similarly overfed and under-exercised due to owner indulgence or ignorance.

Figure 1. Not all Labrador retrievers are overweight, although they may need more preventive maintenance to ensure good body condition.

Certainly, overeating without increased activity will cause an increase in weight, as any of us who have ever overindulged during holidays can attest, but more to obesity exists than this simple explanation.

Obesity is a multifactorial disorder, including environmental, metabolic and genetic factors and their

1 / 7 interactions. We have all had cases of overweight pets where we and the owners have struggled to get the pet to lose weight.

An understanding of some underlying causes of – and predispositions for – obesity may help in understanding why permanent weight loss can be so difficult.

Genetics

In humans, genetic factors account for 40-70% of the variation in body mass index (BMI) – a rough measure of human body fat. Genetic studies have examined several different causative mutations involving obesity loci on different chromosomes.

More than 200 genes in mice and more than 100 genes in humans have been identified that affect bodyweight regulation (Srivastava et al, 2007).

A single-nucleotide polymorphism (SNP; pronounced “snip”) is a DNA sequence variation on a chromosome that occurs when a single nucleotide (for example, adenosine, thymine, cytosine or guanine) differs from that in others of the same species in that genetic location.

An association of SNPs are in the human “fat mass and obesity-associated” gene region with BMI and risk of obesity – that is, a genetic location exists associated with adiposity, although how this gene affects obesity is not clear. Multiple genetic processes may contribute, including those governing appetite and energy expenditure (Fawcett and Barroso, 2010).

A tendency exists for some dog and cat breeds to become overweight, indicating genetics is likely a factor. Labrador retrievers, Shetland sheepdogs, golden retrievers, cocker spaniels, dachshunds, miniature schnauzers, springer spaniels, Chihuahuas, basset hounds and pugs are most likely to be obese than other breeds (Lusby and Kirk, 2009).

Less data exist about obesity risks in cat breeds, although Orientals appear to be affected less frequently, and mixed breed and domestic shorthaired cats may be more at risk than purebred cats (Lund et al, 2005).

A deletion in the canine proopiomelanocortin (POMC) gene has been found in some Labrador retrievers and flat-coated retrievers. This gene is associated with greater body fat and food motivation (Raffan et al, 2016). Three adipokine genes have also been identified as possible markers for Labrador retrievers at risk for obesity (Manowski et al, 2016).

These discoveries in humans and dogs do not explain the increase in the prevalence of obesity and do not fate individuals with “obesity genes” to inevitable obesity. While DNA cannot be changed, the expression of genes and the effects they have can be modified. Some can be modified by diet (nutrigenomics) and by exercise (Figure 1).

2 / 7 Presence of “obesity genes” does mean greater care will likely be needed to prevent it in these individuals and that once it occurs, it may be more difficult to treat.

Environment and management

Diet and feeding factors

Figure 2. Not all cup sizes are the same, so owners may unknowingly be feeding more than they mean or intend to.

Highly palatable diets fed free choice are a very important factor influencing obesity. Feeding table scraps and other treats may also induce many pets to overeat.

In some adult dogs, up to 50% of the calories are from table scraps – particularly in toy breeds – and many owners feed 20-25% of their dog’s calories as human foods (Heuberger and Wakshlag, 2011).

While food type (wet versus dry) doesn’t appear to affect the incidence of canine obesity, feeding premium dry foods has been associated with feline obesity – possibly due to the free choice feeding of these foods (Colliard et al, 2009).

Owners may not know how much to feed or fail to measure food accurately (Figure 2). The majority (nearly 70%) of cat owners feed until their cat stops eating (free choice), with about 16% feeding according to the pet food label, and less than 5% having requested a recommendation from their vet (Pet Food Manufacturers’ Association, 2009).

The cup size used to measure dry food and the feeding bowl size may affect the amount of food fed. Owners given a large cup and bowl provide more food than if small ones are used (Murphy et al, 2010). This is similar to people in which larger serving utensils and plates result in more food being eaten.

The social setting of meals may also influence eating behaviour. Many animals – especially dogs –

3 / 7 increase their food intake when consuming in the presence of other animals. This is referred to as social facilitation. On the other hand, being an only dog also can increase the risk of obesity – likely due to owner feeding management.

Exercise and voluntary activity

Figure 3. So-called "outdoor" cats can enjoy a very active lifestyle.

Several studies have shown low activity is a predictor of obesity. In cats, outdoor access usually increases activity and indoor cats are more at risk for weight gain (Figures 3 and 4).

One study did not find a difference in the risk of obesity between outdoor and strictly indoor cats (Colliard et al, 2009), although this study may have been hampered by a low number of cats and did not describe the activity levels of the cats. In dogs, the risk of being obese decreases by 4% for each additional hour of exercise per week.

In humans, the amount of voluntary movement outside of exercise – for example, fidgeting or cleaning the house, is strongly related to the risk of obesity. The tendency to voluntary movement may have a genetic basis.

This is probably also seen in some nervous or active dogs compared to those dogs who will happily sleep or rest for most of the day. While some breed predisposition to voluntary activity in dogs and possibly in cats is likely, no studies have been done on this.

4 / 7 Gut microbiota

In humans, rodents, dogs and cats, the gut bacteria, other micro-organisms and their environment – collectively termed the microbiome – differ in lean versus obese individuals. The gut microbiome is influenced by the maternal microbiota, diet, environment, antibiotic use and probiotics.

In humans, both the diversity of the microbiota and the Bacteroidetes/Firmicutes ratio are decreased in obese individuals (Compare et al, 2016). In cats, the microbiota differed between lean and obese cats, but was not linked to specific bacterial groups (Kieler et al, 2016). In dogs, the microbiome diversity was lower in the obese individuals and, similar to humans, Firmicutes bacteria were greater in lean dogs and Proteobacteria were predominant in obese dogs (Park et al, 2015).

This “obese microbiota” seems to increase dietary energy absorption and favour weight gain and fat deposition (Compareet al, 2016), although the changes in the microbiota may also be due to a high fat or “obesogenic” diet (Kieler et al, 2016).

The gut microbiota in obese individuals do show changes enabling the microbiota to extract more energy from the diet and interact with host epithelial cells to indirectly control energy expenditure and fat storage.

Another possible effect of the microbiota is to increase gut permeability, which may affect the metabolic inflammatory state seen with obesity (Kobyliak et al, 2016).

Dietary fibre types that function as prebiotics – that is, enhance the growth of beneficial gut bacteria – may shift the microbiome in obese animals to one more similar to that of leaner animals.

Short chain fatty acids (SCFAs) – such as butyrate, acetate and propionate – are produced by the gut bacteria fermentation of dietary fibre. These SCFAs are absorbed and serve as an energy source. They also may act in the gut to regulate energy balance and induce the release of the anorexic peptide YY, which would cause a decrease in appetite (Tilg and Adolph, 2015).

Probiotics may also have a use in modifying the gut bacteria to influence obesity. In mouse studies, some probiotics have shown an inhibition of weight gain in mice on high sugar or high fat diets (Kang et al, 2013; Kondo et al, 2010), although a study in cats using Enterococcus faecium SF68 supplementation did not show any effect on food intake, weight loss or body composition (Kathrani et al, 2016).

As with antibiotics, probiotics are not all the same, and the types and amounts of microorganisms in them have different results in different situations.

Owner factors

5 / 7 Figure 4. Indoor cats are likely to be less active than those that like being outside.

In some studies, the risk of pet obesity increases with decreasing owner income, similar to the risk of human obesity increasing with decreasing income.

The risk of pet obesity increases with increasing owner age, although this is also not affected by the amount of exercise – that is, it appears older owners are not necessarily exercising their dogs less (but perhaps are feeding more?; Courcier et al, 2010).

An association exists between obese owners and obese dogs, but this is not true for cats (Nijland et al, 2010). The association between obese owners and obese dogs also appears to be affected by the amount of time the owners spend walking their dogs.

Summary

While excessive calories definitely will cause weight gain, the tendency to gain weight and the ability to control appetite or begging in pets is driven by many causes. Genetics plays a role, as does the microbiome of the intestines. Educating owners about body condition, feeding and pet exercise is vital.

As we learn more about the effects of gene expression in obesity and the gut microbiome, we will likely find the right diet may also affect these areas, giving us greater control in the pet battle of the bulge and better health for pets.

References

Colliard L, Paragon B, Lemuet B et al (2009). Prevalence and risk factors of obesity in an urban population of healthy cats, J Feline Med Surg 11(2): 135-140. Compare D, Rocco A,

6 / 7 Sanduzzi M et al (2016). The gut bacteria-driven obesity development, Dig Dis 34(3): 221-229. Coucier EA, Thomson RM, Mellor DJ and Yam PS (2010). An epidemiological study of environmental factors associated with canine obesity, J Small Anim Pract 51(7): 362-369. Facett KA and Barroso I (2010). The genetics of obesity: FTO leads the way, Trends Genet 26(6): 266-274. Heuberger R and Wakshlag J (2011). The relationship of feeding patterns and obesity in dogs, J Anim Physiol Anim Nutr (Berl) 95(1): 98-105. Kang JH, Sung IY, Park MH et al (2013). Anti-obesity effect of Lactobacillus gasseri BNR17 in high sucrose diet-induced obese mice, PLoS One 8(1): e54617. Kathrani A, Larsen JA, Kass PH and Fascetti AJ (2016). Effect of short-term probiotic Enterococcus faecium SF68 dietary supplementation in overweight and obese cats without comorbidities, Vet Rec Open 3(1): e000164. Kieler IN, Molbak L, Hansen LL et al (2016). Overweight and the feline gut microbiome – a pilot study, J Anim Physiol Anim Nutr (Berl) 100(3): 478-484. Kobyliak N, Virchenko O and Falalyeyeva T (2016). Pathophysiological role of host microbiota in the development of obesity, Nut J 15(43): 1-12. Kondo S, Xiao JZ, Satoh T et al (2010). Antiobesity effects of Bifidobacterium breve strain B-3 supplementation in a mouse model with high-fat diet-induced obesity, Biosci Biotechnol Biochem 74(8): 1,656-1,661. Lund E, Armstrong PJ, Kirk CA et al (2005). Prevalence and risk factors for obesity in adult cats from private US veterinary practices, Int J Appl Res Vet Med 3(2): 88-98. Lusby AL and Kirk CA (2009). Obesity. In Bonagura JD and Twedt DC (eds), Kirk‘s Current Veterinary Therapy XIV, Saunders Elsevier, St Louis: 191-195. Mankowska M, Stachowiak M, Graczyk A et al (2016). Sequence analysis of three canine adipokine genes revealed an association between TNF polymorphisms and obesity in Labrador dogs, Anim Genet 47(2): 245-249. Murphy M, Lusby AL, Bartges JW and Kirk CA (2012). Size of food bowl and scoop affects amount of food owners feed their dogs, J Anim Physiol Anim Nutr (Berl) 96(2): 237-241. Nijland M, Stam F and Seidell JC (2010). Overweight in dogs, but not in cats, is related to overweight in their owners, Public Health Nutr 13(1): 102-106. Park HJ, Lee SE, Kim HB et al (2015). Association of obesity with serum leptin, adiponectin, and serotonin and gut microflora in beagle dogs, J Vet Intern Med 29(1): 43-50. Pet Food Manufacturers’ Association (2009). Pet obesity report. Raffan E, Dennis RJ, O’Donovan C et al (2016). A deletion in the canine POMC gene is associated with weight and appetite in obesity-prone Labrador retriever dogs, Cell Metabl 23(5): 893-900. Srivastava N, Lakhan R and Mittal A (2007). Pathophysiology and genetics of obesity, Indian J Exp Biol 45(11): 929-936. Tilg H and Adolph TE (2015). Influence of the human intestinal microbiome on obesity and metabolic dysfunction, Curr Opin Pediatr 27(4): 496-501.

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