Health has become one of the most important factors for dog owners when choosing a diet for their pets.1 This growing consciousness in health has resulted in a large number of pet foods that boast various claims. Often, these claims mimic trends in human nutrition.1 Low-carbohydrate, high-protein diets have become increasingly popular for both humans and pets.2–4 An increasing number of pet owners believe that dietary carbohydrates are unnecessary and may even be harmful.3 Obesity, diabetes mellitus, cancer, adverse food reactions, and gastrointestinal diseases are common medical concerns for dogs.5–10 Diet, and carbohydrates in particular, plays an important role in the treatment of these conditions. The intent of the information reported here is to provide an overview of dietary carbohydrates in canine nutrition and examine the role of dietary carbohydrates in the treatment of obesity, diabetes mellitus, cancer, and adverse food reactions in dogs. The role of carbohydrates in gastrointestinal health has been reviewed elsewhere.11–13
Carbohydrate Classification
Carbohydrates are broadly classified as simple or complex on the basis of their chemical structure (Figure 1).14 Monosaccharides are the simplest form of carbohydrates and cannot be further broken down by enzymatic digestion. Complex carbohydrates (oligosaccharides and polysaccharides) consist of 3 to 10 or > 10 sugar units, respectively.14 Starch, the most abundant digestible carbohydrate found in plants, contains glucose molecules bound together by α-glycosidic bonds, which undergo enzymatic digestion by α-amylase in the small intestine of mammals.14–16 Dietary fibers are complex carbohydrates that resist enzymatic digestion in the mammalian small intestine owing to μ-glycosidic bonds between the sugar units.14 Dietary fibers are derived from polysaccharides in plant cell walls and can be classified in several ways on the basis of their rate of fermentation by intestinal microbiota, solubility within the colon, and chemical structure.14,15
Schematic diagram depicting the classification of carbohydrates into simple and complex categories on the basis of chemical structure and degree of polymerization. Simple carbohydrates consist of monosaccharides and disaccharides that contain 1 and 2 sugar units, respectively. Complex carbohydrates include oligosaccharides and polysaccharides that contain 3 to 10 or > 10 sugar units, respectively. Notice for oligosaccharides and polysaccharides that the indicated middle unit (dashed lines) would be repeated 1 to 7 times and > 7 times, respectively.
Citation: Journal of the American Veterinary Medical Association 255, 5; 10.2460/javma.255.5.546
Carbohydrate Digestion, Absorption, and Metabolism in Dogs
Carbohydrate digestion in dogs starts with mechanical breakdown of food within the oral cavity. However, because of the extremely limited production of salivary α-amylase in dogs, enzymatic digestion does not commence in the mouth.17 Instead, μ-amylase is released by the pancreas in dogs, which allows efficient digestion of starch in the small intestine.18 Pancreatic μ-amylase in dogs is sensitive to the quantity of starch in the diet; μ-amylase activity will increase with increasing amounts of dietary starch.19,20 Extruded canine diets containing 35% to 40% DM of starch in the form of barley, corn, potato, rice, sorghum, or wheat all have starch digestibility > 99%.21
Once starch is digested, glucose and galactose are actively transported across the mucosal brush border of the small intestines by SGLT1.15 Dogs express the T1R2/T1R3 heterodimer within the sweet receptor of the tongue, which is necessary for the regulation of SGLT1; thus, it is suggested that dogs are able to upregulate SGLT1 in response to the amount of dietary carbohydrates consumed.22 Dogs reportedly have a glucose absorption rate similar to that of humans.23
Energy needs of the body greatly influence the metabolic fate of dietary glucose. Once glucose is absorbed, it can be used for ATP production through glycolysis, stored in the liver and skeletal muscles as glycogen, or converted to fat and stored as adipose tissue.14,15 Glucokinase or hexokinase (or both) are necessary for the first rate-limiting step in glycolysis, wherein glucose is phosphorylated to produce glucose-6-phosphate.14,15 Glucokinase is found in the liver and pancreatic β cells. In contrast to hexokinase, glucokinase is not inhibited by its product glucose-6-phosphate and has a high affinity for glucose, which allows it to be effective when there is an abundance of glucose. As a result, the liver is able to respond appropriately to the consumption of a starch-rich meal and high blood glucose concentrations.15 The activity of glucokinase in dogs increases in a fed state,21 which means that glucose oxidation is upregulated postprandially.16 Storage of excess dietary glucose as glycogen is vital for maintaining homeostasis of blood glucose. Breakdown of these glycogen reserves allows for the endogenous release of glucose when blood concentrations decrease (eg, during periods when food is withheld), which is critical for maintaining blood glucose homeostasis.14
Dietary Carbohydrate Requirements and Self-selected Intake
Dogs do not have a dietary requirement for carbohydrate, except during pregnancy and lactation.24,25 However, dogs have a metabolic requirement for glucose. Similar to other species, certain tissues and cells (eg, brain and RBCs) rely on glucose for energy needs.15 Carbohydrates in pet foods provide a valuable and important source of glucose, but if carbohydrates are provided in insufficient amounts, protein can provide animals with glucose through gluconeogenic pathways. However, consuming dietary carbohydrates provides metabolic benefits by allowing the body to use the carbohydrates as an energy source so that protein can be used for other important anabolic processes (eg, growth, tissue repair, and the immune response). Protein is also a less efficient energy source than carbohydrates because of the requirement for the body to excrete the nitrogenous waste that is a by-product of amino acid gluconeogenesis.14
The metabolic need for glucose in dogs is especially important during gestation and lactation to support increased demands for energy. The use of carbohydrate-free diets during gestation has resulted in adverse consequences, including an increased mortality rate of puppies as well as hypoglycemia and acetonemia in bitches.24,25
Dietary fiber is also not considered an essential requirement for dogs. However, the addition of fiber to the diet helps to maintain a healthy gastrointestinal tract, promotes regular bowel movements, regulates pH within the colon, and contributes to the growth of beneficial bacteria within the gastrointestinal tract.26 Because dietary fiber is not digested by mammalian enzymes, it provides minimal energy to an animal; thus, fiber can be used to reduce energy density of the diet to help promote weight management.27,28
The ratio of protein, fat, and carbohydrate that dogs will naturally select when provided free-choice access to foods with various macronutrient ratios has been a topic of interest. In a controlled environment, dogs selected a low-carbohydrate diet with 7% of ME from carbohydrate, 30% of ME from protein, and 63% of ME from fat.29 It is unknown whether this macronutrient balance promotes optimal health of dogs or can be attributed to taste preference. Although this ratio differs substantially from the recommended allowance of protein (8.8% of ME) and fat (12.4% of ME) established by the NRC,30 it should be mentioned that the values recommended by the NRC are minimum recommendations and do not necessarily support optimal health. In a recent study,31 investigators assessed the food choices of dogs when the factor of flavor was removed and palatability was balanced among the foods provided. In that study,31 dogs typically selected foods with 36% of ME from carbohydrate, 30% of ME from protein, and 41% of ME from fat. Although the percentages of fat and protein selected again were higher than the values recommended by the NRC, the percentage of carbohydrate was comparable to the quantities found in commercial extruded foods formulated for dogs.32
Carbohydrate Content in Evolutionary Diets
Pet dogs are descended from wolves. Investigators of 1 study33 determined that the adaptation to a starch-rich diet was a crucial step in the early domestication of modern dogs. The authors of that study33 performed whole genomic sequencing of dogs and wolves and identified 36 unique genomic regions that contained 122 genes belonging to dogs. Specifically, 10 genes were identified as having key roles in starch digestion and fat metabolism. Additionally, dogs had greater expression of the pancreatic amylase gene and higher activity of that enzyme, compared with results for wolves. Therefore, this evidence indicated that dogs have evolved to digest dietary starch much more efficiently than do gray wolves.33 This is suggested to be a result of the availability of starch-rich food and waste to which ancestors of modern-day dogs grew accustomed as they became domesticated and the genetic adaptations that followed as a result of the consumption of a starch-rich diet.33 However, the proportion of plant matter consumed by wolves can range from 0% to 50% of the overall diet,34–36 which would suggest that wolves can also metabolize substantial amounts of dietary starch and fiber.
Carbohydrates in Conventional Dry and Wet Dog Foods
Dry pet food comprises the largest share of pet food sold in North America (approx 72% of sales).37 Results of a survey published in 2008 indicate that > 80% of dog owners in the United States and Australia fed their dogs at least half of their diet in the form of a commercial dry food.38 More recently, another survey found that 61% of dogs were fed a commercial dry food daily.39 It is believed that extruded dry food is preferred by dog owners because of the convenience, wide variety of products, and economical price.38,40,41 Carbohydrates play a key functional role in extruded kibble by helping create structural integrity.42 To account for the allowance of protein and fat recommended by the NRC, conventional foods formulated for adult dogs can contain up to 78.8% of ME as carbohydrates. Wet foods also contain carbohydrates to achieve the desired amount of gelatinization and texture,43 although wet foods often contain a smaller percentage of carbohydrates than do extruded kibbles.32
Carbohydrates in the Development and Treatment of Conditions
Carbohydrates have an important role in the development as well as the treatment of several conditions in dogs.
Obesity
Obesity is the most common nutritional disorder affecting dogs. The population of overweight and obese dogs has been estimated as 17% to 44% in developed countries.5,44–51 The main contributor to obesity is a positive energy balance (ie, energy consumed is greater than energy expended).52 Certain diseases and pharmaceuticals may also contribute to the development of obesity. In a 2010 study,53 it was reported that 97% of veterinary practices attributed owner-specific factors (eg, lack of exercise and overfeeding) as the cause of obesity in dogs.
Starch consumed in excess of an animal's immediate energy requirements will be stored as glycogen or converted to body fat.14 Contrary to popular belief, the conversion of dietary carbohydrates to body fat is inefficient in humans, even when carbohydrates are consumed in large quantities.54 The conversion of dietary carbohydrates to fat (and storage as body fat) requires much more energy, compared with that required for the storage of dietary fats.55,56 Additionally, because the body's glycogen stores are small, oxidation of carbohydrates is adjusted to match the intake of carbohydrates by an individual person. In comparison, oxidation of fat is not primarily regulated on the basis of intake.54 Data on conversion of dietary carbohydrates to body fat in dogs are not available. Overall, despite the increasing proportion of overweight and obese dogs, little has been published on the topic of carbohydrates and their influence on weight gain. In 1 study,57 adult dogs fed a high-fat diet (51% of ME from fat and 29% of ME from carbohydrate) gained almost twice the amount of body fat, compared with results for those on a high-carbohydrate diet (23% of ME from fat and 59% of ME from carbohydrate) when food was provided ad libitum. However, dogs fed the high-fat diet also consumed 13% more energy. This was likely attributable to the higher energy density of the high-fat diet and positive influence of dietary fat on palatability. Diets with a higher energy density allow dogs to reach daily energy requirements with a smaller food volume, which causes them to be more likely to consume excess amounts of energy.58,59
In humans, a diet with a high glycemic load or that is rich in starch with a high glycemic index may predispose individuals to a higher risk of weight gain and obesity because these foods may have a less satiating effect.60–63 Only a few studies64,65 have been conducted to test the glycemic index of carbohydrate sources for dogs. Additionally, to the authors' knowledge, no studies have been conducted to investigate the impact of the glycemic index or glycemic load on body weight, body composition, or satiety of dogs. Therefore, information regarding starch and its implications in obesity or satiety of dogs is lacking.
Carbohydrate is often vilified as contributing to weight gain or preventing weight loss, and protein is touted as a beneficial macronutrient for weight loss. Thus, high-protein, low-carbohydrate diets, such as the Atkins diet,66 have remained popular as weight-loss diets for humans. Rate of weight loss or time to reach target body weight did not differ significantly between obese dogs fed a high-protein, low-starch diet (protein, 47.5% DM; starch, 5.3% DM) and a medium-protein, medium-starch control diet (protein, 23.8% DM; starch, 23.9% DM), both of which were fed at 40% to 55% of the dogs' maintenance energy requirements.67 However, the authors of that study67 suggested that high protein content in a weight-loss diet may better conserve lean body mass.
Furthermore, there is a large amount of evidence to support the beneficial effects of dietary fiber for overweight and obese humans.68 The consumption of dietary fiber increases the amount of bulk in the gastrointestinal tract, which allows individuals to feel satiated sooner and thereby limit the quantity of food consumed. Soluble fiber also contributes to delayed gastric emptying and slower transit of food through the small intestine, which further promotes satiation.15 Additionally, dietary fiber may be beneficial for weight loss because it reduces the energy density of the diet and may reduce the efficiency of the gastrointestinal tract to digest macronutrients and extract energy.69 There have been inconsistent results regarding the role of dietary fiber in weight loss of dogs.70–76 These inconsistencies likely stem from the variety of sources and quantities of dietary fiber investigated. However, the inclusion of dietary fiber in weight-loss diets for dogs has provided greater effects on satiation, reductions in body fat, a higher percentage of weight loss, and reductions in voluntary energy intake.71,73,75–77
Diabetes mellitus
Diabetes mellitus is an endocrine disorder that results in hyperglycemia because of insufficient insulin production or decreased insulin sensitivity. The prevalence of diabetes in dogs is believed to have increased during the past 40 years.6 It is estimated that 1.2% of dogs will develop diabetes mellitus before they are 2 years old.7 The autoimmune destruction of β cells, as occurs in humans with type 1 diabetes mellitus, is a common feature of diabetes mellitus in dogs.78 The development of diabetes mellitus in dogs is believed to be a multifactorial phenomenon and can be influenced by a variety of environmental and genetic factors (eg, breed and sex).7,8,79,80 A large proportion of dogs with diabetes mellitus also have pancreatitis.81–87 Thus, it is thought that damage to the pancreatic β cells as a result of chronic or acute pancreatitis could lead to the development of diabetes mellitus in dogs.
Because dogs most commonly develop diabetes mellitus that resembles type 1 diabetes mellitus in humans, carbohydrate intake is generally not considered a risk factor in the pathogenesis of the disease in dogs. Thus, the likelihood that carbohydrate intake will lead to diabetes mellitus in dogs is less of a concern, in contrast to humans and cats, which may develop type 2 diabetes mellitus as a result of chronic hyperglycemia and insulin resistance.88 The authors are not aware of any studies that have been conducted to investigate the relationship between carbohydrate intake and the development of diabetes mellitus in dogs. However, because pancreatitis has been identified as a potential risk factor for the development of diabetes mellitus in dogs,81–87 the amount of fat in a diet should be considered for dogs with both pancreatitis and diabetes mellitus.
Chronic consumption of diets with a low glycemic index or glycemic load by humans has been linked to improved glucose control, insulin sensitivity, and an overall lower risk of developing diabetes mellitus.63,89,90 However, as previously mentioned, there is currently a paucity of studies on the effects of the glycemic index and glycemic load in dogs. Few studies have focused on glycemic response. Investigators of 1 study91 found that the starch content of commercial dog foods has a substantial impact on postprandial glucose concentrations, although the starch sources of the diets were not reported. In addition, feeding pulses or foods that have a low glycemic index (eg, peas and lentils) for humans may also result in a reduced glycemic response in dogs. Feeding of such pulses can cause delayed and prolonged glycemic and insulinemic responses when used as a single ingredient or included in extruded diets.32,64,65 However, the potential physiologic benefits of long-term feeding of diets with a low glycemic index or glycemic load and impacts on the development of diabetes mellitus in dogs currently are unknown.
Veterinarians often consider dietary carbohydrate intake for dogs with diabetes mellitus. Dietary starch intake can be a major determinant of the postprandial glycemic response, regardless of the type of carbohydrate, carbohydrate source, or diet macronutrient profile.91 However, reducing the percentage of carbohydrate in a diet can increase the percentage of fat, which may be contraindicated for diabetic dogs. High-fat diets and hypertriglyceridemia are possible causes of pancreatitis,92,93 and subclinical pancreatitis is difficult to identify in diabetic dogs.94 Dietary fat may also diminish insulin sensitivity and predispose animals to weight gain.57,95 Therefore, it is prudent to consider a diet with low to moderate amounts of fat for all diabetic dogs. In contrast to simply reducing carbohydrate intake, day-to-day consistency in carbohydrate intake in conjunction with insulin treatment is a key component for the management of dogs with diabetes mellitus.96 In general, foods containing < 55% digestible carbohydrate (DM basis) are acceptable for dogs with diabetes mellitus, especially in conjunction with dietary fiber supplementation.97–99 Additionally, modification to the type of carbohydrate in a diet may be considered (including avoiding simple sugars) as well as the addition of dietary fiber to a diet.100 In contrast to simple sugars, starch must be broken down and digested before it is absorbed. As a result, the postprandial glucose and insulin responses after the consumption of these complex carbohydrates will be lower, compared with the responses after ingestion of simple sugars.101
The role of dietary fiber in the management of diabetes mellitus in dogs has been extensively evaluated. The viscosity of fiber allows it to impair and slow the absorption of dietary glucose into the blood, which results in reduced glycemic responses.43,102–104 Both diabetic and healthy dogs have lower blood glucose concentrations and smaller fluctuations in blood glucose concentrations when fed diets with a higher percentage of fiber, which may help to maintain blood glucose homeostasis.105,106 Fiber sources investigated have included soluble (ie, guar gum, pectin, and carboxymethyl cellulose) and insoluble (ie, cellulose) fiber.98,107 However, the role of dietary fiber in improving long-term disease outcomes in diabetic dogs has not been evaluated.
Cancer
Nutrition plays a key role in the prevention and management of cancer. It is estimated that 25% of dogs develop cancer at some point during their lifetime.8 However, research concerning nutrition and cancer in dogs is limited. The effects of carbohydrates on cancer in humans have been an emerging topic of investigation as a result of the altered glucose metabolism in malignant cells.
Because many types of cancer cells rely on glycolysis for energy demands,108–110 the role of simple carbohydrates in the development and progression of cancer has been of special interest. Specifically, hyperglycemia leading to hyperinsulinemia has been investigated to determine effects on cancer progression and survival rates.111–115 Research concerning insulin and malignant cell proliferation in vitro has revealed a positive correlation,115 but in vivo data in mice have not provided conclusive evidence of a positive effect.116–118 The authors are not aware of any similar studies on carbohydrate metabolism and cancer in dogs.
Alterations in macronutrient metabolism have been detected for both human and canine cancer patients.118–123 Because cancer cells rely on anaerobic metabolism for energy needs, simple carbohydrates are converted into lactate.124 Consequently, dogs with lymphoma have higher insulin and lactate concentrations, compared with concentrations in healthy dogs, even after remission following chemotherapy.120,121 As a result, a diet containing a lower concentration of simple carbohydrates and higher concentrations of protein and fat has been suggested for dogs with cancer.125 Effects of diet on energy expenditure and cancer cachexia in dogs have been evaluated.126 In that study,126 dogs with lymphoma received isocaloric amounts of a high-fat (36.87% DM) or high-carbohydrate (58.10% DM) diet. Although the authors reported no significant effect of diet on energy expenditure, conclusions on diet efficacy could not be drawn for this study because analyses of survival time and remission duration were not performed. Similarly, there have been no clinically relevant findings regarding the potential of low-carbohydrate diets for the treatment of cancer in humans.127,128
Adverse food reactions
Adverse food reactions can be described as an abnormal response to the ingestion of a specific food or ingredient.129 Adverse food reactions can be categorized as nonimmunologic (ie, dietary intolerances) or immunologic (ie, dietary allergies or hypersensitivities).129 The prevalence of adverse food reactions among dogs admitted to dermatology referral centers ranges from 7.6% to 12%.10,130 Of dogs with adverse food reactions, 9% to 30.6% have clinical signs compatible with atopy.10,130,131 Similarly, a systematic review of the literature revealed that common gastrointestinal signs (eg, vomiting and diarrhea) occurred in > 20% of dogs and cats with adverse food reactions.132 There is a paucity of published studies regarding the prevalence of adverse food reactions in the general population of dogs because adverse food reactions often mimic clinical signs of other diseases and can often coexist with other types of allergies, such as environmental allergies and flea bite allergies.133
Any dietary protein can potentially be allergenic; however, the most commonly reported food allergens for dogs include beef, dairy, chicken, and wheat.134,135 Carbohydrates typically are not a concern as an allergen, but the protein in carbohydrate-rich products (eg, wheat or soy) typically used in the manufacture of pet food can be responsible for adverse food reactions in some animals.134–136 It has been estimated that wheat and soy are responsible for 13% to 15%135,136 and 6%135,136 of adverse food reactions in dogs, respectively.
Similar to the situation in humans, gluten intolerance may also affect dogs. However, gluten intolerance in dogs is extremely rare and has been well described in only 2 families of Irish Setters.137 Gluten intolerance is linked to the protein fraction of some grains, rather than to the starch or carbohydrate fraction. More specifically, gluten intolerance arises because of the alcohol-soluble protein known as gliadin found within gluten. Gliadin can be found in wheat, barley, and rye.138 The exact prevalence of gluten intolerance in Irish Setters as well as the general population of dogs remains unknown. The cause for the development of gluten intolerance in these dogs also warrants further investigation,139,140 although it has been speculated that an increase in mucosal permeability may play a role in the condition.139,141,142
Inadequate activity of intestinal disaccharidase, as occurs during lactose intolerance, can also affect dogs. Clinical signs of disaccharide intolerance in dogs are similar to those in humans and include diarrhea and bloating.143 Disaccharide intolerance results from a lack of disaccharidase activity in the intestinal brush border and may occur as a result of rapid dietary changes or enteritis.144 Consequently, a transition period of several days is recommended when changing diets fed to dogs to allow for the adaptation to other carbohydrate sources and alterations in their respective disaccharidase activities.144
Modification of the amount of carbohydrate in diets is typically not required for the management of adverse food reactions.144 However, choosing a highly digestible or novel carbohydrate source is often recommended. Highly digestible carbohydrates may be beneficial for patients because of the possibility of malabsorption resulting from inflammation in the gastrointestinal tract.144
Clinical Summary
Despite the large number of dog owners who are averse to feeding carbohydrates to their pets, there is little evidence to support the contention that any negative health effects result from feeding diets that provide dietary carbohydrates in amounts (30% to 60% DM) commonly found in commercial extruded pet foods. There appears to be no association between dietary carbohydrate and the development of obesity, diabetes mellitus, cancer, or adverse food reactions in dogs. In fact, dogs appear to have evolved so that they can metabolize substantial quantities of carbohydrate. Increasing the amount of complex carbohydrates in diets results in the reduction of dietary protein or fat (or both), which may provide benefits for dogs with certain conditions, such as obesity, diabetes mellitus with concurrent pancreatitis, or adverse food reactions.
Acknowledgments
Support for Ms. Rankovic was provided by a grant from Mitacs Accelerate in partnership with Petcurean Pet Nutrition.
Dr. Adolphe is an employee of PPN Ltd Partnership (Petcurean). Dr. Verbrugghe is the Royal Canin Veterinary Diet Endowed Chair in Canine and Feline Clinical Nutrition at the Ontario Veterinary College.
The authors declare that there were no conflicts of interest.
ABBREVIATIONS
| DM | Dry matter |
| ME | Metabolizable energy |
| NRC | National Research Council |
| SGLT1 | Sodium-dependent glucose transporter-I |
References
1. Agriculture and Agri-Food Canada. Pathfinder—global dog and cat food trends. Available at: www.agr.gc.ca/eng/industry-markets-and-trade/international-agri-food-market-intelligence/pathfinder-global-dog-and-cat-food-trends. Accessed Oct 15, 2018.
2. Michel KE. Unconventional diets for dogs and cats. Vet Clin North Am Small Anim Pract 2006;36:1269–1281.
3. Buff PR, Carter RA, Bauer JE, et al. Natural pet food: a review of natural diets and their impact on canine and feline physiology. J Anim Sci 2014;92:3781–3791.
4. Knight C. “We can't go back a hundred million years” low-carbohydrate dieters’ responses to nutritional primitivism. Food Cult Soc 2015;18:441–461.
5. Lund EM, Armstrong PJ, Kirk CA, et al. Prevalence and risk factors for obesity in adult dogs from private US veterinary practices. Int J Appl Res Vet Med 2006;4:177–186.
6. Guptill L, Glickman L, Glickman N. Time trends and risk factors for diabetes mellitus in dogs: analysis of Veterinary Medical Data Base records (1970–1999). Vet J 2003;165:240–247.
7. Fall T, Hamlin HH, Hedhammar A, et al. Diabetes mellitus in a population of 180,000 insured dogs: incidence, survival, and breed distribution. J Vet Intern Med 2007;21:1209–1216.
8. Adams VJ, Evans KM, Sampson J, et al. Methods and mortality results of a health survey of purebred dogs in the UK. J Small Anim Pract 2010;51:512–524.
9. Gaschen FP, Merchant SR. Adverse food reactions in dogs and cats. Vet Clin North Am Small Anim Pract 2011;41:361–379.
10. Chesney CJ. Food sensitivity in the dog: a quantitative study. J Small Anim Pract 2002;43:203–207.
11. Flickinger EA, Fahey GC. Pet food and feed applications of inulin, oligofructose and other oligosaccharides. Br J Nutr 2002;87(suppl 2):S297–S300.
12. Deng P, Swanson KS. Gut microbiota of humans, dogs and cats: current knowledge and future opportunities and challenges. Br J Nutr 2015;113(suppl 1):S6–S17.
13. Hooda S, Minamoto Y, Suchodolski JS, et al. Current state of knowledge: the canine gastrointestinal microbiome. Anim Health Res Rev 2012;13:78–88.
14. Nelson DL, Cox MM. Carbohydrates and glycobiology. In: Lehinger principles of biochemistry. 5th ed. New York: WH Freeman, 2008;235–270.
15. Gropper SS, Smith JL, Groff JL. Carbohydrates. In: Advanced nutrition and human metabolism. 5th ed. Belmont, Calif: Wadsworth Publishing, 2009;63–104.
16. Hoenig M. Carbohydrate metabolism and pathogenesis of diabetes mellitus in dogs and cats. Prog Mol Biol Transl Sci 2014;121:377–412.
17. Contreras-Aguilar MD, Tecles F, Martínez-Subiela S, et al. Detection and measurement of alpha-amylase in canine saliva and changes after an experimentally induced sympathetic activation. BMC Vet Res 2017;13:1–6.
18. Bednar GE, Patil AR, Murray SM, et al. Starch and fiber fractions in selected food and feed ingredients affect their small intestinal digestibility and fermentability and their large bowel fermentability in vitro in a canine model. J Nutr 2001;131:276–286.
19. Kienzle E. Enzymaktivität in pancreas, darmwand und chymus des hundes in abhängigkeit von alter und futterart. J Anim Physiol Anim Nutr (Berl) 1988;60:276–288.
20. Kienzle E. Carbohydrate metabolism of the cat 1. Activity of amylase in the gastrointestinal tract of the cat. J Anim Physiol Anim Nutr (Berl) 1993;69:92–101.
21. Murray SM, Fahey GC, Merchen NR, et al. Evaluation of selected high-starch flours as ingredients in canine diets. J Anim Sci 1999;77:2180–2186.
22. Batchelor DJ, Al-Rammahi M, Moran AW, et al. Sodium/glucose cotransporter-1, sweet receptor, and disaccharidase expression in the intestine of the domestic dog and cat: two species of different dietary habit. Am J Physiol Integr Comp Physiol 2011;300:R67–R75.
23. Pagliassotti MJ, Holste LC, Moore MC, et al. Comparison of the time courses of insulin and the portal signal on hepatic glucose and glycogen metabolism in the conscious dog. J Clin Invest 1996;97:81–91.
24. Romsos DR, Palmer HJ, Muiruri KL, et al. Influence of a low carbohydrate diet on performance of pregnant and lactating dogs. J Nutr 1981;111:678–689.
25. Kienzle E, Meyer H. The effects of carbohydrate-free diets containing different levels of protein on reproduction in the bitch. In: Burger IH, Rivers JPW, eds. Nutrition of the dog and cat: Waltham symposium number 7. Cambridge, England: Cambridge University Press, 1989;243–257.
26. Campos-Vega R, Oomah BD, Vergara-Castaneda HA. In vivo and in vitro studies on dietary fiber and gut health. In: Hosseinian F, Oomah BD, Campos-Vega R, eds. Dietary fiber functionality in food and nutraceuticals—from plant to gut. Chichester, England: John Wiley & Sons, 2017; 123–177.
27. Blundell JE, Burley VJ. Satiation, satiety and the action of fibre on food intake. Int J Obes 1987;11:9–25.
28. Jewell DE, Toll PW, Azain MJ, et al. Fiber but not conjugated linoleic acid influences adiposity in dogs. Vet Ther 2006;7:78–85.
29. Hewson-Hughes AK, Hewson-Hughes VL, Colyer A, et al. Geometric analysis of macronutrient selection in breeds of the domestic dog, Canis lupus familiaris. Behav Ecol 2013;24:293–304.
30. National Research Council. Nutrient requirements and dietary nutrient concentrations. In: Nutrient requirements of dogs and cats. Washington, DC: The National Academies Press, 2006;359–360.
31. Hall JA, Vondran JC, Vanchina MA, et al. When fed foods with similar palatability, healthy adult dogs and cats choose different macronutrient compositions. J Exp Biol 2018;221:1–11.
32. Carciofi AC, Takakura FS, De-Oliveira LD, et al. Effects of six carbohydrate sources on dog diet digestibility and post-prandial glucose and insulin response. J Anim Physiol Anim Nutr (Berl) 2008;92:326–336.
33. Axelsson E, Ratnakumar A, Arendt ML, et al. The genomic signature of dog domestication reveals adaptation to a starch-rich diet. Nature 2013;495:360–364.
34. Bosch G, Hagen-Plantinga EA, Hendriks WH. Dietary nutrient profiles of wild wolves: insights for optimal dog nutrition? Br J Nutr 2015;113(suppl 1):S40–S54.
35. Zlatanova D, Ahmed A, Valasseva A, et al. Adaptive diet strategy of the wolf (Canis lupus L.) in Europe: a review. Acta Zool Bulg 2014;66:439–452.
36. Watts DE, Newsome SD. Exploitation of marine resources by wolves in southwestern Alaska. J Mammal 2017;98:66–76.
37. Packaged Facts. Pet food in the US 13th edition. Available at: www.packagedfacts.com/Pet-Food-13th-Edition-11295405/. Accessed Jun 15, 2018.
38. Laflamme DP, Abood SK, Fascetti AJ, et al. Pet feeding practices of dog and cat owners in the United States and Australia. J Am Vet Med Assoc 2008;232:687–694.
39. Dodd SA, Cave NJ, Adolphe JL, et al. Plant-based (vegan) diets for pets: a survey of pet owner attitudes and feeding practices. PLoS One 2019;14:e02108086.
40. Connolly KM, Heinze CR, Freeman LM. Feeding practices of dog breeders in the United States and Canada. J Am Vet Med Assoc 2014;245:669–676.
41. Michel KE, Willoughby KN, Abood SK, et al. Attitudes of pet owners toward pet foods and feeding management of cats and dogs. J Am Vet Med Assoc 2008;233:1699–1703.
42. Abd El-khalek E. Janssens GP. Effect of extrusion processing on starch gelatinisation and performance in poultry. Worlds Poult Sci J 2010;66:53–64.
43. Karr-Lilienthal LK, Merchen NR, Grieshop CM, et al. Selected gelling agents in canned dog food affect nutrient digestibilities and fecal characteristics of ileal cannulated dogs. Arch Tierernahr 2002;56:141–153.
44. Jerico MM, Scheffer KC. Epidemiological aspects of obese dogs in the city of Sao Paulo. Clin Vet (São Paulo) 2002;37:25–29.
45. Edney AT. Management of obesity in the dog. Vet Med Small Anim Clin 1974;69:46–49.
46. Robertson ID. The association of exercise, diet and other factors with owner-perceived obesity in privately owned dogs from metropolitan Perth, WA. Prev Vet Med 2003;58:75–83.
47. Lund EM, Armstrong PJ, Kirk CA, et al. Health status and population characteristics of dogs and cats examined at private veterinary practices in the United States. J Am Vet Med Assoc 1999;214:1336–1341.
48. Vandendriessche VL, Picavet P, Hesta M. First detailed nutritional survey in a referral companion animal population. Anim Physiol Anim Nutr (Berl) 2017;101:4–14.
49. Montoya-Alonso JA, Bautista-Castaño I, Peña C, et al. Prevalence of canine obesity, obesity-related metabolic dysfunction, and relationship with owner obesity in an obesogenic region of Spain. Front Vet Sci 2017;4:1–4.
50. Mao J, Xia Z, Chen J, et al. Prevalence and risk factors for canine obesity surveyed in veterinary practices in Beijing, China. Prev Vet Med 2013;112:438–442.
51. McGreevy PD, Thomson PC, Pride C, et al. Prevalence of obesity in dogs examined by Australian veterinary practices and the risk factors involved. Vet Rec 2005;156:695–702.
52. German AJ. The growing problem of obesity in dogs and cats. J Nutr 2006;136:1940S–1946S.
53. Bland IM, Guthrie-Jones A, Taylor RD, et al. Dog obesity: veterinary practices’ and owners’ opinions on cause and management. Prev Vet Med 2010;94:310–315.
54. Flatt JP. Use and storage of carbohydrate and fat. Am J Clin Nutr 1995;61:952S–959S.
55. Shah M, McGovern P, French S, et al. Comparison of a low-fat, ad libitum complex-carbohydrate diet with a low-energy diet in moderately obese women. Am J Clin Nutr 1994;59:980–984.
56. Acheson KJ, Schutz Y, Bessard T, et al. Nutritional influences on lipogenesis and thermogenesis after a carbohydrate meal. Am J Physiol 1984;246:E62–E70.
57. Romsos DR, Hornshuh MJ, Leveille GA. Influence of dietary fat and carbohydrate on food intake, body weight and body fat of adult dogs. Proc Soc Exp Biol Med 1978;157:278–281.
58. Stubbs J, Ferres S, Horgan G. Energy density of foods: effects on energy intake. Crit Rev Food Sci Nutr 2000;40:481–515.
59. Rolls BJ, Bell EA. Intake of fat and carbohydrate: role of energy density. Eur J Clin Nutr 1999;53(suppl 1):S166–S173.
60. Rosén LA, Ostman EM, Björck IM. Effects of cereal breakfasts on postprandial glucose, appetite regulation and voluntary energy intake at a subsequent standardized lunch; focusing on rye products. Nutr J 2011;10:1–11.
61. Ball SD, Keller KR, Moyer-Mileur LJ, et al. Prolongation of satiety after low versus moderately high glycemic index meals in obese adolescents. Pediatrics 2003;111:488–494.
62. Ludwig DS, Majzoub JA, Al-Zahrani A, et al. High glycemic index foods, overeating, and obesity. Pediatrics 1999;103:E26.
63. Augustin LSA, Kendall CWC, Jenkins DJA, et al. Glycemic index, glycemic load and glycemic response: an International Scientific Consensus Summit from the International Carbohydrate Quality Consortium (ICQC). Nutr Metab Cardiovasc Dis 2015;25:795–815.
64. Adolphe JL, Drew MD, Huang Q, et al. Postprandial impairment of flow-mediated dilation and elevated methylglyoxal after simple but not complex carbohydrate consumption in dogs. Nutr Res 2012;32:278–284.
65. Adolphe JL, Drew MD, Silver TI, et al. Effect of an extruded pea or rice diet on postprandial insulin and cardiovascular responses in dogs. J Anim Physiol Anim Nutr (Berl) 2015;99:767–776.
66. Atkins RC. Why Atkins works. In: Dr. Atkins’ diet revolution. New York: Bantam Books, 1981;1–90.
67. Diez M, Nguyen P, Jeusette I, et al. Weight loss in obese dogs: evaluation of a high-protein, low-carbohydrate diet. J Nutr 2002;132(suppl 2):1685S–1687S.
68. Slavin JL. Dietary fiber and body weight. Nutrition 2005;21:411–418.
69. Burton-Freeman B. Dietary fiber and energy regulation. J Nutr 2000;130:272S–275S.
70. Butterwick RF, Markwell PJ. Effect of amount and type of dietary fiber on food intake in energy-restricted dogs. Am J Vet Res 1997;58:272–276.
71. Weber M, Bissot T, Servet E, et al. A high-protein, high-fiber diet designed for weight loss improves satiety in dogs. J Vet Intern Med 2007;21:1203–1208.
72. Yamka RM, Frantz NZ, Friesen KG. Effects of 3 canine weight loss foods on body composition and obesity markers. J Appl Res Vet Med 2007;5:125–132.
73. Jackson JR, Laflamme DP, Owens SF. Effects of dietary fiber content on satiety in dogs. Vet Clin Nutr 1997;4:130–134.
74. Bosch G, Verbrugghe A, Hesta M, et al. The effects of dietary fibre type on satiety-related hormones and voluntary food intake in dogs. Br J Nutr 2009;102:318–325.
75. Hours MA, Sagols E, Junien-Castagna A, et al. Erratum to: Comparison of voluntary food intake and palatability of commercial weight loss diets in healthy dogs and cats. BMC Vet Res 2017;13:36.
76. German AJ, Holden SL, Bissot T, et al. A high protein high fibre diet improves weight loss in obese dogs. Vet J 2010;183:294–297.
77. Borne AT, Wolfsheimer KJ, Truett AA, et al. Differential metabolic effects of energy restriction in dogs using diets varying in fat and fiber content. Obes Res 1996;4:337–345.
78. Catchpole B, Kennedy LJ, Davison LJ, et al. Canine diabetes mellitus: from phenotype to genotype. J Small Anim Pract 2008;49:4–10.
79. Hess RS, Kass PH, Ward CR. Breed distribution of dogs with diabetes mellitus admitted to a tertiary care facility. J Am Vet Med Assoc 2000;216:1414–1417.
80. Marmor M, Willeberg P, Glickman LT. Epizootiologic patterns of diabetes mellitus in dogs. Am J Vet Res 1982;43:465–470.
81. Alejandro R, Feldman EC, Shienvold FL, et al. Advances in canine diabetes mellitus research: etiopathology and results of islet transplantation. J Am Vet Med Assoc 1988;193:1050–1055.
82. Ling GV, Lowenstine LJ, Pulley LT, et al. Diabetes mellitus in dogs: a review of initial evaluation, immediate and long-term management, and outcome. J Am Vet Med Assoc 1977;170:521–530.
83. Pápa K, Máthé Á, Abonyi-Tóth Z, et al. Occurrence, clinical features and outcome of canine pancreatitis (80 cases). Acta Vet Hung 2011;59:37–52.
84. Hume DZ, Drobatz KJ, Hess RS. Outcome of dogs with diabetic ketoacidosis: 127 dogs (1993–2003). J Vet Intern Med 2006;20:547–555.
85. Watson PJ, Archer J, Roulois AJ, et al. Observational study of 14 cases of chronic pancreatitis in dogs. Vet Rec 2010;167:968–976.
86. Bostrom BM, Xenoulis PG, Newman SJ, et al. Chronic pancreatitis in dogs: a retrospective study of clinical, clinicopathological, and histopathological findings in 61 cases. Vet J 2013;195:73–79.
87. Mattin MJ, O'Neill DG, Church DB, et al. An epidemiological study of diabetes mellitus in dogs attending first opinion practice in the UK. Vet Microbiol 2014;174:1–7.
88. Rand JS, Fleeman LM, Farrow HA, et al. Canine and feline diabetes mellitus: nature or nurture? J Nutr 2004;134 (suppl 8):2072S–2080S.
89. Ludwig DS. The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. JAMA 2002;287:2414–2423.
90. Barclay AW, Petocz P, McMillan-Price J, et al. Glycemic index, glycemic load, and chronic disease risk—a meta-analysis of observational studies. Am J Clin Nutr 2008;87:627–637.
91. Nguyen P, Dumon H, Biourge V, et al. Glycemic and insulinemic responses after ingestion of commercial foods in healthy dogs: influence of food composition. J Nutr 1998;128:2654S–2658S.
92. Williams DA. Diagnosis and management of pancreatitis. J Small Anim Pract 1994;35:445–454.
93. Simpson KW. Current concepts of the pathogenesis and pathophysiology of acute pancreatitis in dog and cat. Compend Contin Educ Pract Vet 1993;15:247–253.
94. Wiberg ME, Nurmi A-K, Westermarck E. Serum trypsinlike immunoreactivity measurement for the diagnosis of subclinical exocrine pancreatic insufficiency. J Vet Intern Med 1999;13:426–432.
95. Rocchini AP, Marker P, Cervenka T. Time course of insulin resistance associated with feeding dogs a high-fat diet. Am J Physiol 1997;272:E147–E154.
96. Behrend E, Holford A, Lathan P, et al. 2018 AAHA diabetes management guidelines for dogs and cats. J Am Anim Hosp Assoc 2018;54:1–21.
97. Zicker SC, Nelson RW, Kirk CA, et al. Endocrine disorders. In: Hand MS, Thatcher CD, Remillard RL, eds. Small animal clinical nutrition. 5th ed. Topeka, Kan: Mark Morris Institute, 2010;559–584.
98. Nelson RW, Ihle SL, Lewis LD, et al. Effects of dietary fiber supplementation on glycemic control in dogs with alloxan-induced diabetes mellitus. Am J Vet Res 1991;52:2060–2066.
99. Nelson RW, Duesberg CA, Ford SL, et al. Effect of dietary insoluble fiber on control of glycemia in dogs with naturally acquired diabetes mellitus. J Am Vet Med Assoc 1998;212:380–386.
100. Graham PA, Maskell IE, Rawlings JM, et al. Influence of a high fiber diet on glycaemic control and quality of life in dogs with diabetes mellitus. J Small Anim Pract 2002;43:67–73.
101. Jenkins DJ, Wolever TM, Taylor RH. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981;34:362–366.
102. Riccardi G, Rivellese A, Pacioni D, et al. Separate influence of dietary carbohydrate and fibre on the metabolic control in diabetes. Diabetologia 1984;26:116–121.
103. Jenkins DJ, Taylor RH, Wolever TM. The diabetic diet, dietary carbohydrate and differences in digestibility. Diabetologia 1982;23:477–484.
104. O'Connor N, Tredger J, Morgan L. Viscosity differences between various guar gums. Diabetologia 1981;20:612–615.
105. Holt S, Carter DC, Tothill P, et al. Effect of gel fibre on gastric emptying and absorption of glucose and paracetamol. Lancet 1979;1:636–639.
106. Brenelli SL, Campos SD, Saad MJ. Viscosity of gums in vitro and their ability to reduce postprandial hyperglycemia in normal subjects. Braz J Med Biol Res 1997; 30:1437–1440.
107. Blaxter AC, Cripps PJ, Gruffydd-Jones TJ. Dietary fibre and post prandial hyperglycaemia in normal and diabetic dogs. J Small Anim Pract 1990;31:229–233.
108. Klement RJ, Kämmerer U. Is there a role for carbohydrate restriction in the treatment and prevention of cancer? Nutr Metab (Lond) 2011;8:1–16.
109. Warburg O. Uber den stoffwechsel der karzinomezellen. Biochem Z 1924;152:309–344.
110. Devic S. Warburg effect—a consequence or the cause of carcinogenesis? J Cancer 2016;7:817–822.
111. Denley A, Carroll JM, Brierley GV, et al. Differential activation of insulin receptor substrates 1 and 2 by insulin-like growth factor-activated insulin receptors. Mol Cell Biol 2007;27:3569–3577.
112. Melnik BC, John SM, Schmitz G. Over-stimulation of insulin/IGF-1 signaling by Western diet may promote diseases of civilization: lessons learnt from Laron syndrome. Nutr Metab (Lond) 2011;8:1–4.
113. Sengupta S, Peterson TR, Sabatini DM. Regulation of the mTOR complex 1 pathway by nutrients, growth factors, and stress. Mol Cell 2010;40:310–322.
114. Sun Q, Chen X, Ma J, et al. Mammalian target of rapamycin up-regulation of pyruvate kinase isoenzyme type M2 is critical for aerobic glycolysis and tumor growth. Proc Natl Acad Sci U S A 2011;108:4129–4134.
115. Masur K, Vetter C, Hinz A, et al. Diabetogenic glucose and insulin concentrations modulate transcriptom and protein levels involved in tumour cell migration, adhesion and proliferation. Br J Cancer 2011;104:345–352.
116. Ho VW, Leung K, Hsu A, et al. A low carbohydrate, high protein diet slows tumor growth and prevents cancer initiation. Cancer Res 2011;71:4484–4493.
117. Moulton CJ, Valentine RJ, Layman DK, et al. A high protein moderate carbohydrate diet fed at discrete meals reduces early progression of N-methyl-N-nitrosourea-induced breast tumorigenesis in rats. Nutr Metab (Lond) 2010;7:1–7.
118. Fokidis HB, Chin MY, Ho VW, et al. A low carbohydrate, high protein diet suppresses intratumoral androgen synthesis and slows castration-resistant prostate tumor growth in mice. J Steroid Biochem Mol Biol 2015;150:35–45.
119. Mazzaferro EM, Hackett TB, Stein TP, et al. Metabolic alterations in dogs with osteosarcoma. Am J Vet Res 2001;62:1234–1239.
120. Vail DM, Ogilvie GK, Wheeler SL, et al. Alterations in carbohydrate metabolism in canine lymphoma. J Vet Intern Med 1990;4:8–11.
121. Ogilvie GK, Vail DM, Wheeler SL, et al. Effects of chemotherapy and remission on carbohydrate metabolism in dogs with lymphoma. Cancer 1992;69:233–238.
122. Dodesini AR, Benedini S, Terruzzi I, et al. Protein, glucose and lipid metabolism in the cancer cachexia: a preliminary report. Acta Oncol 2007;46:118–120.
123. Sakurai Y, Klein S. Metabolic alteration in patients with cancer: nutritional implications. Surg Today 1998;28:247–257.
124. Heber D, Byerley LO, Chi J, et al. Pathophysiology of malnutrition in the adult cancer patient. Cancer 1986;58(suppl 8):1867–1873.
125. Ogilvie GK. Interventional nutrition for the cancer patient. Clin Tech Small Anim Pract 1998;13:224–231.
126. Ogilvie GK, Walters LM, Salman MD, et al. Energy expenditure in dogs with lymphoma fed two specialized diets. Cancer 1993;71:3146–3152.
127. Champ CE, Palmer JD, Volek JS, et al. Targeting metabolism with a ketogenic diet during the treatment of glioblastoma multiforme. J Neurooncol 2014;117:125–131.
128. Schmidt M, Pfetzer N, Schwab M, et al. Effects of a ketogenic diet on the quality of life in 16 patients with advanced cancer: a pilot trial. Nutr Metab (Lond) 2011;8:54.
129. Cianferoni A, Spergel JM. Food allergy: review, classification and diagnosis. Allergol Int 2009;58:457–466.
130. Proverbio D, Perego R, Spada E, et al. Prevalence of adverse food reactions in 130 dogs in Italy with dermatological signs: a retrospective study. J Small Anim Pract 2010;51:370–374.
131. Wilhelm S, Favrot C. Futtermittelhypersensitivitäts-dermatitis beim hund: möglichkeiten der diagnose. Schweiz Arch Tierheilkd 2005;147:165–171.
132. Mueller RS, Olivry T. Critically appraised topic on adverse food reactions of companion animals (6): prevalence of noncutaneous manifestations of adverse food reactions in dogs and cats. BMC Vet Res 2018;14:341.
133. Kennis RA. Use of atopic dogs to investigate adverse reactions to food. J Am Vet Med Assoc 2002;221:638–640.
134. Roudebush P. Ingredients and foods associated with adverse reactions in dogs and cats. Vet Dermatol 2013;24:293–294.
135. Mueller RS, Olivry T, Prélaud P. Critically appraised topic on adverse food reactions of companion animals (2): common food allergen sources in dogs and cats. BMC Vet Res 2016;12:9.
136. Verlinden A, Hesta M, Millet S, et al. Food allergy in dogs and cats: a review. Crit Rev Food Sci Nutr 2006;46:259–273.
137. Polvi A, Garden OA, Houlston RS, et al. Genetic susceptibility to gluten sensitive enteropathy in Irish Setter dogs is not linked to the major histocompatibility complex. Tissue Antigens 1998;52:543–549.
138. Wieser H. Chemistry of gluten proteins. Food Microbiol 2007;24:115–119.
139. Garden OA, Manners HK, Sórensen SH, et al. Intestinal per meability of Irish Setter puppies challenged with a controlled oral dose of gluten. Res Vet Sci 1998;65:23–28.
140. Batt RM, McLean L, Carter MW. Sequential morphologic and biochemical studies of naturally occurring wheat-sensitive enteropathy in Irish Setter dogs. Dig Dis Sci 1987;32:184–194.
141. Hall EJ, Batt RM. Differential sugar absorption for the assessment of canine intestinal permeability: the cellobiose/mannitol test in gluten-sensitive enteropathy of Irish Setters. Res Vet Sci 1991;51:83–87.
142. Hall EJ, Batt RM. Abnormal permeability precedes the development of a gluten sensitive enteropathy in Irish Setter dogs. Gut 1991;32:749–753.
143. Mundt HC, Meyer H. Pathogenesis of lactose-induced diarrhoea and its prevention by enzymatic-splitting of lactose. In: Burger IH, Rivers JPW, eds. Nutrition of the dog and cat: Waltham symposium number 7. Cambridge, England: Cambridge University Press, 1989;267–274.
144. Roudebush P, Guilford WG, Jackson HA. Adverse reactions to food. In: Hand MS, Thatcher CD, Remillard RL, eds. Small animal clinical nutrition. 5th ed. Topeka, Kan: Mark Morris Institute, 2010;609–636.
