Obesity is an increasingly prevalent health concern in pet dogs.1 Results of various studies2–4 suggest that between 30% and 40% of pet dogs are overweight and between 5% and 20% of pet dogs are obese. Obese dogs are at risk of developing a variety of health problems, such as endocrinopathies, metabolic abnormalities, orthopedic disorders, cardiorespiratory disease, urogenital dysfunction, and neoplasia, which can lead to premature death.1,5–7 Additionally, obese dogs tend to have serum concentrations of inflammatory cytokines and adipokines that are increased from reference limits and contribute to a chronic subclinical inflammatory state.6,8,9 Therefore, it is important that overweight and obese dogs achieve and maintain a healthy body condition by the implementation of appropriate weight management strategies.
Ideal body condition in dogs is defined as 15% to 25% body fat, and most weight loss plans recommend that energy intake be less than or equivalent to that required to maintain an ideal body condition.7,10 Caloric restriction is the primary means for reducing excessive body weight in overweight dogs.6,10,11 The content of essential micronutrients and amino acids in most commercially available adult maintenance dog foods is adjusted on the basis of normal energy intake, and feeding those foods to dogs during periods of caloric restriction can result in malnutrition or loss of excessive LBM.7,12 Moreover, many owners feel like they are depriving their pets when providing them with smaller volumes of food, which may inadvertently encourage the feeding of table scraps and treats. Compared with maintenance foods, foods formulated for weight loss contain less energy and fat and higher concentrations of essential nutrients and fiber to help ensure adequate nutrition and satiety during periods of energy restriction.7,13–16 An ideal food for weight loss would decrease body fat; maintain or minimize the loss of LBM while providing adequate amounts of minerals, vitamins, antioxidants, and essential fatty acids; and safely promote energy metabolism by stimulating metabolic pathways, thereby increasing energy demand. A food that readily achieves satiety when fed would also be a favorable feature so that dogs would self-regulate their food consumption even in instances when they are offered additional food.
Several nutrients have positive effects on metabolism and might be beneficial when incorporated into a dog food formulated for weight loss. Certain dietary fats can increase energy expenditure at the expense of fat deposition; MCFAs are more readily absorbed and rapidly oxidized than are LCFAs.17 Micronutrient supplementation can increase conversion of dietary fat to energy. Carnitine is an essential cofactor in the transfer of LCFAs from the cytosol into the mitochondria of cells where they undergo β-oxidation; therefore, increasing dietary l-carnitine intake may increase the oxidation of LCFAs.18 Lipoic acid is directly involved in energy metabolism and has antioxidant effects in its reduced form.19 The composition of amino acids in a food may reduce the loss of LBM during periods of restricted energy intake. Supplementation with lysine or leucine reduces protein degradation.20,21 Finally, satiety is achieved by both physiologic (ie, hormonal) and physical mechanisms; an increase in the intake of dietary fiber reduces food consumption.22
The purpose of the study reported here was to determine the effect of feeding a food containing coconut oil and supplemental l-carnitine, lipoic acid, lysine, leucine, and fiber (test food) on weight loss and maintenance in overweight or obese dogs. Our hypotheses were that overweight or obese dogs that were fed the test food would have increased fat catabolism, metabolic pathway stimulation, and LBM retention and achieve satiety quicker, compared with similar dogs that were fed an adult maintenance dog food.
Materials and Methods
The study consisted of 2 trials. All study protocols were reviewed and approved by the Institutional Animal Care and Use Committee of Hill's Pet Nutrition Inc.
Trial 1—The objective of trial 1 was to determine whether feeding a reduced-calorie, high-fiber dry test food that contained coconut oil and supplemental l-carnitine, lipoic acid, lysine, and leucine to overweight or obese dogs would result in weight loss.
Animals and housing
Thirty adult Beagles from an animal research centera were recruited for trial 1. All dogs were cared for in accordance with an internal animal welfare policy; were vaccinated against canine distemper virus, adenovirus, parvovirus, Bordetella bronchiseptica, and rabies; were monitored for endoparasites and ectoparasites; received routine heartworm preventative; and had no evidence of chronic disease as determined by results of a physical examination, CBC, serum biochemical analysis, urinalysis, and fecal examination. Only healthy dogs with a body condition score of 4 (overweight) or 5 (obese) on a scale23 of 1 to 5 as determined by the investigators were included in the trial.
Dogs were housed in groups during the day and in pairs with individual places for sleep during the night. Indoor rooms were spacious with natural light. Dogs had access to outdoor runs, and daily behavioral enrichment was provided with toys and interactions with other dogs and caretakers. The dogs had ad libitum access to water. Each dog was individually fed once daily, and the amount of food consumed was determined by weighing the bowl before and after feeding.
Trial design and protocol
Trial 1 was a 20-week (140-day) prospective, randomized controlled trial that consisted to 3 phases (pretreatment, treatment, and posttreatment). During the pretreatment phase, each dog was fed a commercially available dry weight maintenance food (control food) in an amount calculated to meet the daily energy requirements necessary to sustain its body weight for 4 weeks (28 days). For the 8-week (56-day) treatment phase, each dog was randomly assigned by means of a random number generator to 3 groups (10 dogs/group) to be fed a dry maintenance dog food to maintain body weight (group 1) or a dry test food at the same daily amount (group 2) or caloric energy content (group 3) as the control food fed during the pretreatment phase. Thus, the dogs of group 2 were calorically restricted and the dogs of group 3 were calorically matched, compared with the dogs of group 1. During the 8-week posttreatment phase, all dogs were fed the control food at the same amount as that fed during the pretreatment phase.
Each dog was individually weighed at the initiation of the trial (baseline). For each dog throughout the trial, food intake was recorded daily and body weight was recorded weekly. Criteria for a dog to be removed from the trial included the diagnosis of a severe systemic disease, a body condition score ≤ 2 on a scale of 1 to 5, failure to gain weight following an increase in the daily amount of food offered, refusal to eat at least 25% of the allotted food for 4 consecutive days, or a change in food for 4 consecutive days because of a nonserious health problem.
Study foods
The study foods were purchased and manufactured in 2011 and fed in the same year. The nutrient profiles of the controlb and testc foods were summarized (Appendix). The energy density of each food was determined by use of the modified Atwater equation24,25 as follows: metabolizable energy (kcal/kg on a dry-matter basis) = 10([3.5 × crude protein percentage] + [8.5 × crude fat percentage] + [3.5 × nitrogen-free extract percentage]), where the nitrogen-free extract percentage = 100% – (crude protein percentage + crude fat percentage + crude fiber percentage + moisture percentage + ash percentage). Results of a recent study25 indicate that this equation is superior for the calculation of energy density than is the energy-density equation recommended in 2006 by the National Research Council.26
Both foods were fed as dry kibble. The control food was selected because it contained a similar macronutrient composition and micronutrient profile as other commercially available dry adult maintenance dog foods. Both the control and test foods met the 2009 recommendations (recommendations that were current at the time the trial was conducted) of the Association of American Feed Control Officials for adult maintenance dog food.
Trial 2—The objectives of trial 2 were to determine the efficacy of the test food for weight reduction in overweight and obese dogs and to obtain metabolic data from those dogs to determine the effect of the test food on body composition, serum biochemical analytes, and metabolic processes.
Animals
Twenty Beagles were recruited for the treatment group of trial 2 from the same animal research centera used to recruit the dogs for trial 1. All dogs were cared for and housed in the same manner as that described for trial 1. Only healthy dogs with a body condition score of 4 or 5 on a scale23 of 1 to 5 as determined by the investigators and that had > 30% body fat as determined by DEXA were included in the treatment group for trial 2. Those 20 dogs were compared with dogs in 2 control groups that were maintained in accordance with their normal routines (ie, underwent no interventions).
The first control group consisted of the remaining adult Beagles at the animal research center (n = 341) that were considered to have an IBW. The second control group consisted of a cohort of overweight or obese dogs (n = 20) that were matched on the basis of body composition to the 20 dogs of the treatment group and fed to maintain their overweight state. For each control group, the recorded energy intake was calculated as the mean calories consumed per day by the dogs in that group for the duration of the trial. This method of calculating energy intake was chosen because it represented the mean daily caloric consumption necessary for maintaining the mean body weight of the dogs in a given group. All dogs in both control groups were individually weighed prior to trial initiation (baseline) and then once monthly for the duration of the trial. Each dog was individually fed once daily, and the amount of food consumed was determined by weighing the bowl before and after feeding. Food intake for each dog was adjusted as necessary to maintain its body weight. Prior to trial initiation, all dogs in the treatment and control groups underwent DEXA to accurately assess the body composition of each dog at baseline. We chose to use 2 control groups because we wanted to compare the mean energy intake for the dogs in the treatment group with the mean energy intakes for dogs that had an IBW and that were overweight or obese to assess potential diet-associated changes in basal metabolism among the groups, especially during the weight maintenance phase of the trial.
Trial design and protocol
Trial 2 was an 8-month (32-week) prospective clinical trial that consisted of weight loss and weight maintenance phases. The IBW for each dog was estimated to be 1.2 times the original LBM determined by DEXA, and the resting energy requirement was then estimated as 70 × IBW0.75. During the weight loss phase, dogs in the treatment group were fed the test foodc at a rate of 1.6 resting energy requirement equivalents/d for the first week then the caloric intake was adjusted weekly as necessary to achieve a weight loss rate of approximately 1% to 2%/wk. For each dog, food intake was monitored daily and mean food intake was calculated weekly. Each dog in the treatment group remained in the weight loss phase of the trial for 4 months or until it reached a target body condition of 15% to 25% body fat, whichever came first. Subsequently, the dogs began a 4-month weight maintenance phase, in which each dog was fed the test food in an amount calculated to maintain the body weight attained at the end of the weight loss phase, regardless of whether the dog achieved its target body condition. For the dogs of the treatment group during the weight maintenance phase, body weight was measured weekly and the amount of food offered per day was adjusted weekly as necessary. Dogs in the colony and matched-cohort control groups were fed various foods (all of which met the recommendations of the Association of American Feed Control Officials for an adult maintenance dog food) in amounts calculated to maintain their baseline weight for the duration of the trial. The daily maintenance energy requirement for dogs in both control groups was similar to that estimated by the equation recommended by the National Research Council.26 The criteria for removal of a dog from trial 2 were the same as those for trial 1.
DEXA
Dual-energy x-ray absorptiometry was performed on all dogs at the animal research center at baseline and on dogs in the treatment group monthly by use of a commercially available machine,d which was calibrated prior to each use. For the DEXA procedure, each dog had a catheter aseptically placed in a cephalic vein and was anesthetized with propofol (2 to 4 mg/kg, IV to effect) and then positioned in sternal recumbency on the DEXA table. The head and vertebral column of the dog were aligned along the center line of the table, and the forelimbs were flexed approximately 90° at the carpal joint and positioned below the base of the head. Lean body mass, fat mass, body fat percentage, and bone mineral density and content were calculated with commercially available software.e
Serum biochemical, hormone, and metabolomic analyses
For each dog in the treatment group, food was withheld for at least 12 hours and a blood sample (10 mL) was obtained by jugular venipuncture at baseline and monthly thereafter for the duration of the trial. Serum was harvested from each sample. An automated biochemical analyzerf was used to determine the alkaline aminotransferase and alkaline phosphatase activities and albumin, total bilirubin, BUN, calcium, chloride, cholesterol, creatinine, globulin, glucose, magnesium, phosphorous, potassium, sodium, total protein, and triglyceride concentrations and calculate the albumin-to-globulin, BUN-to-creatinine, and sodium-to-potassium concentration ratios. Serum concentrations of insulin,g IGF-1,h glucagon,i and leptinj were determined only for samples obtained during the weight loss phase by the use of commercially available ELISAs.
Serum metabolomic profile analyses were performed by a commercial laboratoryk for all dogs in the treatment group at baseline and at the end of both the weight loss and weight maintenance phases. Samples were prepared by a proprietary methanol-based solvent extraction method. Extracts with analytes were either split and subjected to derivatization and gas chromatography–mass spectrometry or left underivatized and analyzed by liquid chromatography–mass spectrometry in a randomized order. This method provided identification and relative quantification of small endogenous biochemicals representative of metabolic pathways for amino acids, peptides, carbohydrates, lipids, (eg, fatty acids and lysophospholipids), nucleotides, and vitamin cofactors. Data for each analyte were normalized by calculation of the median value for each run-day block (block normalization) to minimize any interday instrument drift without confounding intraday sample variability. Missing values were assumed to be below the detection limits for that compound with the instrumentation used, and when present, were imputed with the observed minimum for that particular compound. Imputed values were added after block-normalization.
Statistical analysis—For trial 1, distributions of the body weight data were assessed for normality by visual evaluation of graphs. At baseline and after each phase (pretreatment, treatment, and posttreatment), a 1-way ANOVA followed by post hoc t tests was used to determine differences in the mean body weight among the 3 groups. Within each group, a paired t test was used to determine the change in body weight from baseline at the end of each phase.
For trial 2, outcomes of interest included changes in body mass and composition, serum biomarkers, and energy intake. For dogs that achieved an ideal body condition in < 4 months, the last observation carried forward method was used to impute missing values for all variables except intake. Each dog served as its own control, and paired t tests were used to evaluate changes from baseline (month, 0) for body mass, body composition, and serum biomarker outcomes.
A mixed linear regression model that accounted for unequal sample sizes among treatment groups was used to compare the respective energy intakes for dogs in the colony and matched-cohort control groups with that for dogs in the treatment (weight loss) group. For each dog, the body weight was standardized to an IBW, which was defined as follows: IBW = LBM (in kg) as determined by DEXA/0.8. Therefore, metabolic body size (kg0.75) could be used to calculate the energy intake (calories/kg of IBW) without bias associated with the increased adiposity of the overweight or obese dogs.
Metabolomic data were used to develop predictive models for body composition. Lean body mass and fat mass were used as dependent variables, and 232 metabolites detected during metabolomics analysis served as possible independent variables. The adjusted R2 was used to select independent variables for entry into a model and as the stop criterion. The corrected Akaike information criterion was used to select the most appropriate predictive model. The top 10 metabolomic variables from each model were selected for further correlation analysis and calculation of the Pearson correlation coefficients. Then, groups of variables (fatty acids and glyceroesters, carnitines and conjugates, cholesterol and bile acids, BCAAs, lipotropes and energy intermediates) were selected as independent variables to predict which groupings were associated with fat reduction during the weight loss phase. Correction for multiple comparisons was performed by the false discovery rate method, and only metabolites with q ≤ 0.10 (a typical cutoff used in metabolomic analyses27) were retained in the final predictive model. All analyses were performed with commercially available software,l and values of P ≤ 0.05 were considered significant unless otherwise specified.
Results
Trial 1—The 30 dogs recruited for trial 1 included 13 castrated males and 17 spayed females, with a mean ± SE age of 9.3 ± 0.4 years (range, 4 to 14 years). At trial enrollment (baseline), the mean ± SE body weight for all dogs was 18.4 ± 0.5 kg (40.5 ± 1.0 lb). All adverse events were determined to be unrelated to the food consumed. One dog in group 2 was euthanized because of a ruptured spleen caused by a non–study-related event, and data from that dog were excluded from all analyses. Four dogs were administered meloxicam for 7 days at various times during the trial for treatment of neck pain or lameness, and 1 dog was administered trimethoprim sulfa for 7 days for treatment of hematuria. One dog developed acute signs of gastrointestinal discomfort and underwent an exploratory laparotomy; however, the cause of the clinical signs was not identified. The dogs that received medical or surgical intervention were dispersed fairly evenly among all 3 groups, and none were removed from the trial.
The daily amount of food offered and consumed by each of the 3 groups of dogs during each phase (pretreatment, treatment, and posttreatment) of trial 1 were summarized (Table 1). The mean ± SE body weight at the end of each phase for each of the 3 groups was likewise summarized (Table 2). The mean daily grams or calories consumed did not differ significantly among the 3 groups during the pretreatment and posttreatment phases. During the treatment phase, the mean daily grams of food consumed by the dogs in group 3 was significantly greater than that consumed by the dogs in groups 1 and 2; however, the mean daily caloric intake by the dogs in group 3 did not differ significantly from that for the dogs in group 1 and was significantly greater than the mean daily caloric intake for the dogs in group 2. The dogs in group 2 consumed significantly fewer calories during the treatment phase than they did during the pretreatment and posttreatment phases. The mean body weight for dogs in group 1 did not differ significantly from that at baseline at any time during trial 1. For the dogs of groups 2 and 3, the mean body weight was decreased significantly from that at baseline at the end of the treatment phase but then returned to approximately the mean baseline body weight at the end of the posttreatment phase.
Mean ± SE daily amount of food offered and consumed by overweight or obese dogs fed a dry adult maintenance dog food (control food) in an amount estimated to provide the energy required to maintain current body weight (group 1; n = 10) or a dry test food formulated for weight loss that contained coconut oil and supplemental l-carnitine, lysine, leucine, and fiber at the same g/d (group 2; 10) or calories/d (group 3; 10) basis as the maintenance food fed to the dogs of group 1 for 8 weeks (trial 1).
| Amount of food offered | Amount of food consumed | ||||
|---|---|---|---|---|---|
| Phase | Group | Grams | Kcal | Grams | Kcal |
| Pretreatment | 1 | 258.5 ± 7.97 | 990.6 ± 30.55 | 256.1 ± 7.97 | 981.6 ± 30.55 |
| 2 | 261.7 ± 9.90 | 1,003.2 ± 45.23 | 255.2 ± 11.57 | 978.2 ± 44.33* | |
| 3 | 258.6 ± 9.42 | 991.2 ± 36.40 | 255.2 ± 9.20 | 978.2 ± 35.26 | |
| Treatment | 1 | 258.5 ± 7.97 | 990.6 ± 30.55 | 244.8 ± 11.42a | 938.3 ± 43.77a |
| 2 | 255.9 ± 8.53 | 790.7 ± 26.37 | 225.2 ± 9.37a | 695.9 ± 28.93b | |
| 3 | 322.0 ± 11.73 | 995.0 ± 36.24 | 290.0 ± 16.73b | 896.1 ± 51.70a | |
| Posttreatment | 1 | 258.5 ± 7.97 | 990.6 ± 30.55 | 248.8 ± 8.98 | 953.7 ± 34.44 |
| 2 | 261.7 ± 9.90 | 1,003.2 ± 45.23 | 258.9 ± 11.23 | 991.6 ± 43.07* | |
| 3 | 258.6 ± 9.42 | 991.2 ± 36.40 | 255.6 ± 9.58 | 979.7 ± 52.53 | |
Trial 1 had a duration of 20 weeks and consisted of 3 phases (pretreatment, treatment, and posttreatment). During the 4-week pretreatment phase, all dogs were fed the control food in an amount estimated to maintain current body weight. During the 8-week treatment phase, dogs were randomly allocated to 3 groups and fed either the control food or test food as specified. During the 8-week posttreatment phase, all dogs were fed the control food in the same amount as that fed during the pretreatment phase. One dog in group 2 was euthanized because of a ruptured spleen caused by a non–study-related event, and data for that dog were excluded from all analyses; thus, the values for group 2 represent the mean ± SE for 9 dogs.
Value differs significantly (P ≤ 0.05) from the corresponding value for the treatment phase.
Within a column and phase, values with different superscript letters differ significantly (P ≤ 0.05).
Mean ± SE body weight (kg) at the end of each phase of trial 1 for the dogs of Table 1.
| Phase | |||||
|---|---|---|---|---|---|
| Group | Pretreatment | Treatment | Posttreatment | Treatment – pretreatment difference | Tosttreatment – treatment difference |
| 1 | 18.8 ± 0.81 | 18.9 ± 0.90 | 19.0 ± 0.89 | 0.12 ± 0.19a | 0.09 ± 0.12a |
| 2 | 19.2 ± 1.04* | 17.4 ± 0.93 | 18.5 ± 0.95* | –1.81 ± 0.20c | 1.2 ± 0.05c |
| 3 | 18.8 ± 0.84* | 18.2 ± 0.89 | 18.7 ± 0.93* | −0.58 ± 0.17b | 0.50 ± 0.16b |
Within a group, value differs significantly (P ≤ 0.05) from the value for the treatment phase.
Within a column, values with different superscript letters differ significantly (P ≤ 0.05).
See Table 1 for remainder of key.
Trial 2—The 20 dogs recruited for the treatment group of trial 2 included 10 castrated males, 2 sexually intact females, and 8 spayed females with a mean ± SE age of 8.5 ± 0.5 years (range, 5 to 15 years). At trial enrollment (baseline), the dogs had a mean ± SE body weight of 17.6 ± 0.7 kg (38.7 ± 7.0 lb) and body fat percentage of 41 ± 1.1%. No adverse events were recorded, and all 20 dogs completed the trial.
Weight loss phase (months 1 to 4)
During the weight loss phase (months 1 to 4), the 20 dogs of the treatment group lost a mean ± SE of 4,015 ± 270 g of body weight, which included 3,700 ± 250 g of body fat mass and 284 ± 132 g of LBM (Figure 1). Compared with baseline values, the mean body weight and body fat mass were significantly (P < 0.01) decreased at the end of each month of the weight loss phase, and the mean LBM was significantly decreased at the end of months 1 (P = 0.02) and 4 (P = 0.04). The dogs had a mean weight loss rate of 1.4%/wk. At the end of the weight loss phase, the mean ± SE body weight for the dogs was 13.6 ± 0.5 kg (29.9 ± 1.1 lb) and body fat percentage was 26 ± 1.5%, and the total body fat was < 26% for 8 of the 20 (40%) dogs (Figure 2).
Concentrations of all serum biochemical analytes and obesity markers were within the respective reference limits at baseline and throughout the weight loss phase, except the baseline triglyceride concentration, which was slightly above the upper reference limit. The mean ± SE serum triglyceride concentration decreased from 115 ± 2.9 mg/dL at baseline to 60 ± 0.7 mg/dL (reference limits, 8 to 78 mg/dL) at the end of the first month and then remained fairly stable for the remainder of the weight loss phase. The mean ± SE serum cholesterol concentration decreased from 215 ± 1.3 mg/dL at baseline to 162 ± 1.1 mg/dL (reference limits, 107 to 313 mg/dL) at the end of the weight loss phase. Compared with baseline concentrations, the mean serum triglyceride and cholesterol concentrations were significantly (P < 0.01) decreased at the end of each month of the weight loss phase. The mean ± SE serum leptin concentration decreased from 14 ± 0.4 ng/mL at baseline to 4 ± 0.2 ng/mL (reference limits, 0 to 20 ng/mL) at the end of month 4 and was significantly (P < 0.01) lower than the baseline concentration at the end of months 1, 2, 3, and 4. The mean serum glucose, glucagon, insulin, and IGF-1 concentrations remained within the respective reference limits and did not vary significantly from baseline at any time during the weight loss phase.
Weight maintenance phase (months 5 to 8)
Compared with the values at the end of the weight loss phase, the mean body weight did not differ significantly, the mean ± SE LBM increased by 248 ± 112 g (P = 0.04), and the mean ± SE body fat mass decreased by 474 ± 199 g (P = 0.03) for the dogs in the treatment group during the weight maintenance phase (Figure 1). Mean bone mineral density and content did not vary significantly during the weight maintenance phase. At the end the weight maintenance phase, the dogs had a mean ± SE body weight of 13.4 ± 0.5 kg (29.5 ± 1.1 lb) and body fat percentage of 23 ± 1.6%; 15 of the 20 (75%) dogs had a body fat percentage < 27%, and all dogs had a body fat percentage < 35% (Figure 2).
Mean body mass for 20 overweight or obese dogs that were fed a high-protein, high-fiber test food that was formulated for weight loss and contained coconut oil and supplemental l-carnitine, lipoic acid, lysine, and leucine immediately before (baseline) and at the end of each month of a 4-month weight loss phase and 4-month weight maintenance phase (trial 2). Lean body mass (black bars), body fat mass (light gray bars), and bone mass (dark gray bars) were determined monthly by DEXA.
Citation: Journal of the American Veterinary Medical Association 247, 4; 10.2460/javma.247.4.375
Concentrations of all serum biochemical analytes remained within the respective reference limits throughout the weight maintenance phase. The mean ± SE cholesterol concentration increased significantly (P < 0.01) from 162 ± 5 mg/dL at the end of the weight loss phase to 186 ± 6 mg/dL at the end of weight maintenance phase. Serum triglyceride and glucose concentrations remained fairly stable throughout the weight maintenance phase.
Energy intake
The mean calorie consumption for the dogs in the treatment group was significantly (P < 0.01) less during months 1 through 5, did not differ significantly during month 6, and was significantly (P < 0.01) greater during months 7 and 8, compared with the mean calorie consumption for the dogs in the colony and matched-cohort control groups (Figure 3).
Metabolomic profiles
For all dogs in the treatment group, the metabolomic profile results at the end of the weight maintenance phase mimicked those at the end of the weight loss phase unless otherwise specified. Results of the metabolomics analyses indicated that consumption of the test food was associated with changes in serum concentrations of fatty acids, carnitine conjugates, sterols, BCAAs, and energy intermediates. Compared with baseline concentrations, the mean concentration of lauric acid was increased by 2- and 3-fold at the end of the weight loss and weight maintenance phases, respectively; the mean concentrations of carnitine and deoxycarnitine were increased by 30% and mean concentrations of butyryl and glutaryl carnintines were increased by 20% and 60%, respectively; the mean concentration of oleoylcarnitine was increased by 70%, but this increase was not significant; the mean concentrations of cholesterol and the cholesterol metabolite 7-α-hydroxy-3-oxo-4-cholestenoate were decreased by 13% and 37%, respectively; the mean concentration of the bile acid cholate was increased by 3- to 4-fold at the end of the weight loss and weight maintenance phases, respectively; the mean concentrations of BCAA metabolites 2-hydroxyisobutyrate, 3-hydroxyisobutyrate, and hydroxyisovalerylcarnitine were increased between 35% and 75%; and the mean concentrations of the gluconeogenic substrate pyruvate and its redox congener lactate were both decreased by 25%.
Number of dogs from Figure 1 with a body fat percentage of 10% to 15% (blue bars), > 15% to 25% (red bars), > 25% to 35% (green bars), > 35% to 45% (purple bars), and > 45% (black bars) at baseline and at the end of the weight loss and weight maintenance phases. The frequency distribution of dogs among the categories for body fat percentage differed significantly (P < 0.01) between baseline and the end of the weight loss phase and between the end of the weight loss phase and the end of the weight maintenance phase. See Figure 1 for remainder of key.
Citation: Journal of the American Veterinary Medical Association 247, 4; 10.2460/javma.247.4.375
Results of the correlation analyses for all observed metabolites indicated that α-hydroxyisocaproate (adjusted R2= 0.44; P < 0.01) and dimethylglycine (adjusted R2 = 0.40; P < 0.01) were the metabolites most highly correlated with LBM, whereas 1,5-anhydroglucitol (adjusted R2 = 0.80; P < 0.01), glutaroyl carnitine (adjusted R2 = −0.63; P < 0.01), and creatine (adjusted R2 = 0.67; P < 0.01) were the metabolites most highly correlated with fat mass. When the metabolites were apportioned into functionally related biochemical classes, results indicated that metabolites involved in BCAA (cumulative adjusted R2 = 0.72) and carnitine (cumulative adjusted R2 = 0.31) metabolism had significant predictive capacity for determining the percentage of body fat loss.
Mean ± SE metabolic IBW (IBW0.75) for the dogs of Figure 1 (dashed line with brackets), compared with that for a colony control group (dashed and dotted line), which consisted of 341 adult dogs from the same research colony as the dogs from Figure 1 that were considered to have an IBW and did not undergo dietary intervention, and a matched-cohort control group (solid line), which consisted of 20 dogs that were matched to the dogs of Figure 1 on the basis of body composition and fed to maintain their body weight. The dotted lines above and below the mean metabolic IBW line for each control group delimit ± 1 SE. *Value differs significantly (P ≤ 0.05) from the corresponding values for both the colony and matched-cohort control groups. See Figure 1 for remainder of key.
Citation: Journal of the American Veterinary Medical Association 247, 4; 10.2460/javma.247.4.375
Discussion
Results of the present study indicated that overweight and obese dogs lost body weight and body fat mass, yet maintained most of their LBM when fed a restricted amount of a reduced-calorie, high-fiber dry dog food that contained coconut oil and supplemental l-carnitine, lipoic acid, lysine, and leucine. Interestingly, following the restricted intake period, those dogs generally gained LBM and continued to lose body fat despite an increase in volume and caloric consumption to maintain body weight. The metabolomic data and the fact that mean daily caloric consumption for the dogs that were fed the test food in trial 2 was significantly greater than that for the dogs in the colony control group during the weight maintenance phase suggested that the test food had a positive effect on energy metabolism and the metabolic rate of overweight and obese dogs. However, the present study was not designed to investigate the effect of the test food on the energy metabolism and metabolic rate of overweight dogs, and additional research is necessary to explore that theory.
The metabolizable energy of both the control and test foods fed during trial 1 was calculated by the incorporation of nutrient analysis results for the respective foods into the modified Atwater equation, which is an accepted method for estimating the caloric density of a food. Because the metabolizable energy was estimated rather than determined directly, it is possible that the test food contained fewer calories or that the control food contained more calories than estimated. Potential errors in the estimated metabolizable energy content of each food were minimized by the use of data obtained from a nutrient analysis of the food instead of predicted values for the individual components of the food. The most accurate method for determining the metabolizable energy content of a food is a digestibility test. Unfortunately, a digestibility test was not performed on either food fed in the present study. However, digestibility trials have been performed for foods with nutritional profiles similar to the nutrient profiles of the control and test foods fed in the present study, and the metabolizable energy contents determined by those digestibility trials did not differ significantly from the metabolizable energy content estimated by the modified Atwater equations (unpublished data). The fact that the dogs fed the test food during trial 2 were able to maintain their body weight during the weight maintenance phase even though their mean daily caloric consumption was greater than that for the colony control group suggested that fairly small alterations in food composition can cause substantial changes in metabolism over time.
The test food fed to the dogs of the present study was formulated to have a positive effect on energy metabolism. Further research is necessary to investigate whether the effects of the test food on the energy metabolism of overweight dogs can be titrated on the basis of varying the balance between the contents of fat and other nutrients. However, the test food contained specific nutrients that positively affect metabolism and weight loss efficiency in other species.28–31 Coconut oil contains a large amount of MCFA-containing triglycerides and glyceroesters with saturated 8- to 12-carbon fatty acids (eg, lauric acid).17 Pancreatic lipase is able to more readily hydrolyze triglycerides that contain MCFAs than those that contain LCFAs, thus MCFAs are absorbed quicker than are LCFAs.28 Once absorbed, MCFAs are transported as free fatty acids directly to the liver via the portal circulation instead of circulating through the peripheral circulation as re-esterified triglycerides in chylomicrons as LCFAs do.28 In dogs, the proportion of MCFAs that are directly transported to the liver by the portal circulation versus the lymphatic system is unknown; however, the insulin and glucagon response in dogs following consumption of large amounts of MCFAs is not as extreme as that following consumption of LCFAs.29 In the liver, fatty acids are either stored as triglycerides or enter catabolic pathways that include mitochondrial β-oxidation and peroxisomal oxidation. Unlike LCFAs, MCFAs are able to pass from the cytosol through the mitochondrial membrane without carnitine conjugation, which increases their use in β-oxidation.28 Compared with LCFAs, the MCFA lauric acid is a preferred substrate for peroxisomal β-oxidation, a process that does not result in the production of ATP, which contributes to the anabolic processes responsible for weight gain.28 Lauric acid also uncouples ATP production from mitochondrial oxidation, and thereby further decreases the potential for weight gain.30 Finally, MCFAs stimulate carbohydrate metabolism, which increases glycolysis and the demand for glucose to maintain euglycemia.28 Consequently, MCFAs enhance energy expenditure, which contributes to weight loss.
Carnitine is required for β-oxidation of LCFAs in mitochondria. Investigators of other studies18,31 suggest that providing dogs and cats with supplemental l-carnitine may increase mitochondrial oxidation of LCFAs, which will decrease adipose formation and preserve muscle glycogen stores. In cats, l-carnitine supplementation causes a decrease in hepatic concentrations of C16:0 and C16:1 fatty acids, possibly subsequent to an increase in the oxidation of 16-carbon fatty acids, and an increase in hepatic omega-3 and omega-6 fatty acid concentrations.31 In dogs, l-carnitine supplementation causes an increase in the concentrations of docosahexaenoic acid in brain phospholipids, unesterified fatty acids, and total lipids despite a lack of dietary omega-3 fatty acids.18 The investigators of that study18 concluded that MCFAs appear to spare preexisting omega-3 fatty acids from oxidation. Hence, the addition of l-carnitine to a dog food that contains MCFAs may have a beneficial synergistic effect by increasing the metabolic rate and sparing essential fatty acids.
Lipoic acid is a cofactor in the pyruvate dehydrogenase complex, which is responsible for the conversion of pyruvate to acetyl-CoA in mitochondria. Acetyl-CoA is used in the tricarboxylic acid cycle to produce ATP, thereby linking glycolysis with the tricarboxylic acid cycle.32 It is generally assumed that endogenous synthesis of lipoic acid is adequate to meet its metabolic demand, but in older or geriatric animals, the biosynthesis of lipoic acid may not be sufficient to meet the physiologic need and dietary supplementation of lipoic acid may be indicated.33 Lipoic acid also decreases inflammation,34,35 decreases blood glucose concentration in diabetic patients by increasing the uptake of glucose by skeletal muscle,36 and in its reduced form, dihydrolipoic acid, acts as an antioxidant in conjunction with glutathione, vitamin E, and vitamin C.19 In obese patients, controlling oxidative stress and inflammation might be critical for the prevention of organ dysfunction and disease.8,37–42
Results of the present study indicated that feeding overweight and obese dogs a reduced-calorie, high-protein, high-fiber food was associated with weight loss and were similar to the findings of other studies.16,43 Lean body mass is dependent on the quantity and quality of protein (ie, the amino acid profile) in the diet. Insufficient quantities of essential amino acids, particularly lysine, in relation to other amino acids can result in a nitrogen retention plateau.44 Once an animal reaches a nitrogen retention plateau, additional amino acids are catabolized and excess nitrogen is excreted, primarily by the kidneys. Thus, consumption of protein in excess of the minimum requirement will not be beneficial unless that protein has an appropriate balance of amino acids.45 Results of other studies20,43 indicate that increasing the lysine concentration-to-calorie ratio of a food decreases protein degradation and may reduce the loss of muscle mass during periods of restricted caloric intake. In rats fed diets with a high concentration of leucine and an adequate energy (glucose) concentration, protein degradation is inhibited and insulin sensitivity is enhanced, which stimulates protein synthesis.21 The balanced amino acid profile of the test food fed in the present study may explain why the dogs maintained or gained LBM throughout the study.
Dogs fed foods with a high-fiber content (20% to 22%) achieve satiety quicker and have decreased food intake and caloric consumption than do dogs fed foods with a low-fiber content (≤ 2%).45,46 Rats fed diets with MCFAs achieve satiety quicker than do rats fed diets with LCFAs.17 During the treatment phase of trial 1, the mean caloric intake for the dogs of group 3 that were fed the test food did not differ significantly from that for the dogs of group 1 that were fed the control food; however, because the test food had a higher fiber content than the control food, the volume of food consumed was significantly greater for the dogs of group 3, compared with that for the dogs of group 1. Although we cannot draw any conclusions regarding the effect of the test food on satiety from the results of the present study, we believe the test food will be beneficial for weight loss in overweight dogs because it will allow owners to restrict the caloric intake of their dogs without having to change the amount or volume of food fed, which may help alleviate any guilt owners might feel about depriving their pets of food.
In trial 2 of the present study, the loss of body fat was associated with a concurrent decrease in serum triglyceride, cholesterol, and leptin concentrations, a finding that was similar to results of other studies.9,47–50 In obese dogs, decreases in serum triglyceride, cholesterol and leptin concentrations during weight loss are associated with a decrease in insulin resistance.8,47 The metabolomic data of trial 2 indicated that serum concentrations of cholesterol and its metabolites decreased, whereas serum concentrations of the bile acid cholate increased from baseline during the weight loss and weight maintenance phases, which suggested a metabolic shift in which sterols were absorbed and fatty acids were excreted. In other studies8,51,52 the serum insulin, IGF-1, and glucose concentrations of obese dogs decreased during periods of weight loss or maintenance of LBM. We did not observe a decrease in the serum insulin and IGF-1 concentrations for the dogs fed the test food during the weight loss phase of trial 2; however, those concentrations were within the respective reference limits at baseline and remained so for the duration of the trial. At the end of the weight maintenance phase of trial 2, the mean serum cholesterol concentration was increased significantly from that at the end of the weight loss phase, although it was still within the reference limits and was less than that at baseline. In humans, consumption of coconut oil, which contains both lauric and myristic fatty acids, is associated with an increase in serum concentrations of high-density lipoprotein, low-density lipoprotein, and total cholesterol.53 Additional research is necessary to assess the long-term effects of lauric and myristic acid consumption on serum cholesterol and lipoprotein concentrations in dogs.
Evaluation of the metabolomic data obtained during trial 2 of the present study suggested that the primary nutritional components of the test food were bioavailable and metabolically active. Consumption of the test food was associated with an increase in the serum concentrations of lauric acid, carnitine, lysine, and leucine metabolites. Serum concentrations of lauric acid and lysine were not correlated with any of the body composition variables assessed and were not included in the final predictive model for fat loss. Conversely, serum concentrations of glutaroyl and acetyl carnitine were included in the final predictive model for fat loss, and the serum concentration of glutaroyl carnitine was inversely correlated with total fat mass at all times assessed. The serum concentration of α-hydroxyisocaproate, a leucine metabolite that has a positive effect on muscle retention and growth,54,55 was positively correlated with canine LBM. Serum concentrations of BCAAs and their metabolites were also included in the final predictive model for fat loss. These results suggested that the efficacy of the test food for weight loss was at least partly associated with the supplemental l-carnitine and leucine it contained.
Obesity is common in dogs, and weight management in obese dogs can be challenging and frustrating for both owners and veterinarians. Each dog is different, and its basal metabolic rate is affected by multiple factors, such as genetics, activity level, body composition, age, sex and neuter status, and nutrition.1,7 The test food fed to the overweight and obese dogs of the present study successfully reduced total body weight and body fat mass and helped maintain LBM. Interestingly, some dogs that were fed the test food continued to lose total body weight and body fat mass and regain or maintain LBM during the weight maintenance phase of trial 2, despite having a mean daily caloric intake that was significantly increased from that during the weight loss phase and compared with that for the dogs in the colony and cohort-control groups. This suggested that consumption of the test food caused an increase in the basal metabolic rate. However, the metabolic rate was not directly measured in the present study, and we cannot rule out that the continued improvement in the body composition of the dogs during the weight maintenance phase was not caused by an increase in activity secondary to weight loss. Veterinarians should be aware that feeding the test food to overweight and obese dogs in their practices is unlikely to produce the same rapid weight loss as was observed in the dogs of the present study because of the potential for owners to not comply with the prescribed feeding protocol and variations in the activity of individual dogs. The mechanism responsible for the apparent increase in the basal metabolic rate of dogs following consumption of the test food is likely multifactorial, but the unique ingredients and nutrient composition in the test food probably played a pivotal role. Further studies are necessary to determine the exact effect each component of the test food has on the body composition of dogs.
ABBREVIATION
| BCAA | Branched chain amino acid |
| DEXA | Dual-energy x-ray absorptiometry |
| IBW | Ideal body weight |
| IGF | Insulin-like growth factor |
| LBM | Lean body mass |
| LCFA | Long-chain fatty acid |
| MCFA | Medium-chain fatty acid |
Ontario Nutrilab Inc, Fergus, ON, Canada.
Canine Medium Adult 25, Royal Canin USA Inc, St Charles, Mo.
Hill's Prescription Diet Canine Metabolic, Hill's Pet Nutrition Inc, Topeka, Kan.
QDR-4500 Acclaim Series Elite, Hologic Inc, Bedford, Mass.
Apex, version 2.3, Hologic Inc, Bedford, Mass.
Cobas c501 analyzer, Hoffmann-La Roche Ltd, Basel, Switzerland.
Mercodia Canine Insulin ELISA, Mercodia Inc, Winston-Salem, NC.
Human IGF-1 ELISA, R&D Systems Inc, Minneapolis, Minn.
Glucagon Human ELISA (multispecies specificity), BioVendor Inc, Asheville, NC.
Canine Leptin ELISA, Millipore Inc, Billerica, Mass.
MVISION, Metabolon, Durham, NC.
SAS, version 9.0, SAS Institute Inc, Cary, NC.
References
1. German AJ. The growing problem of obesity in dogs and cats. J Nutr 2006; 136: 1940S–1946S.
2. Courcier EA, Thomson RM, Mellor DJ, et al. An epidemiological study of environmental factors associated with canine obesity. J Small Anim Pract 2010; 51: 362–367.
3. 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.
4. 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.
5. Kealy RD, Lawler DF, Ballam JM, et al. Effects of diet restriction on life span and age-related changes in dogs. J Am Vet Med Assoc 2002; 220: 1315–1320.
6. Laflamme DP. Understanding and managing obesity in dogs and cats. Vet Clin North Am Small Anim Pract 2006; 36: 1283–1295.
7. Toll PW, Yamka RM, Schoenherr WD, et al. Obesity. In: Hand M, Thatcher C, Remillard R, et al, eds. Small animal clinical nutrition. 5th ed. Topeka, Kan: Mark Morris Institute, 2010; 501–542.
8. German AJ, Hervera M, Hunter L, et al. Improvement in insulin resistance and reduction in plasma inflammatory adipokines after weight loss in obese dogs. Domest Anim Endocrinol 2009; 37: 214–226.
9. Wakshlag JJ, Struble AM, Levine CB, et al. The effects of weight loss on adipokines and markers of inflammation in dogs. Br J Nutr 2011; 106 (suppl 1):S11–S14.
10. German AJ, Holden SL, Bissot T, et al. Dietary energy restriction and successful weight loss in obese client-owned dogs. J Vet Intern Med 2007; 21: 1174–1180.
11. Butterwick RF, Hawthorne AJ. Advances in dietary management of obesity in dogs and cats. J Nutr 1998; 128: 2771S–2775S.
12. Linder DE, Freeman LM, Morris P, et al. Theoretical evaluation of risk for nutritional deficiency with caloric restriction in dogs. Vet Q 2012; 32: 123–129.
13. Linder DE, Freeman LM. Evaluation of calorie density and feeding directions for commercially available diets designed for weight loss in dogs and cats. J Am Vet Med Assoc 2010; 236: 74–77.
14. Blanchard G, Nguyen P, Gayet C, et al. Rapid weight loss with a high-protein low-energy diet allows the recovery of ideal body composition and insulin sensitivity in obese dogs. J Nutr 2004; 134: 2148S–2150S.
15. Burkholder WJ, Bauer JE. Foods and techniques for managing obesity in companion animals. J Am Vet Med Assoc 1998; 212: 658–662.
16. 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.
17. St-Onge MP, Jones PJH. Physiological effects of medium-chain triglycerides: potential agents in the prevention of obesity. J Nutr 2002; 132: 329–332.
18. Hall JA, Jewell DE. Feeding healthy Beagles medium-chain triglycerides, fish oil, and carnitine offsets age-related changes in serum fatty acids and carnitine metabolites. PLoS ONE [serial online] 2012; 7: e49510. Available at: journals.plos.org/plosone/article?id=10.1371/journal.pone.0049510. Accessed Jun 26, 2013.
19. Paetau-Robinson I, Yamka RM, Friesen KG. Foods with lipoic acid and elevated levels of vitamin E and vitamin C correlate with whole blood antioxidant concentrations and may protect geriatric dogs from oxidative stress. Int J Appl Res Vet Med 2008; 6: 93–100.
20. Reeder T, Hibbard G, McLeod KR, et al. Dietary lysine: calorie ratios and their influence on nitrogen metabolism and digestibility in moderately obese mature dogs. Am J Anim Vet Sci 2011; 6: 45–54.
21. Garlick PJ. The role of leucine in the regulation of protein metabolism. J Nutr 2005; 135: 1553S–1556S.
22. Jewell DE, Toll PW. Effects of fiber on food intake in dogs. Vet Clin Nutr 1996; 3: 115–118.
23. Thatcher CD, Hand MS, Remillard RL. Small animal clinical nutrition: an iterative process. In: Hand M, Thatcher C, Remillard R, et al, eds. Small animal clinical nutrition. 5th ed. Topeka, Kan: Mark Morris Institute, 2010; 6.
24. Darden T. AAFCO official publication. Champaign, Ill: Association of American Feed Control Officials, 2013; 180.
25. Hall JA, Melendez LD, Jewell DE. Using gross energy improves metabolizable energy predictive equations for pet foods whereas undigested protein and fiber content predict stool quality. PLoS ONE [serial online] 2013; 8: e54405. Available at: dx.plos.org/10.1371/journal.pone.0054405. Accessed Nov 12, 2013.
26. National Research Council. Nutrient requirements of dogs and cats. Washington, DC: The National Academies Press, 2006; 31–359.
27. Storey JD, Tibshirani R. Statistical significance for genomewide studies. Proc Natl Acad Sci U S A 2003; 100: 9440–9445.
28. Papamandjaris AA, MacDougall DE, Jones PJH. Minireview—medium chain fatty acid metabolism and energy expenditure: obesity treatment implications. Life Sci 1998; 62: 1203–1215.
29. Böttger I, Dobbs R, Faloona GR, et al. The effects of triglyceride absorption upon glucagon, insulin and gut glucagon-like immunoreactivity. J Clin Invest 1973; 52: 2532–2541.
30. Dlasková A, Spacek T, Skobisová E, et al. Certain aspects of uncoupling due to mitochondrial uncoupling proteins in vitro and in vivo. Biochim Biophys Acta 2006; 1757: 467–473.
31. Ibrahim WH, Bailey N, Sunvold GD, et al. Effects of carnitine and taurine on fatty acid metabolism and lipid accumulation in the liver of cats during weight gain and weight loss. Am J Vet Res 2003; 64: 1265–1277.
32. Reed LJ. Multienzyme complexes. Acc Chem Res 1974; 7: 40–46.
33. Ames BN. Micronutrients prevent cancer and delay aging. Toxicol Lett 1998; 102–103:5–18.
34. Zhang WJ, Wei H, Hagen T, et al. Alpha-lipoic acid attenuates LPS-induced inflammatory responses by activating the phosphoinositide 3-kinase/Akt signaling pathway. Proc Natl Acad Sci U S A 2007; 104: 4077–4082.
35. Sola S, Mir MQ, Cheema FA, et al. Irbesartan and lipoic acid improve endothelial function and reduce markers of inflammation in the metabolic syndrome: results of the Irbesartan and Lipoic Acid in Endothelial Dysfunction (ISLAND) study. Circulation 2005; 111: 343–348.
36. Eason RC, Archer HE, Akhtar S, et al. Lipoic acid increases glucose uptake by skeletal muscles of obese-diabetic ob/ob mice. Diabetes Obes Metab 2002; 4: 29–35.
37. Moschen AR, Molnar C, Geiger S, et al. Anti-inflammatory effects of excessive weight loss: potent suppression of adipose interleukin 6 and tumour necrosis factor alpha expression. Gut 2010; 59: 1259–1264.
38. Tilg H, Moschen AR. Adipocytokines: mediators linking adipose tissue, inflammation and immunity. Nat Rev Immunol 2006; 6: 772–783.
39. Gregor MF, Hotamisligil GS. Inflammatory mechanisms in obesity. Annu Rev Immunol 2011; 29: 415–445.
40. Sonta T, Inoguchi T, Tsubouchi H, et al. Evidence for contribution of vascular NAD(P)H oxidase to increased oxidative stress in animal models of diabetes and obesity. Free Radic Biol Med 2004; 37: 115–123.
41. Urakawa H, Katsuki A, Sumida Y, et al. Oxidative stress is associated with adiposity and insulin resistance in men. J Clin Endocrinol Metab 2003; 88: 4673–4676.
42. Tanner AE, Martin J, Thatcher CD, et al. Nutritional amelioration of oxidative stress induced by obesity and acute weight loss. Compend Contin Educ Pract Vet 2006; 28 (suppl 4):72.
43. Yamka RM, Frantz NZ, Friesen KG. Effects of 3 canine weight loss foods on body composition and obesity markers. Int J Appl Res Vet Med 2007; 5: 125–132.
44. Millward DJ, Layman DK, Tome D, et al. Protein quality assessment: impact of expanding understanding of protein and amino acid needs for optimal health. Am J Clin Nutr 2008; 87 (suppl):1576S–1581S.
45. Jewell DE, Toll PW, Novotny BJ. Satiety reduces adiposity in dogs. Vet Ther 2000; 1: 17–23.
46. Jewell DE, Toll PW, Azain MJ, et al. Fiber but not conjugated linoleic acid influences adiposity in dogs. Vet Ther 2006; 7: 78–85.
47. Jeusette IC, Detilleux J, Shibata H, et al. Effects of chronic obesity and weight loss on plasma ghrelin and leptin concentrations in dogs. Res Vet Sci 2005; 79: 169–175.
48. Jeusette IC, Lhoest ET, Istasse LP, et al. Influence of obesity on plasma lipid and lipoprotein concentrations in dogs. Am J Vet Res 2005; 66: 81–86.
49. Diez M, Michaux C, Jeusette I, et al. Evolution of blood parameters during weight loss in experimental obese Beagle dogs. J Anim Physiol Anim Nutr (Berl) 2004; 88: 166–171.
50. Peña C, Suárez L, Bautista I, et al. Relationship between analytic values and canine obesity. J Anim Physiol Anim Nutr (Berl) 2008; 92: 324–325.
51. Tvarijonaviciute A, Ceron JJ, Holden SL, et al. Obesity-related metabolic dysfunction in dogs: a comparison with human metabolic syndrome. BMC Vet Res 2012; 8: 147.
52. Yamka RM, Friesen KG, Frantz NZ. Identification of canine markers related to obesity and the effects of weight loss on the markers of interest. Int J Appl Res Vet Med 2006; 4: 282–292.
53. Katan MB, Zock PL, Mensink RP. Effects of fats and fatty acids on blood lipids in humans: an overview. Am J Clin Nutr 1994; 60 (suppl):1017S–1022S.
54. Mero AA, Ojala T, Hulmi JJ, et al. Effects of alfa-hydroxy-isocaproic acid on body composition, DOMS and performance in athletes. J Int Soc Sports Nutr 2010; 7: 1.
55. Lang CH, Pruznak A, Navaratnarajah M, et al. Chronic α-hydroxyisocaproic acid treatment improves muscle recovery after immobilization-induced atrophy. Am J Physiol Endocrinol Metab 2013; 305: E416–E428.
Appendix
Nutrient composition of the control and test foods fed to dogs in a study conducted to determine the effect of feeding a food containing coconut oil and supplemental l-carnitine, lipoic acid, lysine, leucine, and fiber on weight loss and maintenance in dogs.
| Nutrient | Control food | Test food |
|---|---|---|
| Total protein* | 30.35 | 30.28 |
| Arginine | 1.85 | 1.58 |
| Cystine | 0.34 | 0.41 |
| Histidine | 0.70 | 0.63 |
| Isoleucine | 1.18 | 1.16 |
| Leucine | 2.76 | 2.96 |
| Total lysine | 1.56 | 1.87 |
| Methionine | 0.52 | 1.13 |
| Phenylalanine | 1.40 | 1.43 |
| Threonine | 1.12 | 1.07 |
| Tryptophan | 0.29 | 0.28 |
| Tyrosine | 0.96 | 0.97 |
| Valine | 1.47 | 1.40 |
| Crude fat† | 14.91 | 11.12 |
| Lauric acid (C12:0) | 0.02 | 0.97 |
| Myristic acid (C14:0) | 0.13 | 0.41 |
| Linoleic acid (C18:2) | 3.22 | 2.09 |
| Linolenic acid (C18:3) | 0.24 | 0.77 |
| Sum of omega-3 fatty acids | 0.42 | 0.76 |
| Sum of omega-6 fatty acids | 3.41 | 2.12 |
| Total dietary fiber | 6.33 | 28.48 |
| Insoluble fiber | 3.49 | 25 |
| Soluble fiber | 2.84 | 3.48 |
| Crude fiber | 1.20 | 12.72 |
| Ash | 6.56 | 6.19 |
| Calcium | 1.47 | 0.99 |
| Chloride | 0.74 | 0.92 |
| Magnesium | 0.12 | 0.21 |
| Phosphorus | 1.08 | 0.86 |
| Potassium | 0.69 | 1.08 |
| Sodium | 0.42 | 0.41 |
| l-carnitine (ppm) | 91 | 391 |
| β-carotene (ppm) | 140 | 421 |
| Lipoic acid (μg/g)‡ | — | 105 |
| Energy (kcal/kg [kcal/cup])‡ | 3,833 (361) | 3,090 (253) |
| Protein (g/calorie)‡ | 7 | 9 |
Values represent the percentage of the diet on a dry-matter basis unless otherwise specified.
Determined by the Kjeldahl method.
Determined by acid hydrolysis.
Predicted on an as-fed basis.
— = Not detected.
