Obesity is a prevalent and growing health problem in pet cats.1 Investigators of various studies2–6 have estimated that 25% to 40% of pet cats are overweight or obese. Overweight and obese cats are at an increased risk for a variety of health problems, such as diabetes mellitus, hepatic lipidosis, oral disease, dermatopathies, orthopedic disorders, cardiovascular disease, lower urinary tract disease, and neoplasias, which may lead to premature death.1,2,7 Furthermore, obese animals tend to be in a chronic, subclinical systemic inflammatory state because serum concentrations of inflammatory cytokines and adipokines are increased above reference limits, which may exacerbate disease.7,8 Consequently, it is important that overweight cats achieve and maintain a healthy body condition with appropriate weight management strategies.
Ideal body condition in cats is defined as 15% to 25% body fat.9 Daily energy intake less than or equal to that required to maintain IBW is recommended for weight loss plans9; therefore, limited caloric intake is the principal approach for the reduction of excessive body weight in overweight or obese cats.7,10 In standard adult maintenance pet foods, amino acid and essential micronutrient contents are adjusted on the basis of normal energy intake; thus, the use of one of those foods for caloric restriction may cause malnutrition and loss of LBM.9 Compared with maintenance foods, foods formulated for weight loss contain less energy and fat and higher concentrations of essential amino acids, vitamins, minerals, and fiber so that adequate nutrition is provided during periods of caloric restriction.9,11,12 An ideal food for weight loss would decrease body fat by safely stimulating energy metabolism, maintain LBM while providing adequate amounts of essential nutrients, and promote healthy body weight management by decreasing markers of inflammation and oxidative stress and improving insulin sensitivity.
Several nutrients have positive effects on metabolism, lean tissue preservation, and insulin regulation. Certain dietary fats increase energy expenditure at the expense of fat deposition; MCFAs are more readily absorbed and rapidly oxidized than are LCFAs.13 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 LCFA oxidation.14–16 The amino acid composition of a food may reduce the loss of LBM during periods of restricted energy intake. Supplementation with lysine or leucine decreases or prevents protein degradation.17,18 Finally, protein and fiber are involved in the control of glycemia, which may help minimize the risk of diabetes mellitus.19,20
The purpose of the study reported here was to determine the effect of feeding a food containing coconut oil and supplemental l-carnitine, lysine, leucine, and fiber (test food) on weight loss and maintenance in overweight or obese cats. Our hypotheses were that overweight cats fed the test food would lose body fat and maintain LBM despite being offered either the same amount of calories or the same amount of grams as similar cats that were fed a commercially available weight maintenance food (control food), that the cats fed the test food would regain weight when switched to the control food, and that the cats fed the test food would maintain the weight attained during a weight loss phase when calorie intake was returned to maintenance requirements. We also predicted that serum concentrations of biochemical analytes and obesity indicators (insulin, IGF-1, and leptin) would remain within reference limits for all cats throughout the study, whereas the metabolomic data for the cats fed the test food would suggest that the coconut oil, l-carnitine, lysine, leucine, and fiber contained in that food were bioavailable and used in vivo.
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 a reduced-calorie, high-fiber dry test food that contained coconut oil and supplemental l-carnitine, lysine, and leucine provided additional benefits for weight loss and maintenance in overweight cats that were previously fed a commercially available weight maintenance food.
Animals and housing
Thirty cats from a research colonya were recruited for trial 1. All cats were cared for in accordance with an internal animal welfare policy, were routinely vaccinated, 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 cats with a body condition score of 4 (overweight) or 5 (obese) on a scale21 of 1 to 5 as determined by 2 investigators were included in the trial.
Cats were housed indoors in groups in spacious rooms with natural light that varied with the season. Daily behavioral enrichment was provided with toys and interaction with other cats and caretakers. The cats had ad libitum access to water. Each cat was offered a specified amount of fresh food daily by the use of individual electronic feeders that identified each cat by its microchip and monitored the amount of food it consumed by the change in the weight of the food bowl at the beginning and end of each feeding session. The allotted daily portion of food was available beginning in the morning, and cats had unlimited access to the electronic feeders throughout the day until the food was consumed. For each day, once the allotted portion of food was consumed, the feeder would no longer open for that cat until the following morning when the next day's food became available.
Trial design and protocol
Trial 1 was a 20-week (140-day) prospective randomized controlled trial that consisted of 3 phases (pretreatment, treatment, and posttreatment). During the pretreatment phase, each cat 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, cats were randomly assigned by means of a random number generator to 3 groups (10 cats/group) to be fed a dry maintenance cat 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 cats of group 2 were calorically restricted and the cats of group 3 were calorically matched, compared with the cats of group 1. During the 8-week (56-day) posttreatment phase, all cats were fed the control food at the same amount as that fed during the pretreatment phase.
Each cat was individually weighed at the initiation of the trial (baseline). For each cat throughout the trial, food intake was recorded daily and body weight was recorded weekly. Criteria for a cat 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 equation22 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 study23 indicate that this equation is superior for calculation of energy density than is the energy-density equation recommended in 2006 by the National Research Council.24 The control food was selected because it contained a similar macronutrient composition and micronutrient profile as other commercially available dry adult maintenance cat foods. Both the control and test foods met the 2009 recommendations (recommendations that were current at the time the trial was conducted) of the AAFCO for an adult maintenance cat food.
Trial 2—The objectives of trial 2 were to determine the efficacy of the test food for weight reduction in overweight and obese cats and to obtain metabolic data from those cats to determine the effect of the test food on body composition, serum biochemical analytes, and metabolic processes.
Animals and housing
Twenty cats were recruited for the treatment group of trial 2 from the same research colonya used to recruit the cats for trial 1. All cats were cared for and housed in the same manner as that described for trial 1. Only healthy cats with a body condition score of 4 or 5 on a scale21 of 1 to 5 as determined by 2 investigators and that had > 30% body fat as determined by DEXA were included in the treatment group for trial 2. Those 20 cats were compared with cats 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 cats in the research colonya (n = 418) that were considered to have an IBW. The second control group consisted of a cohort of overweight or obese cats (n = 20) that were matched on the basis of body composition to the 20 cats 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 cats in that group for the duration of the trial. This method of calculating energy intake was chosen because it represented the mean caloric consumption necessary for maintaining the mean body weight of the cats in a given group. All cats in both control groups were individually weighed prior to trial initiation (baseline) and then once monthly for the duration of the trial. Food intake for each cat was adjusted as necessary to maintain its body weight. Prior to trial initiation, all cats in the treatment and control groups underwent DEXA to accurately assess the body composition of each cat at baseline. We chose to use 2 control groups because we wanted to compare the mean energy intake for the cats of the treatment group with the mean energy intakes for cats 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. All foods fed throughout the trial were in the form of dry kibble. The IBW for each cat was estimated as 1.2 times the original LBM determined by DEXA, and the resting energy requirement was estimated as 70 × IBW0.75. During the weight loss phase, cats in the treatment group were fed the test foodc at a rate of 0.8 resting energy requirement equivalents/d during the first week then caloric intake was adjusted as necessary to achieve a weight loss rate of approximately 1%/wk. For each cat, food intake was monitored daily and mean food intake was calculated weekly. Each cat 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 cats began a 4-month weight maintenance phase, in which each cat 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 cat achieved its target body condition. For the cats 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. Cats in the colony and matched-cohort control groups were fed various foods (all of which met the recommendations of the AAFCO for an adult maintenance cat food) in amounts calculated to maintain their baseline weight for the duration of the trial. The daily maintenance energy requirement for cats in both control groups was similar to that estimated by the equation recommended by the National Research Council.24 The criteria for removal of a cat from trial 2 were the same as those for trial 1.
DEXA
Dual-energy x-ray absorptiometry was performed on all cats in the research colony at baseline and on cats 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 cat was anesthetized and positioned in sternal recumbency on the DEXA table. Isoflurane was administered via a face mask when necessary to maintain anesthesia for the duration of the procedure. The head and vertebral column of the cat 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 cat in the treatment group, food was withheld for at least 12 hours and a blood sample (9 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 ALT and alkaline phosphatase activities and albumin, total bilirubin, BUN, calcium, chloride, cholesterol, creatinine, globulin, glucose, magnesium, phosphorus, potassium, sodium, total protein, and triglyceride concentrations and calculate the albumin-to-globulin, BUN-to-creatinine, and sodium-to-potassium concentration ratios. Serum insulin,g IGF-1,h and leptini concentrations were determined by use of commercially available ELISAs.
Serum metabolomic profile analyses were performed by a commercial laboratoryj for all cats 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 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 cats 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 cat served as its own control, and paired t tests were used to evaluate the respective 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 cats in the colony and matched-cohort control groups with that for cats in the treatment (weight loss) group. For each cat, the body weight was standardized to an IBW 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 cats.
Metabolomic data were used to develop predictive models for body composition. Lean body mass and fat mass were used as dependent variables, and the 264 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, groupings of variables (fatty acids and glyceroesters, carnitines and conjugates, cholesterol and bile acids, BCAAs, lipotropes, and energy intermediates) were selected as the independent variables for models in which LBM and fat mass were the dependent 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 analyses25) were retained in the final predictive model. All analyses were performed with commercially available software,k and values of P ≤ 0.05 were considered significant unless otherwise specified.
Results
Trial 1—The 30 cats recruited for trial 1 included 18 castrated males and 12 spayed females with a mean ± SE age of 9.3 ± 1.7 years (range, 7 to 13 years). At trial enrollment (baseline), the mean ± SE body weight for all cats was 6.38 ± 0.2 kg (14.04 ± 0.5 lb). One cat in group 3 was removed from the trial during the treatment phase because of poor food intake, and data for that cat were excluded from all analyses. All other adverse events were determined to be unrelated to the cat food fed.
The daily amount of food offered and consumed by each of the 3 groups of cats 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). During the treatment phase, cats in group 1 consumed significantly more calories/d than did the cats in groups 2 and 3. Cats in groups 2 and 3 consumed significantly fewer calories during the treatment phase than they did during the pretreatment and posttreatment phases. The mean body weight for cats in group 1 did not differ significantly from that at baseline at any time during trial 1. For the cats 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 cats fed a dry adult maintenance cat 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 cats of group 1 for 8 weeks (trial 1).
| Amount of food offered | Amount of food consumed | ||||
|---|---|---|---|---|---|
| Phase | Group | Grams | Kcal | Grams | Kcal |
| Pretreatment | 1 | 87.7 ± 4.90 | 335.8 ± 18.78 | 74 ± 5.88 | 283.4 ± 22.53 |
| 2 | 87.6 ± 2.94 | 335.5 ± 11.19 | 68 ± 4.78 | 260.4 ± 18.28 | |
| 3 | 88.1 ± 3.35 | 337.4 ± 12.84 | 75 ± 4.14 | 287.3 ± 15.87 | |
| Treatment | 1 | 87.7 ± 4.90 | 335.8 ± 18.78 | 71 ± 6.32 | 271.9 ± 24.22* |
| 2 | 83.7 ± 2.78 | 274.0 ± 9.12 | 65.8 ± 3.45 | 215.4 ± 11.29† | |
| 3 | 103.1 ± 4.13 | 337.0 ± 13.43 | 68.3 ± 4.83 | 223.5 ± 15.83† | |
| Posttreatment | 1 | 87.7 ± 4.90 | 335.8 ± 18.78 | 69 ± 7.65 | 264.3 ± 29.31 |
| 2 | 87.6 ± 2.94 | 335.5 ± 11.19 | 79.3 ± 3.76 | 303.7 ± 14.42‡ | |
| 3 | 88.1 ± 3.53 | 337.4 ± 13.53 | 78.5 ± 4.50 | 300.6 ± 17.23‡ | |
Trial 1 had a duration of 20 weeks and consisted of 3 phases (pretreatment, treatment, and posttreatment). During the 4-week pretreatment phase, all cats were fed the control food in an amount estimated to maintain current body weight. During the 8-week treatment phase, cats were randomly allocated to 3 groups and fed either the control food or test food as specified. During the 8-week posttreatment phase, all cats were fed the control food in the same amount as that fed during the pretreatment phase. One cat in group 3 was removed from the trial during the treatment phase because of poor intake and was excluded from all analyses; thus, the values for group 3 represent the mean ± SE for 9 cats.
Within a phase, value differs significantly (P ≤ 0.05) from the corresponding values for groups 2 and 3.
Value differs significantly (P ≤ 0.05) from the corresponding value during the pretreatment phase.
Value differs significantly (P ≤ 0.05) from the corresponding value during the treatment phase.
Mean ± SE body weight (kg) at the end of each phase of trial 1 for the cats of Table 1.
| Phase | |||||
|---|---|---|---|---|---|
| Group | Pretreatment | Treatment | Posttreatment | Treatment – pretreatment difference | Posttreatment – treatment difference |
| 1 | 6.6 ± 0.51 | 6.7 ± 0.54 | 6.6 ± 0.57 | 0.07 ± 0.08a | –0.05 ± 0.07a |
| 2 | 6.6 ± 0.35* | 6.3 ± 0.35 | 6.6 ± 0.38* | –0.23 ± 0.04b | 0.33 ± 0.04b |
| 3 | 6.6 ± 0.41* | 6.3 ± 0.37 | 6.6 ± 0.40* | –0.3 ± 0.09b | 0.27 ± 0.07b |
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 cats recruited for the treatment group of trial 2 included 13 castrated males and 7 spayed females with a mean ± SE age of 8.2 ± 0.5 years (range, 4 to 11 years). At trial enrollment (baseline), the cats had a mean ± SE body weight of 6.56 ± 0.3 kg (14.4 ± 0.66 lb) and body fat percentage of 40 ± 1.6%. All adverse events were determined to be unrelated to the cat food fed. One cat died acutely of severe hemoperitoneum caused by a generalized hepatocellular carcinoma during the weight maintenance phase of the trial, and data for that cat were excluded from all analyses that involved that phase.
Weight loss phase (months 1 to 4)
During the weight loss phase (months 1 to 4), the 20 cats of the treatment group lost a mean ± SE of 1,559 ± 106 g of body weight, which included 1,348 ± 105 g of body fat mass and 204 ± 30 g of LBM (Figure 1). Compared with baseline values, the mean body weight, body fat mass, and LBM were significantly decreased at the end of each of the 4 months of the weight loss phase. The cats had a mean weight loss rate of 1.25%/wk. At the end of the weight loss phase, the mean ± SE body weight for the cats was 5.0 ± 0.27 kg (11.0 ± 0.59 lb) and body fat percentage was 26.1 ± 1.5%, and the total body fat was < 26% for 10 of the 20 (50%) cats (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. However, from baseline to the end of the weight loss phase, the mean ± SE serum triglyceride concentration decreased from 43 ± 0.7 mg/dL to 29 ± 0.4 mg/dL (reference limits, 3 to 77 mg/dL), creatinine concentration decreased from 1.25 ± 0.01 mg/dL to 1.00 ± 0.1 mg/dL (reference limits, 0.8 to 1.8 mg/dL), and cholesterol concentration decreased from 158 ± 2.0 mg/dL to 143 ± 2.0 mg/dL (reference limits, 69 to 205 mg/dL). Compared with baseline concentrations, the serum triglyceride, creatinine, and cholesterol concentrations were significantly decreased at the end of each month of the weight loss phase. Serum glucose concentration remained stable and within the reference limits throughout the weight loss phase. Mean ± SE serum leptin concentration decreased from 2.9 ± 0.1 ng/mL at baseline to 1.6 ± 0.1 ng/mL (reference limits, 0 to 20 ng/mL) at the end of month 4 and was significantly decreased from the baseline concentration at the end of month 2 (P < 0.01), 3 (P = 0.04), and 4 (P = 0.01). Mean ± SE serum IGF-1 concentration decreased from 5.0 ± 0.1 ng/mL to 3.9 ± 0.1 ng/mL from baseline to the end of month 4 and was significantly (P < 0.01) decreased from the baseline concentration at the end of each month. The serum insulin concentration did not differ significantly from the baseline concentration and remained within the reference limits throughout the weight loss phase.
Weight maintenance phase (months 5 to 8)
Compared with values at the end of the weight loss phase, the mean ± SE LBM increased by 152 ± 42 g (P < 0.01), body fat mass decreased by 276 ± 52 g (P < 0.01), and body weight decreased by 123 ± 57 g (P = 0.04) for the cats 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 of the weight maintenance phase, the cats had a mean ± SE body weight of 4.9 ± 0.25 kg (10.78 ± 0.55 lb) and body fat percentage of 20.7 ± 1.7%, and 15 of the remaining 19 cats had a body fat percentage < 26% (Figure 2).
Concentrations of all serum biochemical analytes and obesity markers were within the respective reference limits at baseline and throughout the weight maintenance phase. However, from the end of the weight loss phase to the end of the weight maintenance phase, the mean ± SE serum triglyceride concentration increased from 29 ± 1.8 mg/dL to 51 ± 6 mg/dL (P < 0.01), ALT activity increased from 48 ± 2.4 mg/dL to 60 ± 4 mg/dL (reference limits, 25 to 87 mg/dL; P < 0.01), total bilirubin concentration increased from 0.09 ± 0.01 mg/dL to 0.15 ± 0.01 mg/dL (reference limits, 0 to 0.2 mg/dL; P < 0.01), and BUN concentration increased from 17 ± 0.7 mg/dL to 23 ± 0.9 mg/dL (reference limits, 15 to 30 mg/dL; P < 0.01). Mean ± SE serum creatinine concentration decreased from 1.00 ± 0.04 mg/dL to 0.92 ± 0.04 mg/dL (P < 0.01) and glucose concentration decreased from 79 ± 3.5 mg/dL to 68 ± 4 mg/dL (reference limits, 52 to 141 mg/dL; P < 0.01) from the end of the weight loss phase to the end of the weight maintenance phase. Serum cholesterol concentration remained stable throughout the weight maintenance phase. Mean ± SE serum IGF-1 concentration increased from 3.9 ± 0.4 ng/mL at the end of month 4 to 4.8 ± 0.4 ng/mL at the end of month 8 and was significantly (P < 0.01) increased from the concentration at the end of the weight loss phase and at the end of months 6, 7, and 8. The serum insulin and leptin concentrations did not differ significantly from the corresponding concentrations at the end of the weight loss phase and remained within the respective reference limits throughout the weight maintenance phase.
Energy intake
Compared with the mean calorie consumption for cats in the colony control group, the mean calorie consumption for cats in the treatment group was significantly (P < 0.01) less during months 1 through 6 and greater during month 8. Compared with the mean calorie consumption for cats in the matched-cohort control group, the mean calorie consumption for cats in the treatment group was significantly (P < 0.01) less during months 2 through 4 and greater during months 7 and 8 (Figure 3).
Mean body mass for 20 overweight or obese cats that were fed a high-protein, high-fiber test food that was formulated for weight loss and contained coconut oil and supplemental l-carnitine, 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. The body mass data for the weight maintenance phase represents the mean for 19 cats because 1 cat died acutely of severe hemoperitoneum caused by a generalized hepatocellular carcinoma during that phase, and data for that cat were excluded from all analyses for that phase.
Citation: Journal of the American Veterinary Medical Association 247, 4; 10.2460/javma.247.4.365
Number of cats 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 cats 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.247.4.365
Metabolomic profiles
For all cats 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. Serum concentrations of carnitine and lauric acid, components of the test food, were significantly increased from baseline concentrations. Serum concentrations for indicators of protein catabolism and turnover including leucine, isoleucine, valine, and 3-methylhistidine were significantly decreased from baseline concentrations as were serum concentrations for metabolites of BCAAs including α-hydroxyisovalerate, 3-methyl-2-oxobutyrate, and 3-methyl-2-oxovalerate; indicators of oxidative stress such as hypoxanthine and inosine; indicators of inflammation such as arachidonate and thromboxane B2; cholesterol; creatinine; 2-hydroxybutyrate; and the free fatty acids palmitate, stearate, and oleate. Serum concentrations of the oxidized congener glutathione disulfide and proximal indicators of glutathione flux (5-oxoproline and ophthalmic acid) were also significantly decreased from baseline concentrations, which indicated that the test food caused a decrease in the demand for glutathione. Five BCAA metabolites including 2-hydroxybutyrate, α-hydroxyisovalerate, 3-hydroxyisobutyrate, and γ-glutamylvaline (cumulative adjusted R2 = 0.72); 19 fatty acid and glyceroester metabolites including linolenate, eicosapentaenoate, arachidonate, laurate, docosapentaenoate, palmitate, and glycerophosphorylcholine (cumulative adjusted R2 = 0.98); and 5 energy intermediates including malate, β-alanine, alanine, creatine, and ATP (cumulative adjusted R2 = 0.73) had significant predictive capacity for determining the percentage of body fat loss.
Mean ± SE metabolic IBW (IBW0.75) for the cats of Figure 1 (solid line with brackets), compared with that for a colony control group (dashed and dotted line), which consisted of 418 adult cats from the same research colony as the cats from Figure 1 that were considered to have an IBW and did not undergo dietary intervention, and a matched-cohort control group (dashed line), which consisted of 20 cats that were matched to the cats 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 value for the colony control group. †Value differs significantly (P ≤ 0.05) from the corresponding value for the matched-cohort control group. See Figure 1 for remainder of key.
Citation: Journal of the American Veterinary Medical Association 247, 4; 10.2460/javma.247.4.365
Discussion
Results of the present study indicated that overweight and obese cats 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 cat food that contained coconut oil and supplemental l-carnitine, lysine, and leucine. Interestingly, following the restricted intake period, those cats generally gained LBM and continued to lose body fat despite an increase in caloric consumption and intake to maintain body weight. The metabolomic data and the fact that the mean daily caloric consumption for the cats that were fed the test food in trial 2 was significantly greater than that for the cats 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 cats. However, the present study was not designed to investigate the effect of the test food on the energy metabolism and metabolic rate of overweight cats, and further research is necessary to explore that theory.
For both the test and control foods used in trial 1, the metabolizable energy content 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 content was estimated instead of determined directly, it is possible that the test food contained fewer calories or the control food contained more calories than estimated. Digestibility tests were not performed on either food at the time the present study was conducted. However, the measured metabolizable energy content of test food that was made after the study (but was produced in an identical manner as that fed in study) as determined by results of a digestibility trial that was performed in accordance with standards established by the AAFCO was 4.6% greater than that predicted by the modified Atwater equation. This suggested that it was unlikely that the caloric density of the test food fed in the present study was less than that estimated by the modified Atwater equation. The fact that the cats in the treatment group of trial 2 consumed more calories on a daily basis than did the cats in the colony control group without gaining body weight during the weight maintenance phase suggested that fairly small alterations in food composition can cause substantial changes in metabolism over time.
The test food used in 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 cats can be titrated on the basis of varying the balance between the contents of fat and other nutrients, and determine whether the results of the present study can be replicated. Although we cannot rule out that the positive effects of dietary protein intake and an increase in activity did not contribute to weight loss in the overweight and obese cats of the present study, the test food fed to those cats contained nutrients that positively affect metabolism and the efficiency of weight loss in cats and other species.26–32 Coconut oil contains a large amount of MCFA-containing triglycerides and glyceroesters with saturated 8- to 12-carbon fatty acids (eg, lauric acid).13 Unlike LCFAs, MCFAs are directly transported from the intestine to the liver without entering the systemic circulation, thereby decreasing their uptake by adipose tissue. Additionally, MCFAs are able to pass from the cytosol through mitochondrial membranes without conjugation with carnitine, which increases their use in β-oxidation.26 Compared with LCFAs, the MCFA lauric acid is a preferred substrate for peroxisomal β-oxidation,26 and it uncouples ATP production from mitochondrial oxidation and promotes thermogenesis.27 Carbohydrate metabolism can be stimulated by MCFAs, which increases glucose utilization.26 For the overweight and obese cats in the treatment group of trial 2, metabolomic data indicated that the serum concentration of lauric acid was increased from the baseline concentration following consumption of the test food, which suggested that the lauric acid in the food was bioavailable. Thus, the MCFAs contained in the test food might have increased the total energy expenditure of the cats to which it was fed and contributed to the observed weight loss in those cats.
Metabolomic data obtained during trial 2 also indicated that the serum carnitine concentration increased in cats following consumption of the test food, which suggested that the formulation of l-carnitine contained in the food was bioavailable. Carnitine is required for β-oxidation of LCFAs in mitochondria, and supplemental dietary l-carnitine might increase mitochondrial oxidation of LCFAs.14 An increase in the oxidation of LCFAs might cause a decrease in adipose formation and preserve muscle glycogen stores,14 and multiple studies14–17 have been conducted to evaluate that hypothesis. Dietary MCFAs and supplemental l-carnitine might act synergistically to influence metabolic rate and spare essential fatty and amino acids. Results of a study14 that involved cats suggest that supplemental l-carnitine causes a decrease in concentrations of C16:0 and C16:1 fatty acids, possibly subsequent to an increase in oxidation of C16 fatty acids, and an increase in hepatic omega-3 and omega-6 fatty acid concentrations. In a another study,28 healthy dogs fed supplemental MCFAs had a subsequent 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. The investigators of that study28 concluded that MCFAs appear to spare preexisting omega-3 fatty acids from oxidation. Supplemental dietary carnitine might also spare methionine and lysine concentrations because those amino acids are used to synthesize l-carnitine in vivo.29
Results of the present study were similar to those of other studies30–32 and suggested high dietary intake of protein, such as that provided by the test food, was beneficial for weight loss and the maintenance of LBM in overweight and obese cats during periods of restricted caloric intake. The quantity and quality of the protein (ie, the amino acid profile) is imperative for the production and maintenance of LBM. Results of another study17 indicate that an increase in the dietary lysine concentration-to-calorie ratio results in a decrease in protein degradation and may reduce muscle loss during periods of calorie restriction in geriatric cats. In rats, high concentrations of dietary leucine in conjunction with adequate energy (glucose) intake, inhibits protein degradation and stimulates protein synthesis by enhancing insulin sensitivity.18 In the present study, the cats of the treatment group lost a significant amount of LBM (13% of the total weight loss) during the weight loss phase of trial 2 but gained almost all of that LBM back during the weight maintenance phase, likely because of the balanced amino acid profile of the test food and the increase in protein intake.
The test food fed to the cats of the present study might help modify the pathophysiologic processes associated with obesity, such that its consumption may aid healthy body weight management. In cats, obesity is frequently accompanied by chronic inflammation and chronic disruptions in redox homeostasis and oxidative stress.33 Evidence that the test food fed in the present study contributed to healthy body weight management of overweight cats included a decrease in the circulating concentrations of inflammatory (arachidonate and thromboxane B2) and oxidative stress (hypoxanthine and inosine) indicators. The test food also appeared to reduce the demand for glutathione, an endogenous free radical scavenger, which may be useful for combating obesity-associated oxidative stress.
During the treatment phase of trial 1, the cats in groups 2 and 3 had the same caloric intake and lost the same amount of weight, even though the cats in group 3 were offered a greater amount of food than were the cats of the group 2. We anticipated that the cats in group 3 would maintain their body weight; however, most of the cats in trial 1 appeared to habitually eat approximately the same volume of food daily, regardless of whether they were offered additional food. Aside from habituation, cats may consistently consume the same volume of food for physiologic reasons associated with satiety including gastric volume and nutrient signals such as sufficient blood concentrations of glucose, fatty acids, amino acids, and hormones (eg, insulin and cholecystokinin). When the cats of groups 2 and 3 were fed the control food during the posttreatment phase, their caloric intake increased from that during the treatment phase and they regained all of the weight they had lost. Because the mean daily grams of food consumed did not differ significantly among the 3 groups of cats throughout trial 1, it is likely that the weight loss observed in the cats of groups 2 and 3 was associated with the lower caloric density and higher fiber content of the test food in comparison with the control food. However, during trial 2, the amount of test food consumed by the cats in the treatment group steadily increased during the weight maintenance phase. This increase in food consumption suggested that changes in body composition, specifically LBM, over time (ie, > the 2-month duration of trial 1) caused an increase in energy metabolism and consumption was no longer limited by the bulk of the test food.
For the cats of the treatment group of trial 2, mean serum concentrations of triglyceride, cholesterol, creatinine, IGF-1, and leptin at the end of the weight loss phase were significantly decreased from the corresponding baseline concentrations. In cats, a decrease in serum leptin concentration can increase insulin sensitivity.34 In trial 2, the mean serum glucose concentration at the end of the weight maintenance phase was significantly lower than that at the end of the weight loss phase. That decrease in serum glucose concentration might have been a consequence of weight loss or the consumption of the high-protein, high-fiber test food, which may have facilitated a decrease in serum leptin concentration. The decrease in serum leptin concentration was supported by a concurrent decrease in the serum concentrations of the insulin resistance indicators 2-hydroxybutyrate and creatinine.35,36 The reason that the mean serum IGF-1 concentration was decreased from the baseline concentration at the end of the weight loss phase and then returned to approximately the baseline concentration at the end of the weight maintenance phase is unknown; however, the changes in mean serum IGF-1 concentration remained within reference limits throughout trial 2 and did not appear to be clinically relevant.
Mean serum ALT activity and BUN, triglyceride, and total bilirubin concentrations at the end of the weight maintenance phase of trial 2 were significantly higher than the corresponding activity and concentrations at the end of the weight loss phase. However, all activities and concentrations remained within the respective reference limits, and changes in those activities and concentrations did not appear to be clinically relevant because all cats remained healthy. It is unknown why the mean serum concentrations of biochemical analytes associated with liver function (eg, ALT and total bilirubin) did not increase significantly from baseline concentrations during the weight loss phase, but we were not surprised that those concentrations increased during the weight maintenance phase because most of the cats continued to lose body fat during that phase. Increases in serum ALT activity and bilirubin concentration have been observed in obese cats during periods of weight loss.14 In that study,14 the hepatic lipid content was higher and the number of hepatocyte mitochondria was lower in overweight and obese cats, compared with those in clinically normal or lean cats. Consequently, obese cats that undergo abrupt weight loss are at risk of developing clinical hepatic lipidosis; however, results of that study14 indicate that increases in hepatic lipid content and serum concentrations of biomarkers associated with hepatic lipidosis in obese cats that undergo weight loss by means of gradual energy restriction are not sufficient to cause clinical signs of hepatic liposis. It has been suggested that hepatic lipidosis in cats is caused by a decrease in mitochondrial or peroxisomal oxidation or a combination of both.14,37 Therefore, feeding cats a food with supplemental carnitine may facilitate healthy body weight management by helping to minimize clinical signs associated with hepatic lipidosis during weight loss.9,14 Additional long-term studies are necessary to further evaluate the effects of weight loss in overweight or obese cats on the incidence and severity of hepatic lipidosis.
Overweight and obese cats can become refractory to weight loss interventions, which makes weight management in those cats challenging and frustrating for both owners and veterinarians. Each cat 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.1,9 The test food fed to the overweight and obese cats of the present study successfully reduced total body weight and body fat mass, helped maintain LBM, and caused a decrease in metabolomic indices associated with protein catabolism, which suggested that this food might be beneficial for cats with sarcopenic obesity. Interestingly, some cats that were fed the test food continued to lose total body weight and body fat mass during the weight maintenance phase of trial 2, despite significantly increasing their caloric intake from that during the weight loss phase. Although the goal of the weight maintenance phase of trial 2 was to equilibrate total body weight, results suggested that a feeding protocol that involved steady modulation of caloric intake was unable to keep up with metabolic demands. Thus, once overweight cats achieve an IBW, weight equilibration for cats fed the test food may take > 4 months when caloric intake is only gradually increased on a weekly basis. It is likely that the rapid weight loss observed in the overweight and obese cats of the present study might not be reproduced in cats maintained in a home environment because of noncompliant owners and variability in the activity level of individual cats. The mechanism responsible for the apparent increase in the basal metabolic rate of cats 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 cats.
ABBREVIATIONS
| AAFCO | Association of American Feed Control Officials |
| ALT | Alanine aminotransferase |
| 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.
Feline Adult Fit 32, Royal Canin USA Inc, St Charles, Mo.
Hill's Prescription Diet Feline 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 Feline Insulin ELISA, Mercodia Inc, Winston-Salem, NC.
Human IGF-1 ELISA, R&D Systems Inc, Minneapolis, Minn.
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. Lund E, Armstrong P, Kirk C, et al. Prevalence and risk factors for obesity in adult cats from private US veterinary practices. Int J Appl Res Vet Med 2005; 3: 88–96.
3. Colliard L, Paragon B, Lemuet B, et al. Prevalence and risk factors for obesity in an urban population of healthy cats. J Feline Med Surg 2009; 11: 135–140.
4. Courcier EA, O'Higgins R, Mellor DJ, et al. Prevalence and risk factors for feline obesity in a first opinion practice in Glasgow, Scotland. J Feline Med Surg 2010; 12: 746–753.
5. Sloth C. Practical management of obesity in dogs and cats. J Small Anim Pract 1992; 33: 178–182.
6. Scarlett JM, Donoghue S. Associations between body condition and disease in cats. J Am Vet Med Assoc 1998; 212: 1725–1731.
7. Laflamme DP. Understanding and managing obesity in dogs and cats. Vet Clin North Am Small Anim Pract 2006; 36: 1283–1295.
8. German AJ, Ryan VH, German AC, et al. Obesity, its associated disorders and the role of inflammatory adipokines in companion animals. Vet J 2010; 185: 4–9.
9. 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.
10. Butterwick RF, Hawthorne AJ. Advances in dietary management of obesity in dogs and cats. J Nutr 1998; 128: 2771S–2775S.
11. 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.
12. Burkholder WJ, Bauer JE. Foods and techniques for managing obesity in companion animals. J Am Vet Med Assoc 1998; 212: 658–662.
13. St-Onge MP, Jones PJH. Physiological effects of medium-chain triglycerides: potential agents in the prevention of obesity. J Nutr 2002; 132: 329–332.
14. 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.
15. Center SA, Warner KL, Randolph JF, et al. Influence of dietary supplementation with l-carnitine on metabolic rate, fatty acid oxidation, body condition, and weight loss in overweight cats. Am J Vet Res 2012; 73: 1002–1015.
16. Center SA, Harte J, Watrous D, et al. The clinical and metabolic effects of rapid weight loss in obese pet cats and the influence of supplemental oral l-carnitine. J Vet Intern Med 2000;14: 598–608.
17. Frantz NZ, Yamka RM, Friesen KG. The effect of diet and lysine:calorie ratio on body composition and kidney health in geriatric cats. Int J Appl Res Vet Med 2007; 5: 25–36.
18. Garlick PJ. The role of leucine in the regulation of protein metabolism. J Nutr 2005; 135: 1553S–1556S.
19. Frank G, Anderson W, Pazak H, et al. Use of a high-protein diet in the management of feline diabetes mellitus. Vet Ther 2001; 2: 238–246.
20. Nelson RW, Scott-Moncrieff JC, Feldman EC, et al. Effect of dietary insoluble fiber on control of glycemia in cats with naturally acquired diabetes mellitus. J Am Vet Med Assoc 2000; 216: 1082–1088.
21. 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; 7.
22. Darden T. AAFCO official publication. Champaign, Ill: Association of American Feed Control Officials, 2013; 180.
23. 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.
24. National Research Council. Nutrient requirements of dogs and cats. Washington, DC: National Academies Press, 2006; 31–366.
25. Storey JD, Tibshirani R. Statistical significance for genomewide studies. Proc Natl Acad Sci U S A 2003; 100: 9440–9445.
26. Papamandjaris AA, MacDougall DE, Jones PJH. Minireview—medium chain fatty acid metabolism and energy expenditure: obesity treatment implications. Life Sci 1998; 62: 1203–1215.
27. 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.
28. 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 Nov 12, 2013.
29. Blanchard G, Paragon BM, Milliat F, et al. Dietary l-carnitine supplementation in obese cats alters carnitine metabolism and decreases ketosis during fasting and induced hepatic lipidosis. J Nutr 2002; 132: 204–210.
30. Vasconcellos RS, Borges NC, Goncalves KNV, et al. Protein intake during weight loss influences the energy required for weight loss and maintenance in cats. J Nutr 2009; 139: 855–860.
31. Nguyen P, Leray V, Dumon H, et al. High protein intake affects lean body mass but not energy expenditure in nonobese neutered cats. J Nutr 2004; 134: 2084S–2086S.
32. Laflamme DP, Hannah SS. Increased dietary protein promotes fat loss and reduces loss of lean body mass during weight loss in cats. Int J Appl Res Vet Med 2005; 3: 62–68.
33. Tanner AE, Martin J, Saker KE. Oxidative stress and inflammatory state induced by obesity in the healthy feline. J Anim Physiol Anim Nutr (Berl) 2007; 91: 163–166.
34. Appleton DJ, Rand JS, Sunvold GD. Plasma leptin concentrations are independently associated with insulin sensitivity in lean and overweight cats. J Feline Med Surg 2002; 4: 83–93.
35. Gall WE, Beebe K, Lawton KA, et al. α-Hydroxybutyrate is an early biomarker of insulin resistance and glucose intolerance in a nondiabetic population. PLoS ONE [serial online] 2010; 5: e10883. Available at: journals.plos.org/plosone/article?id=10.1371/journal.pone.0010883. Accessed Nov 12, 2013.
36. Kronborg J, Jenssen T, Njølstad I. Metabolic risk factors associated with serum creatinine in a non-diabetic population. Eur J Epidemiol 2007; 22: 707–713.
37. Center SA, Guida L, Zanelli MJ, et al. Ultrastructural hepatocellular features associated with severe hepatic lipidosis in cats. Am J Vet Res 1993; 54: 724–731.
Appendix
Nutrient composition of the control and test foods fed to cats in a study conducted to determine the effect of feeding a food containing coconut oil and supplemental l-carnitine, lysine, leucine, and fiber on weight loss and maintenance in cats.
| Nutrient | Control food | Test food |
|---|---|---|
| Total protein* | 35.50 | 38.32 |
| Arginine | 2.08 | 2.06 |
| Cystine | 0.36 | 0.62 |
| Histidine | 0.84 | 0.77 |
| Isoleucine | 1.45 | 1.55 |
| Leucine | 3.77 | 4.36 |
| Total lysine | 1.86 | 1.93 |
| Methionine | 0.95 | 1.21 |
| Phenylalanine | 1.73 | 1.97 |
| Threonine | 1.40 | 1.41 |
| Tryptophan | 0.33 | 0.31 |
| Tyrosine | 1.26 | 1.37 |
| Valine | 1.78 | 1.96 |
| Crude fat† | 16 | 12.02 |
| Lauric acid (C12:0) | 0.02 | 0.78 |
| Myristic acid (C14:0) | 0.13 | 0.35 |
| Linoleic acid (C18:2) | 3.49 | 2.23 |
| Linolenic acid (C18:3) | 0.28 | 0.92 |
| Sum of omega-3 fatty acids | 0.47 | 0.90 |
| Sum of omega-6 fatty acids | 3.65 | 2.36 |
| Total dietary fiber | 10.68 | 17.37 |
| Insoluble fiber | 7.9 | 14.90 |
| Soluble fiber | 2.78 | 2.47 |
| Crude fiber | 3.84 | 9.65 |
| Ash | 8.17 | 5.85 |
| Calcium | 1.28 | 1.10 |
| Chloride | 0.79 | 0.68 |
| Magnesium | 0.12 | 0.11 |
| Phosphorus | 1.19 | 0.93 |
| Potassium | 0.75 | 0.77 |
| Sodium | 0.63 | 0.32 |
| l-carnitine (ppm) | 40 | 809 |
| β-carotene (ppm) | 224 | 341 |
| Energy (kcal/kg [kcal/cup])‡ | 3,830 (350) | 3,273 (288) |
| Protein (g/calorie)‡ | 9 | 11 |
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.
