Bioavailability of lysine for kittens in overheated casein is underestimated by the rat growth assay method.

Growth assays were performed to determine lysine bioavailability for kittens and rats in untreated and heated casein; these values were compared with estimates obtained with an in vitro method. Body weight, food intake, nitrogen and dry matter digestibility, and plasma lysine were determined during an 80-day growth trial using kittens (n = 16). Body weight and food intake were determined during a 21-day growth trial using weanling rats (n = 80). The growth data showed bioavailable lysine to be 102.4% and 100.2% (for untreated casein) and 66.1% and 51.7% (for heated casein) for kittens and rats, respectively. There was no relationship between plasma lysine and dietary lysine concentrations for kittens. There were no significant differences in nitrogen or dry matter digestibility among diets for kittens. The chemically reactive lysine content of untreated casein was 99.6%, and of heated casein was 67.1%. Heat treatment of casein resulted in significantly decreased lysine bioavailability as estimated by all methods. For untreated casein, both growth assays showed good agreement with the in vitro method for available lysine. For heated casein, the rat growth assay significantly underestimated bioavailable lysine as determined in kittens while the in vitro method closely approximated this value for the cat.

Dietary crude protein has minimal effect on the activity of selected enzymes of methionine catabolism in kittens fed diets near-limiting in methionine.

Previous experiments have shown that increasing the dietary crude protein (CP) of cats does not increase urea cycle enzymes or alanine amino transferase as occurs in rats. Also when an essential amino acid (EAA) is limiting in a diet for growing kittens, the kittens do not exhibit an amino acid imbalance when other EAAs are added to the diet. To study the metabolic basis for these observations which are different from that found in omnivores and herbivores, the hypothesis that increased dietary CP decreases methionine catabolism, so more is spared for growth, was tested. Fifteen male kittens were randomly assigned to one of three dietary treatments. Each diet contained 2.5 g l-methionine/kg diet and 200, 300 or 500 g CP/kg diet. The livers and kidneys were removed and assayed for methionine transaminase (MTA), cystathionase (CASE) and cystathionine synthase (CS). Free amino acid concentrations were determined in liver, kidney and plasma. The 300 and 500 g CP/kg groups had significantly greater kidney weights and body weight gains than the 200 g CP/kg group. Hepatic MTA activity was lower in the 300 than the 200 or 500 g CP/kg groups (p < 0.05). Renal MTA and CASE activities were 35% and 50% greater, respectively, for the 500 g CP/kg group than for the 200 g CP/kg diet group (p < 0.05). Renal CS activities for the 300 and 500 g CP/kg groups were 29% (p > 0.05) and 38% (p < 0.05) greater, respectively, than the 200 g CP/kg group. Cyst(e)ine concentrations were lower in the livers of the 500 g CP/kg group than the 200 g CP/kg group (p < 0.05). Cystathionine was lower in plasma and kidney from the 500 g CP/kg diet group than from the 200 g CP/kg diet group (p < 0.05). It was concluded that the metabolic basis for the increased growth of kittens fed diets marginally limiting in methionine, with increasing concentrations of dietary CP, was not mediated through decreased enzyme activity associated with the catabolism of methionine, but was the result of an increase in food (methionine) intake.

Testosterone increases urinary free felinine, N-acetylfelinine and methylbutanolglutathione excretion in cats (Felis catus).

Two days after castration, urinary free felinine plus N-acetylfelinine decreased 24% in male cats, but, by day 5, the concentration had not decreased to that routinely found in males that have been castrated for several months. In a second experiment, three groups of castrated adult male cats received different subcutaneous injections: control (carrier), testosterone, testosterone plus estradiol. A fourth group of intact adult female cats received a testosterone injection. Urine was collected and analysed for free felinine, N-acetylfelinine and 3-methylbutanolglutathione. Baseline blood testosterone and estradiol concentrations were low during the pre-period, but increased sharply after hormone injections. The concentration of all three urinary metabolites increased as a result of testosterone injections with estradiol not modulating the effect. The effect of testosterone was not gender dependent. The concentration of free felinine, N-acetylfelinine and 3-methylbutanolglutathione in the urine remained low in the placebo control group throughout the study. The relative molar contribution of free felinine to the total amount of felinine containing compounds increased due to testosterone treatment, while the contribution of 3-methylbutanolglutathione and N-acetylfelinine decreased. Testosterone increases free felinine, N-acetylfelinine and 3-methylbutanolglutathione excretion in castrated adult male and intact female cats, whereas estradiol does not modulate this effect.

Increasing dietary crude protein does not increase the methionine requirement in kittens.

The objective of this study was to determine if the methionine (met) requirement of kittens is correlated with the concentration of dietary crude protein (CP). The study used 48 male kittens in two replications of six 4 x 4 Latin squares, each representing one concentration of met (1.5, 2.5, 3.5, 4.5, 6.0 or 9.0 g/kg diet) with four CP concentrations (150, 200, 300 and 500 g/kg diet) in 2-week periods. Cystine was present in the lowest CP diet at 5.3 g/kg diet and increased as dietary CP increased. Body weight gain, food intake, nitrogen balance and plasma amino acids, glucose, insulin, cortisol, somatomedin C, T(3) and T(4) concentrations on day 12 were measured. From breakpoint analysis of the nitrogen retention curves, the met requirement of kittens was found to be 3.1, 3.8, 3.1 and 2.4 g met/kg for the 150, 200, 300 and 500 g CP/kg diets, respectively. When met was limiting (1.5 or 2.5 g/kg diet), increasing dietary CP did not decrease, but rather increased food intake, body weight gain and nitrogen retention. Plasma met concentrations increased as dietary met increased and at 2.5-3.5 g met/kg diet were not different among kittens fed the various CP diets. Total plasma T(3) and T(4) increased significantly as dietary CP increased in kittens given the 2.5 and 4.5 g met/kg diets. Results indicate that food intake and possibly altered hormonal secretion play a role in this growth response. In conclusion, the met requirement of growing kittens, unlike omnivores and herbivores studied, was not positively correlated with the concentration of dietary CP.

Excess dietary cystine intensifies the adverse effect of a methionine deficiency in the cat.

Foot pad dermatitis has been observed in turkeys, puppies and kittens fed diets deficient in methionine. Excess cystine aggravated the lesions and decreased body weight gain in puppies and turkeys. The objective of this study was to determine whether methionine deficiency induced perioral and foot pad lesions in kittens and whether excess cystine exacerbated the lesions. Eighteen kittens were divided into three groups and offered one of three diets: diet 1, low-methionine, low-cystine (LMLC; 1.6 g methionine and 1.6 g cystine/kg diet); diet 2, low-methionine, high-cystine (HMHC; 1.6 methionine and 15 g cystine/kg diet); diet 3, high-methionine, high-cystine (HMHC; 15 g methionine and 15 g cystine/kg diet). Kittens in the LMLC group lost body weight, whereas those in the LMHC group maintained their body weight and those in the HMHC group gained weight. Plasma methionine concentrations were significantly higher (p < 0.001) for the HMHC group than for the LMLC and LMHC groups. Plasma cyst(e)ine (sum of cysteine and cystine) concentrations were different (p < 0.001) among all the three groups. Two kittens given the LMLC diet developed mild perioral lesions. All kittens receiving the LMHC diet developed foot pad lesions and severe perioral lesions. Histopathological changes observed in perioral biopsy specimens were similar to those described in protein deficiency. In conclusion, the results showed that a diet severely deficient in methionine causes perioral lesions in kittens, and that addition of excess cystine to the diet aggravates the perioral lesions and also causes foot pad lesions.

Increasing dietary crude protein does not increase the essential amino acid requirements of kittens.

Essential amino acid (EAA) requirements of omnivores and herbivores (e.g. chicks, lambs, pigs and rats) are directly related to the concentration of dietary crude protein (CP). When an EAA is limiting in the diet, addition of a mixture of EAA lacking the limiting one (which increases dietary CP) results in a decrease in food intake and weight gain. This interaction has been referred to as an AA imbalance and has not been studied in depth in strict carnivores. The objectives of these experiments were to examine the effects on growing kittens (2-week periods) of the addition to diets of a mixture of AA lacking the limiting one. The control diets were at the requirement of the respective limiting EAA (or about 85% of the 1986 National Research Council requirement). In experiment 1, with the dietary EAAs at the minimally determined requirements, the concentration of the essential or dispensable amino acids was increased to determine if CP or an EAA was limiting. Results of growth rates (n = 12) and plasma AA concentrations indicated that tryptophan was limiting, but increased body weight gain also occurred when the concentration of CP was increased as dispensable amino acids without additional tryptophan. Experiment 1 was repeated in experiment 2 using a crossover design. Again, when tryptophan was limiting additional concentrations of dispensable AAs increased body weight gain. This response is the opposite of that in herbivores and omnivores. Experiment 3 consisted of 10 separate crossover trials, one for each of the 10 EAA and examined the effect of two concentrations of dietary CP (200 and 300 g CP/kg diet) on body weight gain of kittens (n = 8) offered diets limiting in each respective EAA. Body weight gain was numerically greater when diets contained 300 g CP/kg than 200 g CP/kg for eight of 10 EAAs (p < 0.05 for only isoleucine and threonine) when each amino acid was limiting. This response is the reverse of that which occurs in chicks, lambs, pigs and rats when an EAA is limiting and dietary CP lacking the limiting EAA is increased. These results indicate that the EAA requirements of kittens are not positively correlated with dietary CP concentrations.

Elevation of plasma cholecystokinin concentration following a meal is increased by gonadectomy in male cats.

An overweight or obese body condition commonly develops after gonadectomy (GX) in domestic cats. The cause appears to be a rapid, quantal (approximately 12%), increase in food intake that is sustained and probably mediated by withdrawal of gonadal hormone. Recently, an interaction of gonadal hormone and cholecystokinin (CCK) effectiveness has been suggested. A reduction in the satiating potency of intestinal CCK was presently hypothesized to contribute to the disturbance of food intake control caused by GX in domestic cats. Pre- and post-prandial intestinal CCK secretion as indicated by plasma CCK concentrations were determined in 16 adult male cats (5.1 +/- 0.1 kg) 8 weeks before and 57 weeks after eight of the cats were gonadectomized. During ad libitum intake of a commercial dry, expanded diet, body weight increased from 22% to 28% in gonadectomized cats and was unchanged in intact cats. Baseline CCK concentrations were not different between gonadectomized and intact cats. Amounts of diet ingested during CCK determinations were 15-19% of daily metabolizable energy requirement and were not different between gonadectomized and intact cats. The post-prandial area under the curve (AUC; 0-400 min) CCK concentration increased linearly with meal size (p < 0.01) and was not correlated with body weight. Area under the curve CCK concentration, when normalized for meal size, was 34% greater (p < 0.01) in gonadectomized cats than that in intact cats. The findings indicate GX increases meal-induced intestinal CCK secretion and therefore, do not support the study hypothesis. The findings indicate GX may slow digestion and absorption and attenuate inhibition of food intake by CCK.

Localizing the X-linked orange colour phenotype using feline resource families.

Many genes influencing mammalian coat colours are well conserved. While genes responsible for pelage phenotypes in one species provide strong evidence for a candidate gene in a different species, the X-linked orange phenotype of the domestic cat is unique within mammals. The orange locus (O) undergoes X-inactivation, producing females that express both wildtype black (wt) and orange (variant) phenotypes when heterozygous (tortoiseshell). The orange locus has not yet been localized on the X chromosome. Tortoiseshell male cats have been identified but have been shown to be sex chromosome trisomies (XXY). To localize the cat orange locus, 10 feline-derived X-linked microsatellites were analysed in two extended cat pedigrees consisting of 79 and 55 individuals, respectively, segregating for the orange phenotype. Linkage analyses excluded close association of orange in the vicinity of the nine informative X-linked microsatellites. One marker was not polymorphic within either family. Several markers suggested exclusion (Z < -2.0) at distances of 7.5-33 cM. Exclusion analyses suggested a possible location for orange a 14 cM region near Xcen. Recombination distances of markers in the segregating feline pedigrees were reduced as compared with the feline interspecies backcross family. Thus, the presented pedigrees may be useful as reference families for the domestic cat because more accurate recombination rates for domestic cats can be determined.

Mammalian isovalthine metabolism.

Isovalthine is a branched-chain sulphur amino acid, which has been found in the urine of normal cats. The concentrations of isovalthine in the urine of healthy adult cats are approximately 24-66 micromol/l and are not affected by the gender of the cat. Isovalthinuria can be induced in other species (rats, rabbits, guinea-pigs, humans, dogs) following the administration of certain inducing agents such as some hypocholesterolaemic agents, bile acids, hormones or cholesterol precursors. The method of induction of isovalthinuria was studied extensively during the 1960s, and efforts were made to understand its biosynthesis. However, although the origin of the sulphur atom in isovalthine was shown to be from cysteine or methionine, the origin of the carbon skeleton remains unknown. Interest in isovalthine metabolism was generated in part because it was reportedly found in the urine of patients with hypercholesterolaemia. The validity of this finding however, was brought into question following reports that administration of the drug Bromural (alpha-bromoisovalerylurea), to humans results in the generation of compounds which break down to yield isovalthine following acid hydrolysis. This article presents a review and discussion of the experimental data on isovalthine metabolism.

Lysine requirement of kittens given purified diets for maximal growth.

Three experiments were conducted using a total of 15 male and 15 female weaned specific pathogen-free kittens given amino acid-based purified diets containing varying concentrations of lysine (from 4.0 to 11.3 g/kg diet) in a Latin square design of 10 day periods. In experiment 1, the predicted lysine requirement was 7.7 g/kg diet, and in experiments 2 and 3, maximal weight gain occurred at 8.0 g lysine/kg diet. In experiment 3, nitrogen balance was not different for kittens given diets containing 8.0 and 9.0 g lysine/kg. These experiments support a requirement of 8.0 g lysine (free base)/kg diet, in a diet with a calculated metabolizable energy value of 4.7 kcal/g.

Lipoic acid is 10 times more toxic in cats than reported in humans, dogs or rats.

The antioxidant lipoic acid (LA) is administered to humans and pets. We described acute toxicity and maximum tolerated dose (MTD) of LA in cats. In progression, 10 healthy adult male cats received orally 60 (high), 30 (low), or 0 mg LA/kg (control). Serum enzyme activities and concentrations of bile acids, ammonia, amino acids (AA), LA and dihydrolipoic acid (DHLA) were measured, and tissues examined microscopically. Significant clinical toxicity with changes in ammonia and AA concentrations occurred in all high-dose cats. Oral LA produced hepatocellular toxicity and MTD was < 30 mg/kg in cats.

Influences of stage of lactation, teat position and sequential milk sampling on the composition of domestic cat milk (Felis catus).

Milk from 11 domestic shorthair cats (Felis catus; n=7 fed dry low-fat diet, n=4 fed dry high-fat diet) was collected weekly for 6 weeks following parturition, and analysed for total solids (TS), crude protein (CP), fat, lactose and ash. Samples were collected in 1-ml sequential fractions to determine whether within-sampling changes in composition existed Samples of extracted milk fat were also analysed for fatty acid content. Two commercia kitten milk replacers were analysed according to the same procedures utilized for mil samples. In statistical analyses individual cat, diet, stage of lactation, litter size, and teat position influenced concentrations of milk components; parity and sequential sampling had no effect. Averaged cat milk was 27.9% TS, and 8.7% CP, 12.7% fat, 4.2% lactose and 1.3% ash (on a wet basis). Milk protein percentage increased over lactation for both diet groups, but fat percentage increased only for queens fed the high-fat diet. Milk replacers were lower in fat and protein content than milk from queens, and had considerably lower levels of arachidonic acid. Data from this study contribute to the limited information available regarding the composition of domestic cat milk, and give possible reasons for poor growth occasionally observed in kittens fed unsupplemented commercial milk replacers.

Teratogenic effects of chronic ingestion of high levels of vitamin A in cats.

High concentrations of retinoids occur in some commercial cat food formulations as a result of the use of animal liver as an ingredient. Our objective was to study the teratogenic potential of dietary vitamin A in cats. We investigated the incidence of birth defects in kittens of queens given diets with retinyl acetate concentrations of 6000, 306000, or 606000 retinol equivalents (RE)/kg diet (control, 306K, or 606K groups, respectively) for approximately 3 years [1 RE=1 micro g retinol=3.3 International Units (IU)]. Each group comprised 12-15 age-matched, nulliparous domestic short-haired queens that were exposed to toms. There were a total of 396 kittens born in 97 litters. Pregnancy rate, number of kittens per gestation and gestations per year were not significantly different among treatment groups. A total of 2, 5 and 11 malformed kittens occurred in the control, 306K and 606K groups, respectively. Malformations included cleft palate, cranioschisis, foreshortened mandible, stenotic colon, enlarged heart and agenesis of the spinal cord and small intestine, which are typical foetal defects consistent with ingestion of excess retinoids in other species. This study demonstrated that a concentration of 306000 RE/kg diet has a potential for causing birth defects in the kittens.

Determination of the selenium requirement in kittens.

The purpose of this study was to determine the selenium (Se) requirement in kittens. Thirty-six specific-pathogen-free kittens (9.8 weeks old) were utilized in a randomized complete block design to determine the Se requirement in cats with gender and weight used as blocking criteria. Kittens were fed a low Se (0.02 mg/kg Se) torula yeast-based diet for 5 weeks (pre-test) after which an amino acid-based diet (0.027 mg Se/kg diet) was fed for 8 weeks (experimental period). Six levels of Se (0, 0.05, 0.075, 0.10, 0.20 and 0.30 mg Se/kg diet) as Na2SeO3 were added to the diet and were used to construct a response curve. Response variables included Se concentrations and Se-dependent glutathione peroxidase activities (GSHpx) in plasma and red blood cells (RBC) as well as plasma total T3 (TT3) and total T4 (TT4). No significant changes in food intake, weight gain or clinical signs of Se deficiency were noted. Estimates of the kitten's Se requirement (i.e. breakpoints) were determined for RBC and plasma GSHpx (0.12 and 0.15 mg Se/kg diet, respectively), but no definitive breakpoint was determined for plasma Se. Plasma TT3 increased linearly, whereas plasma TT4 and the ratio of TT4 : TT3 decreased in a quadratic fashion to dietary Se concentration. The requirement estimate determined in this study (0.15 mg Se/kg) for kittens is in close agreement with other species. As pet foods for cats contain a high proportion of animal protein with a Se bioavailability of 30%, it is recommended that commercial diets for cats contain 0.5 mg Se/kg DM.

Taurine status in normal dogs fed a commercial diet associated with taurine deficiency and dilated cardiomyopathy.

Taurine (Tau) deficiencies have been associated with the feeding of commercial lamb-meal and rice diets to dogs. We hypothesized that the poor digestibility of some lamb-meals may limit sulphur amino acids availability for Tau synthesis and/or increase of Tau degradation in the gut. Growing dogs were fed either a lamb-meal-based (Diet A) or poultry by-product-based (Diet B) commercial diet. Plasma, whole blood and urinary Tau were measured for 22 weeks. Plasma and whole blood Tau concentrations were similar between the groups throughout the study. Urinary excretion of Tau in dogs fed diet A was 3.2 times greater than that from dogs fed Diet B, suggesting greater renal reabsorption and the need for conservation of Tau in the Diet A group. Food restriction affected Tau status as indicted by a positive correlation of food intake and urinary Tau. Dogs fed Diet A were given antibiotics to inhibit bacterial activity in the gut. Increases in breath hydrogen, indicative of increased bacterial activity, correlated negatively with urinary Tau. Urinary Tau increased by 54% when methionine (Met) was supplemented to Diet A, supporting the suggestion of a low bioavailability of sulphur amino acids and/or an increased fecal loss of Tau in dogs consuming Diet A.

Taurine concentrations in animal feed ingredients; cooking influences taurine content.

The aim of this study was to determine the taurine content in a variety of animal feeds. There is very little information on the taurine content of ingredients used in home-prepared diets for dogs and cats, and foods fed to wild animals in captivity. This study reports the taurine content of both common and alternative feed ingredients, and compares taurine loss as a result of different methods of food preparation. Foods were selected based on their use in commercial and home-prepared diets. Animal muscle tissue, particularly marine, contained high taurine concentrations. Plant products contained either low or undetectable amounts of taurine. The amount of taurine that remained in a feed ingredient after cooking depended upon the method of food preparation. When an ingredient was constantly surrounded by water during the cooking process, such as in boiling or basting, more taurine was lost. Food preparation methods that minimized water loss, such as baking or frying, had higher rates of taurine retention.

Plasma and whole blood taurine in normal dogs of varying size fed commercially prepared food.

The objective of the present study was to examine the effect of signalment, body size and diet on plasma taurine and whole blood taurine concentrations. A total of 131 normal dogs consuming commercially prepared dog food had blood drawn 3-5 h post-prandially to be analysed for plasma amino acids and whole blood taurine. Body weight and morphometric measurements of each dog were taken. Plasma and whole blood taurine concentrations were 77 +/- 2.1 nmol/ml (mean +/- SEM) and 266 +/- 5.1 nmol/ml (mean +/- SEM), respectively. No effect of age, sex, body weight, body size, or diet was seen on plasma and whole blood taurine concentrations. Mean whole blood taurine concentrations were lower in dogs fed diets containing whole grain rice, rice bran or barley. The lowest whole blood concentrations were seen in dogs fed lamb or lamb meal and rice diets. Plasma methionine and cysteine concentrations were lower in dogs fed diets with animal meals or turkey, and whole grain rice, rice bran or barley. Fifteen of 131 dogs had plasma taurine concentrations lower than, or equal, to the previously reported lowest mean food-deprived plasma taurine concentration in normal dogs of 49 +/- 5 nmol/ml (mean +/- SEM) (Elliott et al., 2000). These findings support the theory that taurine deficiency in dogs may be related to the consumption of certain dietary ingredients. Scientific and clinical evidence supports the hypothesis that dilated cardiomyopathy is associated with low blood taurine concentration in dogs; therefore, further work is indicated to determine the mechanism by which diet can affect taurine status in dogs.

A low-selenium diet increases thyroxine and decreases 3,5,3'triiodothyronine in the plasma of kittens.

The effect of a low-selenium diet on thyroid hormone metabolism was investigated in growing kittens. Twelve specific-pathogen-free kittens with ages ranging from 16 to 18 weeks were divided into two groups of equal number with equal sex distribution in each group. One group was fed a yeast-based low-selenium diet (0.02 mg Se/kg diet) while the other group was fed the same diet supplemented with Na2SeO3 at 0.4 mg Se/kg diet for 8 weeks. Food intake, body weight and body weight gain were not affected by the low-Se diet during the study period. However, kittens given the low-Se diet had significantly reduced plasma selenium concentration and glutathione peroxidase activity. Plasma total thyroxine (T4) increased and total 3,5,3'triiodothyronine (T3) decreased significantly in kittens fed the low-Se diet at the end of the study. These results suggest that type I deiodinase in cats is a selenoprotein- or a selenium-dependent enzyme.

Dietary crude protein concentration does not affect the leucine requirement of growing dogs.

The objective of the present study was to examine the interaction between graded levels of leucine and dietary crude protein. Dose-response curves were generated using four 3 x 3 Latin squares (two dogs/square). Each square represented one of two concentrations of crude protein (140 or 280 g/kg diet) and one of two combinations of three concentrations of leucine (5.0, 7.0 and 9.0 g/kg diet or 9.0, 11 and 13 g/kg diet). An additional experiment was performed by feeding crude protein at 210 g/kg diet with either 7.0 or 11 g leucine/kg diet. Weight gain, food intake, nitrogen retention, plasma albumin and plasma amino acids were measured. The requirement was determined to be the minimum leucine concentration required to maximize weight gain and nitrogen retention. For 8-14-week-old male Beagle dogs, 140 g crude protein/kg diet in a diet containing 18 kJ metabolizable energy/g does not appear to support maximal growth. The leucine requirement was not affected by doubling the dietary crude protein level from 140 to 280 g/kg diet. From these results, the leucine requirement of 8-14-week-old Beagle dogs appears to be 11 g leucine/kg diet independent of the level of dietary crude protein, whereas dogs over 14 weeks require only 7 g leucine/kg diet for maximal nitrogen retention.

Quantitation of urinary 3-methylhistidine excretion in growing dogs as an index of in vivo skeletal muscle catabolism.

Purpose: To quantitate urinary 3-methylhistidine (3-mh) excretion as an index of in vivo muscle catabolism in dogs fed diets containing either normal or high protein levels.Methods: Twelve male, 5-month-old Beagle dogs were housed individually in metabolism cages and fed a non-meat, purified diet. They were divided into two diet groups of six dogs each, receiving 22.6% (NP) or 41.1% (HP) DM crude protein, respectively. Three dogs from each group received an intravenous injection of 385 +/- 29 kBq [14C] 3-mh. HCl. Urine and feces were collected daily until radioactivity returned to background levels (17 days). Urinary 3-mh was measured using an amino acid analyzer and percentage of bound 3-mh was estimated via acid hydrolysis.Results: Results are reported as means +/- SEM. 3-mh recovery in urine and feces of dogs were 263 +/- 28 kBq and 50.7 +/- 2.2 kBq and 327 +/- 45 kBq and 25.9 +/- 25.9 kBq for the NP and HP groups, respectively. The total cumulative 3-mh recoveries for the NP and HP groups were 81.8% +/- 2.8 and 91.4% +/- 2.7, respectively. Bound 3-mh accounted for 2.1 to 4.8% of urinary 14C-3-mh.Conclusions: Growing Beagle dogs excrete a higher percentage of 3-mh in feces (13.5% vs. 6.7%) when consuming the NP versus the HP diet. It appears that some of the 14C was lost in CO(2) and/or re-circulated in the body, as reported for sheep and pigs. We conclude that urinary 3-mh does not appear to be a quantitative index of in vivo muscle catabolism in growing dogs.