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.

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.

Vitamin K deficiency in cats fed commercial fish-based diets.

Clinical signs of vitamin K deficiency have been observed in cats offered two commercial canned diets high in salmon or tuna. Some of the queens and kittens offered these diets had died while survivors had increased coagulation times. Necropsies revealed hepatic and, or, gastrointestinal haemorrhages. Coagulation times of survivors returned to normal after vitamin K therapy. The purpose of this study was to induce a vitamin K deficiency in kittens and determine the dietary requirement. Kittens were offered vitamin K-deficient purified diets containing antibiotics and, or, substances inherent in canned fish diets that may have contributed to the deficiency. Clinical signs of vitamin K deficiency were not observed, even though one purified diet contained only 4 micrograms K1/kg diet compared with 60 micrograms in the commercial tuna diet. Therefore, a minimum vitamin K requirement could not be determined using purified diets; nevertheless, canned commercial diets formulated primarily with fish should contain more than 60 micrograms K1/kg diet.