Thousands of pet cats die each year with dilated cardiomyopathy, the cause of which is unknown. Although taurine is present in millimolar concentrations in the myocardium of all mammals, taurine depletion has not previously been associated with a decrease in myocardial function in any species. In this study, low plasma taurine concentrations associated with echocardiographic evidence of myocardial failure were observed in 21 cats fed commercial cat foods and in 2 of 11 cats fed a purified diet containing marginally low concentrations of taurine for 4 years. Oral supplementation of taurine resulted in increased plasma taurine concentrations and was associated with normalization of left ventricular function in both groups of cats. Since myocardial concentrations of taurine are directly related to plasma concentrations and low plasma concentrations were found to be associated with myocardial failure in cats, a direct link between decreased taurine concentration in the myocardium and decreased myocardial mechanical function is proposed.

From the foregoing discussion of the nutritional requirements and some of the metabolic anomalies of the cat, it is clear that the cat is adapted to eating a carnivorous diet. It may, however, have less capability than omnivores and herbivores to adapt to wide ranges in dietary composition. For example, the lack of ability to synthesize sufficient vitamin A from carotene, ornithine from glutamic acid, arachidonate from linoleate, and taurine from cysteine results from a complete deletion or severe limitation of the enzyme or pathway that makes each nutrient. Other nutrient requirements, such as the absolute requirement for niacin and the high protein requirement, appear to result from the high activity of one or more enzymes and the fact that these enzymes are not adaptive in the cat. For example, the cat cannot decrease picolinic carboxylase in order to force tryptophan toward the niacin-synthetic pathway (244) nor can it decrease the urea cycle enzymes when dietary protein is decreased in the diet in order to conserve nitrogen (209). Indeed, the cat appears to have less capability to adapt to most changes in dietary composition because it cannot change the quantities of enzymes involved in the metabolic pathways (209). This evolutionary development has resulted in more stringent nutritional requirements for cats than for omnivores such as the rat, dog, and man. What little evidence exists for other carnivore species leads us to suggest that this pattern may well be common among other strict carnivores. The metabolic differences between the cat and omnivores provide the researcher with a useful animal model for studying the biochemical basis of some nutrient requirements. For example, because there is no significant conversion of linoleate to arachidonate in cat liver (101, 150, 231), the physiological functions of linoleate can be determined independent of it having a role as a precursor of arachidonate (150). This has not been possible with other species. It is anticipated that further studies of the nutrition of the cat will increase our understanding of metabolic adaptation and nutrient functions.

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.

Gonadectomy predisposes domestic cats to undesired body weight gain and obesity. The disturbance responsible for this disregulation of energy balance has not been clearly identified. Energy intake and expenditure, body composition and plasma concentrations of leptin, insulin, glucose and triacylglycerol were determined during a 36-wk period in adult male (2-5 y) gonadectomized (n = 8) and intact (n = 8) normal cats and gonadectomized (n = 8) and intact (n = 8) lipoprotein lipase (LPL)-deficient cats. Cats were housed individually in temperature- and light-controlled rooms and continuously provided a commercial dry-type diet. In normal and LPL-deficient cats, body weight increased (P < 0.05) after gonadectomy by 27 to 29%, mostly as a result of fat accretion. There was a rapid increase (P < 0.05) in food intake of approximately 12% after gonadectomy of normal and LPL-deficient cats. The metabolic rate (kJ.kg(-1).d(-1)), determined in normal intact (319 +/- 20, n = 5) and gonadectomized (332 +/- 36, n = 5) cats, did not differ after gonadectomy. After gonadectomy, plasma concentrations of glucose and triacylglycerol did not change, whereas plasma insulin and leptin concentrations increased (P < 0.05), but not coincidentally with body weight gain. A stair-step increase in energy intake, and not decreased energy expenditure, appears to drive the weight gain associated with gonadectomy. Body fat mass appears to increase until the energy intake supports no further expansion. Adiposity signaling through insulin or leptin does not appear to mediate the energy intake effect. LPL deficiency did not preclude development of the overweight body condition. Therefore, gonadectomy-induced weight gain in cats is not a result of changed adipose LPL activity, as previously suggested.

The activities of three urea cycle enzymes, several nitrogen catabolic, gluconeogenic, and lipogenic enzymes were measured in the liver of adult cats fed: a commercial kibble; a 17.5 or 70% protein purified diet, or starved for 5 days. Except for an increase in tyrosine transaminase (EC 2.6.1.5) after feeding the high protein diet, there were no changes in the activities of the hepatic enzymes as influenced by dietary protein level. Likewise, starvation had a minimal effect on the activities of these enzymes as compared to that found in similar experiments in rats. These results indicate that the cat may have only minimal capabilities for enzyme adaptation as compared to that found in many herbivores and omnivores and may provide an explanation as to why cats have an unusually high protein requirement as compared to many other mammals.

Leptin is in the serum of domestic cats in free (> 78%) and apparently bound forms. The relationship between body fat and serum leptin concentration was similar to that observed in humans and rodents and indicative of a lipostatic role for leptin in cats. Cats that have an overabundance of body fat appear to be less sensitive to the weight-normalizing action of leptin than cats of ideal body condition.

No abstract

Plasma amino acid concentrations were measured in 36 dogs diagnosed with superficial necrolytic dermatitis (SND) via skin biopsy. The median age of the dogs was 10 years, and 27 out of 36 (75%) were male. Twenty-two out of 36 (61%) of the dogs were accounted for by six breeds; West Highland white terriers (six), Shetland sheepdogs (five), cocker spaniels (four), Scottish terriers (three), Lhasa apsos (two) and Border collies (two). The mean concentration (+/- standard deviation) was calculated for each measured plasma amino acid and compared to previously documented concentrations of plasma amino acids measured in dogs with acute and chronic hepatitis. The ratio of branched chain amino acids to aromatic amino acids in the dogs with SND was 2.6, slightly lower than that in normal dogs. The mean plasma amino acid concentrations for dogs with SND were significantly lower than for dogs with acute and chronic hepatitis. A metabolic hepatopathy in which there is increased hepatic catabolism of amino acids is hypothesized to explain the hypoaminoacidaemia seen in SND.