It has long been appreciated that cats are unable to use the -carotene from plants as a source of vitamin A (MacDonald, 1984). Cats lack the enzymes required to cleave the carotene molecule to retinal. Vitamin A metabolites particularly retinoic acid plays a key role in the maturation of cells of many tissues particularly the skin. Vitamin A is also required for fetal development, and in its absence, fetuses develop with congenital defects, one of the common ones in kittens being cleft palate. Excessive amounts of vitamin A or retinoic acid in many animals, including humans, during early pregnancy induces a wide range of teratological changes in the fetus. Teratological defects can occur from either a deficiency or an excess of vitamin A in the diet. A continual diet of liver has been reported to produce skeletal changes such as exostoses of the spine in cats in countries such as Australia and Argentina where livers are from cattle grazing on pasture before slaughter. Liver is commonly used to produce digests or as an ingredient in cat foods explaining the high levels of vitamin A that are observed in some commercial foods. Studies were designed to evaluate if those levels could be associated with health problems.
Queens were given diets containing either a normal level of vitamin A, with 1 million or with 2 million I U of vitamin A as retinyl acetate/kg diet (Freytag 1998). Even at that highest level of 2 million IU/kg there was only a very low incidence of teratological changes in kittens born to the queens. It appears that cats are resistant to vitamin A toxicity. One clue to the resistance is that cats have high levels of retinyl esters, retinyl palmitate and retinyl stearate in their plasma, whereas other animals have mainly retinol combined with retinyl binding protein. It is possible that these retinyl esters are rapidly cleared from plasma preventing their conversion to retinoic acid. In the wild, cats would receive a high load of vitamin A from their prey so it is perhaps not unexpected that cats would be more resistant to vitamin A toxicity than other animals.
For most animals, vitamin D is a conditional nutrient in the diet in that it is only when that animal does not receive exposure to sunlight that it becomes an essential nutrient. Cats have a predilection for lying in the sun, which raises the question of "are they doing it to obtain vitamin D or for hedonic reasons".
Dr J.G. Morris studied the ability of kittens to synthesize vitamin D by feeding them a vitamin D-free diet and exposing them for 3 hours a day, 5 days a week to summer sunlight in Davis, California (Morris 1997). A control group of kittens was kept indoors and not exposed to ultraviolet light. To test if the hair covering the body was the impediment to synthesis, one kitten exposed to light had the back shaved. In all kittens the concentration of 25-hydroxyvitamin D (the main metabolite of vitamin D in blood) declined at the same rate indicating that there was no perceptible synthesis. Several of the cats exposed to sunlight developed clinical signs of vitamin D deficiency. Analysis of cat skin showed that the concentration of the precursor for vitamin D, 7-dehydrocholesterol (7-DHC), was very low in cats compared to that of animals such as rats, sheep and pigs that synthesize vitamin D. When cats were given an inhibitor of the enzyme that converts 7-DHC to cholesterol, the concentration of 7-DHC in skin increased and cats exposed to ultraviolet light synthesized large quantities of vitamin D. Thus, the reason cats do not synthesize vitamin D is that cats have a very active enzyme that converts 7-DHC to cholesterol, and there is not sufficient 7-DHC in skin to allow synthesis to occur. In the wild state cats obtain sufficient vitamin D from prey. Analysis of wild rats, mice and birds showed that they contain sufficient vitamin D to meet the needs of growing kittens. Although we know now that vitamin D is an essential nutriment in cats, the dietary levels already recommended in commercial foods will fulfill all their requirements (AAFCO 1998, NRC 1986).
Most veterinarians warn their clients to be cautious when supplementing with vitamin preparations containing vitamin A and D because of the potential for toxicity. While it is still a good advice, cats are much more resistant to vitamin D toxicity than it could be expected.
Long term (>18 month) experiments with breeding queens given diets containing about 30,000 IU of vitamin D3 (cholecalciferol) /kg diet (over 100 times the requirement for growing kittens) have been undertaken at Davis, and they have been unable to demonstrate any pathological changes due to this high intake of vitamin D. Cats given these diets maintain high circulating levels of vitamin D and 25-OHD in plasma. It is possible that other dietary conditions than those tested may augment the toxicity of vitamin D to cats.
Most animals can obtain the vitamin niacin from two sources: - preformed nicotinamides in food or from the metabolism of the amino acid tryptophan. While cats possess all the enzymes for nicotinic acid synthesis from tryptophan, catabolism synthesis is ineffective (MacDonald 1984). Synthesis is prevented by the high activity of an enzyme that directs the metabolism of an intermediate in the pathway along an alternate pathway not leading to nicotinic acid synthesis. A strict carnivorous diet is always well supplied with niacin, so there has been no advantage for cats to synthesize a nutrient already present in abundant levels in the diet.
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