Vitamin A metabolism in the cat
Dijk, S. van
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The vitamin A metabolism in cats appears to be different, at some levels, from other species. However, there is still much unknown. The main conclusions are: - Cats depend on retinyl esters in their diet, in contrast to species that can use β-carotene. • - Instead of transporting retinol in blood bound to Retinol Binding Protein, cats transport retinyl esters • bound to lipoproteins. - It appears that the vitamin A level in blood is not homeostatically regulated. • - Cats have a reduced urinary vitamin A excretion compared to dogs.• Deforming cervical spondylosis is often associated with hypervitaminosis A. However, we suggest that there is an interaction between vitamin A and vitamin D. To increase the understanding about this subject, we have reviewed literature. Unfortunately, potential interactions between vitamins A and D have not been examined in cats. Thus, there is still much to be investigated. The second subject of this study was to determine whether the enzymes CYP24A1, CYP27B1, CYP1A2, CYP26A1, CYP26B1 and LRAT are expressed in cat liver, using quantitative PCR. The enzymes CYP24A1 and CYP27B1 from the vitamin D metabolism were not detected in the cat liver. This is similar to other species. The enzymes of the vitamin A metabolism, CYP1A2 CYP26A1, CYP26B1 and LRAT, are expressed in cat liver. In addition we made a comparison of the quantitative expression between healthy and cirrhotic livers, to see if a shift would occur. The hyperostoses are often seen in older cats, which generally have cirrhotic livers. A shift in expression was significant for CYP26A1. The expression in young livers is very low, while the expression in old livers is relatively high. This is remarkable, because CYP26 is responsible for the breakdown of vitamin A. The results of this study does not indicate a direct effect of the examined enzymes in the pathophysiology of the metabolic bone disease. We suggest that this disease is most likely multifactorial. More research should be done to understand the pathophysiology of deforming cervical spondylosis.