Abstract
The relationship between dietary vitamin A and all-trans-retinoic acid levels in serum and tissues had not been quantified. We determined the impact of dietary vitamin A on retinoid levels in serum, liver, kidney, testis, and epididymal white adipose of five mouse strains: AKR/J; BALB/cByJ; C3H/HeJ; C57BL/6J; 129S1/SvImJ. Retinoids were quantified in mice fed copious vitamin A (lab chow, ≥20 IU/g) followed by one month feeding a vitamin A-sufficient diet (4 IU/g), or after three generations of feeding a vitamin A-sufficient diet. Retinol and retinyl esters were measured by high-performance liquid chromatography with ultraviolet absorbance detection. All-trans-retinoic acid was quantified by liquid chromatography tandem mass spectrometry. The amounts of dietary vitamin A had long-term strain-specific effects on tissue retinyl ester, retinol and all-trans-retinoic acid concentrations. Three generations of feeding a vitamin A-sufficient diet decreased all-trans-retinoic acid in most tissues of most strains, in some cases more than 60%, compared to a diet with copious vitamin A. With both diets, all-trans-retinoic acid concentrations maintained an order of liver ≈ testis > kidney > white adipose tissue ≈ serum. Neither retinol nor all-trans-retinoic acid in serum reflected all-trans-retinoic acid concentrations in tissues. Strain and tissue-specific differences in retinol and all-trans-retinoic acid altered by different amounts of dietary vitamin A could have profound effects on retinoid action. This would be the case especially with the increased all-trans-retinoic acid values associated with the amounts of vitamin A and its precursors (carotenoids) in chow diets.
Highlights
Vitamin A is essential for diverse physiological processes in post-natal vertebrates, including modulating energy metabolism, supporting neurogenesis and nervous system function, and sustaining the immune response [1,2,3]
Previous reports with mice fed copious vitamin A have shown that liver retinyl esters (RE) correlate directly with dietary vitamin A levels when mice are challenged with even greater dietary vitamin A, or fed a vitamin A-deficient diet [21,22]
The present study addressed these issues, and revealed that the transition of copious to sufficient dietary vitamin A affects retinoid homeostasis with strain and tissue-specificity
Summary
Vitamin A (retinol) is essential for diverse physiological processes in post-natal vertebrates, including modulating energy metabolism, supporting neurogenesis and nervous system function, and sustaining the immune response [1,2,3]. Standard rodent chow consists of natural sources, which vary in precise compositions, and contains copious amounts of nutrients, including vitamins [12]. Semi-purified diets provide a consistent nutrient composition in amounts that meet the National Research Council recommendations for rodent nutrient intake, while avoiding delivery of copious amounts of vitamins that can confound studies of nutrient functions. The American Institute of Nutrition (AIN) has determined that the minimum amount of vitamin A necessary for rodents is 2.9 IU/g diet, and recommends an intake of 4 IU/g diet to provide a margin of safety [13,14]. Vitamin A in rodent chow diet is ,5 times the recommended intake for rodents, and is exceptionally copious
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