RAT ADIPOSE-TISSUE RAPIDLY ACCUMULATES AND SLOWLY RELEASES AN ORALLY-ADMINISTERED HIGH VITAMIN-D DOSE

We investigated the effect of oral high-dose cholecalciferol on plasma and adipose tissue cholecalciferol and its subsequent release, and on plasma 25-hydroxyvitamin D (25(OH)D). Female Wistar rats (n 126) rece ived 37.5 mu g cholecalciferol/d for 14 d and were subsequently studie d for a further 88 d. Two subgroups of eighteen rats each were fasted for 3 d immediately after treatment (days 14-17) and at the end of tie study (days 98-101). During treatment, plasma cholecalciferol increas ed rapidly to reach a steady-state. Plasma 25(OH)D and adipose tissue cholecalciferol increased linearly for 1-2 d after treatment. Serum Ca and inorganic phosphate also increased. Subsequently half-lives of pl asma cholecalciferol and 25(OH)D, and perirenal and subcutaneous adipo se tissue were: 1.4, 22.5, 97.5 and 80.9 d respectively. Fasting, as c ompared with ad libitum feeding, caused increased plasma free fatty ac ids, weight loss up to 14 % and increased adipose tissue cholecalcifer ol (nmol/g wet weight). It did not affect plasma cholecalciferol immed iately after cholecalciferol treatment, but raised plasma 25(OH)D. Fas ting at the end of the study decreased plasma cholecalciferol and incr eased plasma 25(OH)D. We conclude that orally-administered cholecalcif erol rapidly accumulates in adipose tissue and that it is very slowly released while there is energy balance. Fasting causes preferential lo ss of triacylglycerols from adipose tissue, as opposed to cholecalcife rol, but nevertheless augments plasma 25(OH)D. Adipose tissue may act as a 'buffer to functional vitamin D status' by preventing, to a certa in extent, unregulated production of 25(OH)D from dietary vitamin D, a nd by slowly releasing vitamin D under fasting conditions.