Brouwer D A, van Beek J, Ferwerda H, Brugman A M, van der Klis F R, van der Heiden H J, Muskiet F A
Central Laboratory for Clinical Chemistry, University Hospital Groningen, The Netherlands.
Br J Nutr. 1998 Jun;79(6):527-32. doi: 10.1079/bjn19980091.
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) received 37.5 micrograms cholecalciferol/d for 14 d and were subsequently studied 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 the study (days 98-101). During treatment, plasma cholecalciferol increased 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 plasma cholecalciferol and 25(OH)D, and perirenal and subcutaneous adipose tissue were: 1.4, 22.5, 97.5 and 80.9 d respectively. Fasting, as compared with ad libitum feeding, caused increased plasma free fatty acids, weight loss up to 14% and increased adipose tissue cholecalciferol (nmol/g wet weight). It did not affect plasma cholecalciferol immediately after cholecalciferol treatment, but raised plasma 25(OH)D. Fasting at the end of the study decreased plasma cholecalciferol and increased plasma 25(OH)D. We conclude that orally-administered cholecalciferol rapidly accumulates in adipose tissue and that it is very slowly released while there is energy balance. Fasting causes preferential loss of triacylglycerols from adipose tissue, as opposed to cholecalciferol, but nevertheless augments plasma 25(OH)D. Adipose tissue may act as a 'buffer to functional vitamin D status' by preventing, to a certain extent, unregulated production of 25(OH)D from dietary vitamin D, and by slowly releasing vitamin D under fasting conditions.
我们研究了口服大剂量胆钙化醇对血浆和脂肪组织中胆钙化醇及其后续释放的影响，以及对血浆25-羟基维生素D（25(OH)D）的影响。雌性Wistar大鼠（n = 126）连续14天每天接受37.5微克胆钙化醇，随后再研究88天。两个亚组，每组18只大鼠，分别在治疗后立即（第14 - 17天）和研究结束时（第98 - 101天）禁食3天。治疗期间，血浆胆钙化醇迅速升高至稳态。治疗后1 - 2天，血浆25(OH)D和脂肪组织胆钙化醇呈线性增加。血清钙和无机磷也升高。随后，血浆胆钙化醇和25(OH)D以及肾周和皮下脂肪组织的半衰期分别为：1.4天、22.5天、97.5天和80.9天。与自由采食相比，禁食导致血浆游离脂肪酸增加、体重减轻达14%，脂肪组织胆钙化醇（nmol/g湿重）增加。在胆钙化醇治疗后，禁食对血浆胆钙化醇无立即影响，但会升高血浆25(OH)D。研究结束时禁食会降低血浆胆钙化醇并升高血浆25(OH)D。我们得出结论，口服胆钙化醇会在脂肪组织中迅速蓄积，在能量平衡时其释放非常缓慢。与胆钙化醇不同，禁食导致脂肪组织中三酰甘油优先丢失，但仍会增加血浆25(OH)D。脂肪组织可能通过在一定程度上防止膳食维生素D不受调控地产生25(OH)D，并在禁食条件下缓慢释放维生素D，从而起到“功能性维生素D状态缓冲器”的作用。
