Cantorna M T, Munsick C, Bemiss C, Mahon B D
Department of Nutrition, College of Health and Human Development, The Pennsylvania State University, University Park, PA 16802, USA.
J Nutr. 2000 Nov;130(11):2648-52. doi: 10.1093/jn/130.11.2648.
Anecdotal data suggest that the amount of vitamin D available in the environment either from sunshine exposure or diet may be an important factor affecting the development of inflammatory bowel disease (IBD) in humans. We tested the vitamin D hypothesis in an experimental animal model of IBD. Interleukin (IL)-10 knockout (KO) mice, which spontaneously develop symptoms resembling human IBD, were made vitamin D deficient, vitamin D sufficient or supplemented with active vitamin D (1,25-dihydroxycholecalciferol). Vitamin D-deficient IL-10 KO mice rapidly developed diarrhea and a wasting disease, which induced mortality. In contrast, vitamin D-sufficient IL-10 KO mice did not develop diarrhea, waste or die. Supplementation with 50 IU of cholecalciferol (5.0 microgram/d) or 1, 25-dihydroxycholecalciferol (0.005 microgram/d) significantly (P < 0. 05) ameliorated symptoms of IBD in IL-10 KO mice. 1, 25-Dihydroxycholecalciferol treatment (0.2 microgram/d) for as little as 2 wk blocked the progression and ameliorated (P < 0.05) symptoms in IL-10 KO mice with already established IBD.
轶事数据表明,环境中通过阳光照射或饮食获取的维生素D量可能是影响人类炎症性肠病(IBD)发病的一个重要因素。我们在IBD实验动物模型中验证了维生素D假说。白细胞介素(IL)-10基因敲除(KO)小鼠会自发出现类似人类IBD的症状,我们将其分为维生素D缺乏组、维生素D充足组或补充活性维生素D(1,25-二羟胆钙化醇)组。维生素D缺乏的IL-10 KO小鼠迅速出现腹泻和消瘦疾病,并导致死亡。相比之下,维生素D充足的IL-10 KO小鼠未出现腹泻、消瘦或死亡。补充50 IU胆钙化醇(5.0微克/天)或1,25-二羟胆钙化醇(0.005微克/天)可显著(P<0.05)改善IL-10 KO小鼠的IBD症状。仅用1,25-二羟胆钙化醇(0.2微克/天)治疗2周就能阻止已患IBD的IL-10 KO小鼠病情进展并改善(P<0.05)症状。