Department of Biochemistry, University of Wisconsin-Madison, 433 Babcock Drive, Madison, WI 53706-1544, USA.
Arch Biochem Biophys. 2011 Sep 15;513(2):140-3. doi: 10.1016/j.abb.2011.07.005. Epub 2011 Jul 19.
Multiple sclerosis incidence is clearly inversely related to sun exposure. This observation led to the idea that vitamin D might be responsible for this relationship. Providing super-physiologic doses of the hormonal form of vitamin D, 1α,25-dihydroxyvitamin D₃, suppresses an animal model of multiple sclerosis, i.e. experimental autoimmune encephalomyelitis (EAE) but causes unwanted hypercalcemia. Further, dietary calcium is needed for this activity of 1α,25-dihydroxyvitamin D₃. B10PL mice were maintained on a vitamin D-deficient diet for two generations to produce frank vitamin D deficiency. These animals showed delayed onset and reduced severity of EAE compared to control animals on the same diet and given vitamin D₃ or provided a vitamin D-containing chow diet. Thus, vitamin D deficiency interferes with the development of this autoimmune disease rather than increasing susceptibility.
多发性硬化症的发病率显然与阳光照射呈负相关。这一观察结果促使人们认为维生素 D 可能对此关系负责。给予超生理剂量的维生素 D 激素形式，1α，25-二羟维生素 D₃，可抑制多发性硬化症的动物模型，即实验性自身免疫性脑脊髓炎（EAE），但会导致不必要的高钙血症。此外，1α，25-二羟维生素 D₃ 的这种活性需要膳食钙。将 B10PL 小鼠维持在维生素 D 缺乏饮食中两代以产生明显的维生素 D 缺乏症。与给予维生素 D₃ 或提供含维生素 D 的饲料饮食的同饮食对照动物相比，这些动物的 EAE 发病时间延迟且严重程度降低。因此，维生素 D 缺乏症会干扰这种自身免疫性疾病的发展，而不是增加易感性。
