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维生素D和1,25 - 二羟维生素D3作为免疫系统的调节剂。

Vitamin D and 1,25-dihydroxyvitamin D3 as modulators in the immune system.

作者信息

Mathieu Chantal, van Etten Evelyne, Decallonne Brigitte, Guilietti Annapaula, Gysemans Conny, Bouillon Roger, Overbergh Lut

机构信息

LEGENDO, Katholieke Universiteit Leuven, O&N, Herestraat 49, 3000 Leuven, Belgium.

出版信息

J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):449-52. doi: 10.1016/j.jsbmb.2004.03.014.

Abstract

Treatment from weaning until old age with 1,25-dihydroxyvitamin D (1,25(OH)(2)D(3)) prevents diabetes in NOD mice. It is mainly through its actions on dendritic cells (DCs), that 1,25(OH)(2)D(3) changes the function of potentially autoreactive T lymphocytes. In contrast, early life treatment (from 3 to 70 days of age) of NOD mice with vitamin D or 1,25(OH)(2)D(3) did not influence final diabetes incidence at 200 days of age. Also in spontaneous diabetic BB rats, diabetes could not be prevented by early life treatment (from 3 to 50 days of age) with vitamin D (1000 IU per day) or 1,25(OH)(2)D(3) (0.2 microg/kg per day or 1 microg/kg per 2 days). However, when NOD mice were made vitamin D deficient in early life (until 100 days of age), diabetes onset occurred earlier and final incidence was increased. These data further support a role for vitamin D and its metabolites in the pathogenesis of type 1 diabetes in NOD mice.

摘要

从断奶到老年用1,25 - 二羟维生素D(1,25(OH)₂D₃)治疗可预防非肥胖糖尿病(NOD)小鼠患糖尿病。1,25(OH)₂D₃主要通过作用于树突状细胞(DCs)来改变潜在自身反应性T淋巴细胞的功能。相比之下,用维生素D或1,25(OH)₂D₃对NOD小鼠进行早期治疗(3至70日龄)并不影响200日龄时最终的糖尿病发病率。同样,在自发性糖尿病BB大鼠中,早期治疗(3至50日龄)给予维生素D(每天1000国际单位)或1,25(OH)₂D₃(每天0.2微克/千克或每2天1微克/千克)也无法预防糖尿病。然而,当NOD小鼠在生命早期(直到100日龄)维生素D缺乏时,糖尿病发病更早且最终发病率增加。这些数据进一步支持了维生素D及其代谢产物在NOD小鼠1型糖尿病发病机制中的作用。

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