Basal concentrations of various steroids in the nonobese diabetic (NOD) mouse and effect of immobilization stress

被引:17
作者
Durant, S [1 ]
Christeff, N [1 ]
Coulaud, J [1 ]
Nunez, EA [1 ]
Dardenne, M [1 ]
Homo-Delarche, F [1 ]
机构
[1] CNRS, URA 1461, F-75730 Paris 15, France
关键词
NOD mouse; immobilization; corticosterone; dehydroepiandrosterone; sex steroids; castration; adrenalectomy;
D O I
10.3109/08916939808995373
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The progression of type I diabetes in the NOD mouse is modulated by, among other things, stressful events and steroids. We measured in 2-month-old prediabetic NOD mice various circulating steroids (progesterone, corticosterone, dehydroepiandrosterone, Delta 4-androstenedione, testosterone, estrone and estradiol) under basal and stressful conditions (1.5h immobilization), Basal progesterone concentrations were low but measurable in randomized cycling NOD females and under the detection limit in NOD males. Immobilization increased progesterone concentrations in both sexes, Serum corticosterone concentrations also increased after immobilization but with the sexual dimorphism normally observed in rodents. Dehydroepiandrosterone concentrations were similar in both sexes and remained unaffected by stress. Testosterone and Delta 4-androstenedione were drastically reduced after immobilization in NOD males. Serum estrone and estradiol were not found to be statistically different in NOD females and males, but slightly higher to that described in the literature, and immobilization increased estrone concentrations in NOD males. In conclusion, while nonspecific to the NOD mouse, the modulation of circulating corticosteroids, estrogens and androgens induced by environmental factors may be part of the mechanism(s) by which these factors modulate the progression of type I diabetes. The hormonal changes may act in a complex manner at different levels: the immune system, the islet of Langerhans and the other structures involved in glucose homeostasis.
引用
收藏
页码:249 / 258
页数:10
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