reverse effect of mammalian hypocalcemic cortisol in fish cortisol stimulates ca2+ uptake via glucocorticoid receptor-mediated vitamin d3 metabolism反向的影响哺乳动物hypocalcemic皮质醇在鱼类皮质醇刺激通过糖皮质激素受体介导ca2 +吸收维生素d3的新陈代谢.pdfVIP

reverse effect of mammalian hypocalcemic cortisol in fish cortisol stimulates ca2+ uptake via glucocorticoid receptor-mediated vitamin d3 metabolism反向的影响哺乳动物hypocalcemic皮质醇在鱼类皮质醇刺激通过糖皮质激素受体介导ca2 +吸收维生素d3的新陈代谢.pdf

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reverseeffectofmammalianhypocalcemiccortisolinfishcortisolstimulatesca2uptakeviaglucocorticoidreceptor-mediatedvitamind3metabolism反向的影响哺乳动物hypocalcemic皮质醇在鱼类皮质醇刺激通过糖皮质激素受体介导ca2吸收维生素d3的新陈代谢

Reverse Effect of Mammalian Hypocalcemic Cortisol in Fish: Cortisol Stimulates Ca2+ Uptake via Glucocorticoid Receptor-Mediated Vitamin D3 Metabolism 1,2 3 4 5 1,2,4 Chia-Hao Lin , I-Lun Tsai , Che-Hsien Su , Deng-Yu Tseng , Pung-Pung Hwang * 1 Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, Republic of China, 2 Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan, Republic of China, 3 Department of Aquaculture, National Pingtung University of Science and Technology, Pingtung, Taiwan, Republic of China, 4 Institute of Fishery Science, National Taiwan University, Taipei, Taiwan, Republic of China, 5 Department of Biological Sciences and Technology, National University of Tainan, Tainan, Republic of China Abstract Cortisol was reported to downregulate body-fluid Ca2+ levels in mammals but was proposed to show hypercalcemic effects in teleostean fish. Fish, unlike terrestrial vertebrates, obtain Ca2+ from the environment mainly via the gills and skin rather than by dietary means, and have to regulate the Ca2+ uptake functions to cope with fluctuating Ca2+ levels in aquatic environments. Cortisol was previously found to regulate Ca2+ uptake in fish; however, the molecular mechanism behind this is largely unclear. Zebrafish were used as a model to explore this issue. Acclimation to low-Ca2+ fresh water stimulated Ca2+ influx and expression of epithelial calcium channel (ecac), 11b-hydroxylase and the glucocorticoid receptor (gr). Exogenous cortisol increased Ca2+ influx and the expressions of ecac and hydroxysteroid 11-beta dehydrogenase 2 (hsd

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