Glucocorticoid-stimulated utilization of substrates in hepatic mitochondria☆
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Glucocorticoid receptor isoforms in human hepatocarcinoma HepG2 and SaOS-2 osteosarcoma cells: Presence of glucocorticoid receptor alpha in mitochondria and of glucocorticoid receptor beta in nucleoli
2005, International Journal of Biochemistry and Cell BiologyCitation Excerpt :As GRβ does not bind glucocorticoids, its action cannot be directly modulated by these hormones but through interaction with GRα (Bamberger et al., 1995; Lu & Cidlowski, 2004) or/and other agents, such as nucleolin. Lastly, steroid and thyroid hormones, in addition to their genomic action, exert rapid effects on substrate utilization, mitochondrial permeability and ionic concentrations (Wakat & Haynes, 1977). A possible role of mitochondrial steroid/thyroid hormone receptors in the rapid genomic actions of the respective hormones should be considered.
Glucocorticoid and thyroid hormone receptors in mitochondria of animal cells
2003, International Review of CytologyEffect of dexamethasone on mitochondrial maturation in the fetal rat brain
2002, American Journal of Obstetrics and GynecologyCitation Excerpt :Simon et al23 have also reported that glucocorticoids decreased cytochrome c oxidase activity of isolated rat kidney mitochondria. On the contrary, Wakat and Haynes24 have shown, after a short-term administration of glucocorticoids to rats, an increase of substrate use by isolated hepatic mitochondria. These differences indicate that the glucocorticoid effects on mitochondria vary with age and organs.
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This work was supported by National Institutes of Health Grants AM-14347, AM-17042, and F32 AM05165 (DW is the recipient of a Postdoctoral Fellowship from the Institute for Arthritis, Metabolism, and Digestive Diseases). A preliminary report of this work has been presented (17).