{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T11:51:55Z","timestamp":1790423515976,"version":"4.1.0"},"reference-count":88,"publisher":"Bioscientifica","issue":"1","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2019,1]]},"abstract":"<jats:p>\n                    Glucocorticoid signaling is context dependent, and in certain scenarios, glucocorticoid receptors (GRs) are able to engage with other members of the nuclear receptor subfamily. Glucocorticoid signaling can exert sexually dimorphic effects, suggesting a possible interaction with androgen sex hormones. We therefore set out to determine the crosstalk between glucocorticoids and androgens in metabolic tissues including white adipose tissue, liver and brown adipose tissue. Thereto we exposed male C57BL\/6J mice to elevated levels of corticosterone in combination with an androgen receptor (AR) agonist or an AR antagonist. Systemic and local glucocorticoid levels were determined by mass spectrometry, and tissue expression of glucocorticoid-responsive genes and protein was measured by RT-qPCR and Western blot, respectively. To evaluate crosstalk\n                    <jats:italic>in vitro<\/jats:italic>\n                    , cultured white and brown adipocytes were exposed to a combination of corticosterone and an AR agonist. We found that AR agonism potentiated transcriptional response to GR\n                    <jats:italic>in vitro<\/jats:italic>\n                    in white and brown adipocytes and\n                    <jats:italic>in vivo<\/jats:italic>\n                    in white and brown adipose tissues. Conversely, AR antagonism substantially attenuated glucocorticoid signaling in white adipose tissue and liver. In white adipose tissue, this effect could partially be attributed to decreased 11B-hydroxysteroid dehydrogenase type 1-mediated glucocorticoid regeneration upon AR antagonism. In liver, attenuated GR activity was independent of active glucocorticoid ligand levels. We conclude that androgen signaling modulates GR transcriptional output in a tissue-specific manner.\n                  <\/jats:p>","DOI":"10.1530\/joe-18-0503","type":"journal-article","created":{"date-parts":[[2018,10,4]],"date-time":"2018-10-04T08:06:47Z","timestamp":1538640407000},"page":"51-63","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":29,"title":["Androgens modulate glucocorticoid receptor activity in adipose tissue and liver"],"prefix":"10.1530","volume":"240","author":[{"given":"Dieuwertje C E","family":"Spaanderman","sequence":"first","affiliation":[{"name":"1Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, the Netherlands"},{"name":"2Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Nixon","sequence":"additional","affiliation":[{"name":"3BHF Centre for Cardiovascular Science, The Queen\u2019s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacobus C","family":"Buurstede","sequence":"additional","affiliation":[{"name":"1Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, the Netherlands"},{"name":"2Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hetty H C M","family":"Sips","sequence":"additional","affiliation":[{"name":"1Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, the Netherlands"},{"name":"2Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maaike","family":"Schilperoort","sequence":"additional","affiliation":[{"name":"1Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, the Netherlands"},{"name":"2Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eline N","family":"Kuipers","sequence":"additional","affiliation":[{"name":"1Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, the Netherlands"},{"name":"2Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emma A","family":"Backer","sequence":"additional","affiliation":[{"name":"1Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, the Netherlands"},{"name":"2Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sander","family":"Kooijman","sequence":"additional","affiliation":[{"name":"1Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, the Netherlands"},{"name":"2Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick C N","family":"Rensen","sequence":"additional","affiliation":[{"name":"1Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, the Netherlands"},{"name":"2Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natalie Z M","family":"Homer","sequence":"additional","affiliation":[{"name":"3BHF Centre for Cardiovascular Science, The Queen\u2019s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian R","family":"Walker","sequence":"additional","affiliation":[{"name":"3BHF Centre for Cardiovascular Science, The Queen\u2019s Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom"},{"name":"4Institute for Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Onno C","family":"Meijer","sequence":"additional","affiliation":[{"name":"1Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, the Netherlands"},{"name":"2Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan","family":"Kroon","sequence":"additional","affiliation":[{"name":"1Division of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, the Netherlands"},{"name":"2Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"ref481","doi-asserted-by":"crossref","first-page":"1539","DOI":"10.1038\/ijo.2015.102","article-title":"Estrogens protect male mice from obesity complications and influence glucocorticoid metabolism","volume":"39","year":"2015","journal-title":"International Journal of Obesity"},{"key":"ref731","doi-asserted-by":"crossref","first-page":"41","DOI":"10.1016\/j.mce.2012.12.014","article-title":"How glucocorticoid receptors modulate the activity of other transcription factors: a scope 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