Novel Causes of Generalized Glucocorticoid Resistance
Abstract Glucocorticoid resistance is a rare condition characterized by generalized, partial, target-tissue insensitivity to glucocorticoids. Compensatory elevations in circulating adrenocorticotropic hormone (ACTH) concentrations lead to increased secretion of cortisol and adrenal steroids with min...
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| Veröffentlicht in: | Hormone and metabolic research 2007-06, Vol.39 (6), p.445-450 |
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| creator | Charmandari, E. Kino, T. |
| description | Abstract
Glucocorticoid resistance is a rare condition characterized by generalized, partial, target-tissue insensitivity to glucocorticoids. Compensatory elevations in circulating adrenocorticotropic hormone (ACTH) concentrations lead to increased secretion of cortisol and adrenal steroids with mineralocorticoid and/or androgenic activity, but no clinical evidence of hypercortisolism. The clinical spectrum of the condition is broad, ranging from asymptomatic to severe cases of hyperandrogenism, fatigue and/or mineralocorticoid excess. The molecular basis of glucocorticoid resistance has been ascribed to mutations in the human glucocorticoid receptor (hGR) gene, which impair glucocorticoid signal transduction, thereby altering tissue sensitivity to glucocorticoids. The study of functional defects of natural hGR mutants enhances our understanding of the molecular mechanisms of hGR action and highlights the importance of integrated cellular and molecular signaling mechanisms for maintaining homeostasis and preserving normal physiology. |
| doi_str_mv | 10.1055/s-2007-980196 |
| format | Article |
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Glucocorticoid resistance is a rare condition characterized by generalized, partial, target-tissue insensitivity to glucocorticoids. Compensatory elevations in circulating adrenocorticotropic hormone (ACTH) concentrations lead to increased secretion of cortisol and adrenal steroids with mineralocorticoid and/or androgenic activity, but no clinical evidence of hypercortisolism. The clinical spectrum of the condition is broad, ranging from asymptomatic to severe cases of hyperandrogenism, fatigue and/or mineralocorticoid excess. The molecular basis of glucocorticoid resistance has been ascribed to mutations in the human glucocorticoid receptor (hGR) gene, which impair glucocorticoid signal transduction, thereby altering tissue sensitivity to glucocorticoids. The study of functional defects of natural hGR mutants enhances our understanding of the molecular mechanisms of hGR action and highlights the importance of integrated cellular and molecular signaling mechanisms for maintaining homeostasis and preserving normal physiology.</description><identifier>ISSN: 0018-5043</identifier><identifier>EISSN: 1439-4286</identifier><identifier>DOI: 10.1055/s-2007-980196</identifier><identifier>PMID: 17578762</identifier><language>eng</language><publisher>Germany</publisher><subject>Adrenocorticotropic Hormone - blood ; Drug Resistance ; Glucocorticoids - pharmacology ; Humans ; Mutation ; Receptors, Glucocorticoid - genetics ; Review ; Signal Transduction</subject><ispartof>Hormone and metabolic research, 2007-06, Vol.39 (6), p.445-450</ispartof><rights>Georg Thieme Verlag KG Stuttgart · New York</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c328t-932b379f78c441d403d55c1e3d38d5c6cc696641bb348a08365a6c7234b997683</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.thieme-connect.de/products/ejournals/pdf/10.1055/s-2007-980196.pdf$$EPDF$$P50$$Gthieme$$H</linktopdf><linktohtml>$$Uhttps://www.thieme-connect.de/products/ejournals/html/10.1055/s-2007-980196$$EHTML$$P50$$Gthieme$$H</linktohtml><link.rule.ids>314,776,780,3004,3005,27901,27902,54534,54535</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17578762$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Charmandari, E.</creatorcontrib><creatorcontrib>Kino, T.</creatorcontrib><title>Novel Causes of Generalized Glucocorticoid Resistance</title><title>Hormone and metabolic research</title><addtitle>Horm Metab Res</addtitle><description>Abstract
Glucocorticoid resistance is a rare condition characterized by generalized, partial, target-tissue insensitivity to glucocorticoids. Compensatory elevations in circulating adrenocorticotropic hormone (ACTH) concentrations lead to increased secretion of cortisol and adrenal steroids with mineralocorticoid and/or androgenic activity, but no clinical evidence of hypercortisolism. The clinical spectrum of the condition is broad, ranging from asymptomatic to severe cases of hyperandrogenism, fatigue and/or mineralocorticoid excess. The molecular basis of glucocorticoid resistance has been ascribed to mutations in the human glucocorticoid receptor (hGR) gene, which impair glucocorticoid signal transduction, thereby altering tissue sensitivity to glucocorticoids. The study of functional defects of natural hGR mutants enhances our understanding of the molecular mechanisms of hGR action and highlights the importance of integrated cellular and molecular signaling mechanisms for maintaining homeostasis and preserving normal physiology.</description><subject>Adrenocorticotropic Hormone - blood</subject><subject>Drug Resistance</subject><subject>Glucocorticoids - pharmacology</subject><subject>Humans</subject><subject>Mutation</subject><subject>Receptors, Glucocorticoid - genetics</subject><subject>Review</subject><subject>Signal Transduction</subject><issn>0018-5043</issn><issn>1439-4286</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEtLw0AURgdRbK0u3UpWrhyd92MpRatQFETXw2RygylJR2cSQX-9KSm4cnW5cDjwHYTOKbmmRMqbjBkhGltDqFUHaE4Ft1gwow7RnBBqsCSCz9BJzpvxFZaKYzSjWmqjFZsj-RS_oC2WfsiQi1gXK9hC8m3zA1WxaocQQ0x9E2JTFS-Qm9z7bYBTdFT7NsPZ_i7Q2_3d6_IBr59Xj8vbNQ6cmR5bzkquba1NEIJWgvBKykCBV9xUMqgQlFVK0LLkwnhiuJJeBc24KK3VyvAFupy8Hyl-DpB71zU5QNv6LcQhO00U14zREcQTGFLMOUHtPlLT-fTtKHG7Ti67XSc3dRr5i714KDuo_uh9mBG4moD-vYEO3CYOaTtO_cf3C0UZbuE</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>Charmandari, E.</creator><creator>Kino, T.</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20070601</creationdate><title>Novel Causes of Generalized Glucocorticoid Resistance</title><author>Charmandari, E. ; Kino, T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c328t-932b379f78c441d403d55c1e3d38d5c6cc696641bb348a08365a6c7234b997683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adrenocorticotropic Hormone - blood</topic><topic>Drug Resistance</topic><topic>Glucocorticoids - pharmacology</topic><topic>Humans</topic><topic>Mutation</topic><topic>Receptors, Glucocorticoid - genetics</topic><topic>Review</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Charmandari, E.</creatorcontrib><creatorcontrib>Kino, T.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Hormone and metabolic research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Charmandari, E.</au><au>Kino, T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Novel Causes of Generalized Glucocorticoid Resistance</atitle><jtitle>Hormone and metabolic research</jtitle><addtitle>Horm Metab Res</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>39</volume><issue>6</issue><spage>445</spage><epage>450</epage><pages>445-450</pages><issn>0018-5043</issn><eissn>1439-4286</eissn><abstract>Abstract
Glucocorticoid resistance is a rare condition characterized by generalized, partial, target-tissue insensitivity to glucocorticoids. Compensatory elevations in circulating adrenocorticotropic hormone (ACTH) concentrations lead to increased secretion of cortisol and adrenal steroids with mineralocorticoid and/or androgenic activity, but no clinical evidence of hypercortisolism. The clinical spectrum of the condition is broad, ranging from asymptomatic to severe cases of hyperandrogenism, fatigue and/or mineralocorticoid excess. The molecular basis of glucocorticoid resistance has been ascribed to mutations in the human glucocorticoid receptor (hGR) gene, which impair glucocorticoid signal transduction, thereby altering tissue sensitivity to glucocorticoids. The study of functional defects of natural hGR mutants enhances our understanding of the molecular mechanisms of hGR action and highlights the importance of integrated cellular and molecular signaling mechanisms for maintaining homeostasis and preserving normal physiology.</abstract><cop>Germany</cop><pmid>17578762</pmid><doi>10.1055/s-2007-980196</doi><tpages>6</tpages></addata></record> |
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| ispartof | Hormone and metabolic research, 2007-06, Vol.39 (6), p.445-450 |
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| language | eng |
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| source | MEDLINE; Thieme Connect Journals |
| subjects | Adrenocorticotropic Hormone - blood Drug Resistance Glucocorticoids - pharmacology Humans Mutation Receptors, Glucocorticoid - genetics Review Signal Transduction |
| title | Novel Causes of Generalized Glucocorticoid Resistance |
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