Common polymorphisms in the glucocorticoid receptor gene are associated with adrenocortical responses to psychosocial stress.
Identifieur interne : 000746 ( PubMed/Corpus ); précédent : 000745; suivant : 000747Common polymorphisms in the glucocorticoid receptor gene are associated with adrenocortical responses to psychosocial stress.
Auteurs : Stefan Wüst ; Elisabeth F C. Van Rossum ; Ilona S. Federenko ; Jan W. Koper ; Robert Kumsta ; Dirk H. HellhammerSource :
- The Journal of clinical endocrinology and metabolism [ 0021-972X ] ; 2004.
English descriptors
- KwdEn :
- Adrenal Cortex (physiopathology), Adrenocorticotropic Hormone (metabolism), Adult, Alleles, Cosyntropin (pharmacology), Dexamethasone (pharmacology), Genotype, Glucocorticoids (pharmacology), Heterozygote, Humans, Hydrocortisone (metabolism), Male, Polymorphism, Genetic, Receptors, Glucocorticoid (genetics), Reference Values, Saliva (metabolism), Stress, Psychological (genetics).
- MESH :
- chemical , genetics : Receptors, Glucocorticoid.
- chemical , metabolism : Adrenocorticotropic Hormone, Hydrocortisone.
- chemical , pharmacology : Cosyntropin, Dexamethasone, Glucocorticoids.
- genetics : Stress, Psychological.
- metabolism : Saliva.
- physiopathology : Adrenal Cortex.
- Adult, Alleles, Genotype, Heterozygote, Humans, Male, Polymorphism, Genetic, Reference Values.
Abstract
Chronic dysregulation of hypothalamus-pituitary-adrenal axis activity is related to several stress-related disorders. Evidence suggests that polymorphisms in the glucocorticoid receptor (GR) gene may have an impact on this neuroendocrine system. In the present investigation, 112 healthy males were studied to estimate the impact of three GR gene polymorphisms (BclI RFLP, N363S, ER22/23EK) on cortisol and ACTH responses to psychosocial stress (Trier Social Stress Test) and pharmacological stimulation (1 microg ACTH(1-24), 0.5 mg dexamethasone). Because only four ER22/23EK heterozygotes were identified, these subjects were not statistically analyzed. Compared with subjects with the wild-type GR genotype (n = 36), 363S allele carriers (n = 10) showed significantly increased salivary cortisol responses to stress, whereas the BclI genotype GG (n = 18) was associated with a diminished cortisol response. BclI heterozygotes and homozygotes (GG) exhibited a trend toward lower ACTH responses, compared with wild-type subjects and 363S carriers. The cortisol response to ACTH(1-24) administration was not significantly different between genotypes. After dexamethasone ingestion, 363S carriers showed a trend toward an enhanced cortisol suppression. This is the first report documenting an impact of GR gene polymorphisms on cortisol (and perhaps ACTH) responses to psychosocial stress. These variants may contribute to the individual vulnerability for hypothalamus-pituitary-adrenal-related disorders.
DOI: 10.1210/jc.2003-031148
PubMed: 14764763
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Koper</name></author><author><name sortKey="Kumsta, Robert" sort="Kumsta, Robert" uniqKey="Kumsta R" first="Robert" last="Kumsta">Robert Kumsta</name></author><author><name sortKey="Hellhammer, Dirk H" sort="Hellhammer, Dirk H" uniqKey="Hellhammer D" first="Dirk H" last="Hellhammer">Dirk H. Hellhammer</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2004">2004</date><idno type="RBID">pubmed:14764763</idno><idno type="pmid">14764763</idno><idno type="doi">10.1210/jc.2003-031148</idno><idno type="wicri:Area/PubMed/Corpus">000746</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000746</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Common polymorphisms in the glucocorticoid receptor gene are associated with adrenocortical responses to psychosocial stress.</title><author><name sortKey="Wust, Stefan" sort="Wust, Stefan" uniqKey="Wust S" first="Stefan" last="Wüst">Stefan Wüst</name><affiliation><nlm:affiliation>Department of Psychobiology, University of Trier, Johanniterufer 15, 54290 Trier, Germany. wuest@uni-trier.de</nlm:affiliation></affiliation></author><author><name sortKey="Van Rossum, Elisabeth F C" sort="Van Rossum, Elisabeth F C" uniqKey="Van Rossum E" first="Elisabeth F C" last="Van Rossum">Elisabeth F C. Van Rossum</name></author><author><name sortKey="Federenko, Ilona S" sort="Federenko, Ilona S" uniqKey="Federenko I" first="Ilona S" last="Federenko">Ilona S. Federenko</name></author><author><name sortKey="Koper, Jan W" sort="Koper, Jan W" uniqKey="Koper J" first="Jan W" last="Koper">Jan W. Koper</name></author><author><name sortKey="Kumsta, Robert" sort="Kumsta, Robert" uniqKey="Kumsta R" first="Robert" last="Kumsta">Robert Kumsta</name></author><author><name sortKey="Hellhammer, Dirk H" sort="Hellhammer, Dirk H" uniqKey="Hellhammer D" first="Dirk H" last="Hellhammer">Dirk H. Hellhammer</name></author></analytic><series><title level="j">The Journal of clinical endocrinology and metabolism</title><idno type="ISSN">0021-972X</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenal Cortex (physiopathology)</term><term>Adrenocorticotropic Hormone (metabolism)</term><term>Adult</term><term>Alleles</term><term>Cosyntropin (pharmacology)</term><term>Dexamethasone (pharmacology)</term><term>Genotype</term><term>Glucocorticoids (pharmacology)</term><term>Heterozygote</term><term>Humans</term><term>Hydrocortisone (metabolism)</term><term>Male</term><term>Polymorphism, Genetic</term><term>Receptors, Glucocorticoid (genetics)</term><term>Reference Values</term><term>Saliva (metabolism)</term><term>Stress, Psychological (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, Glucocorticoid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adrenocorticotropic Hormone</term><term>Hydrocortisone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Cosyntropin</term><term>Dexamethasone</term><term>Glucocorticoids</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Stress, Psychological</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Saliva</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Adrenal Cortex</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Alleles</term><term>Genotype</term><term>Heterozygote</term><term>Humans</term><term>Male</term><term>Polymorphism, Genetic</term><term>Reference Values</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Chronic dysregulation of hypothalamus-pituitary-adrenal axis activity is related to several stress-related disorders. Evidence suggests that polymorphisms in the glucocorticoid receptor (GR) gene may have an impact on this neuroendocrine system. In the present investigation, 112 healthy males were studied to estimate the impact of three GR gene polymorphisms (BclI RFLP, N363S, ER22/23EK) on cortisol and ACTH responses to psychosocial stress (Trier Social Stress Test) and pharmacological stimulation (1 microg ACTH(1-24), 0.5 mg dexamethasone). Because only four ER22/23EK heterozygotes were identified, these subjects were not statistically analyzed. Compared with subjects with the wild-type GR genotype (n = 36), 363S allele carriers (n = 10) showed significantly increased salivary cortisol responses to stress, whereas the BclI genotype GG (n = 18) was associated with a diminished cortisol response. BclI heterozygotes and homozygotes (GG) exhibited a trend toward lower ACTH responses, compared with wild-type subjects and 363S carriers. The cortisol response to ACTH(1-24) administration was not significantly different between genotypes. After dexamethasone ingestion, 363S carriers showed a trend toward an enhanced cortisol suppression. This is the first report documenting an impact of GR gene polymorphisms on cortisol (and perhaps ACTH) responses to psychosocial stress. These variants may contribute to the individual vulnerability for hypothalamus-pituitary-adrenal-related disorders.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">14764763</PMID><DateCreated><Year>2004</Year><Month>02</Month><Day>06</Day></DateCreated><DateCompleted><Year>2004</Year><Month>03</Month><Day>26</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0021-972X</ISSN><JournalIssue CitedMedium="Print"><Volume>89</Volume><Issue>2</Issue><PubDate><Year>2004</Year><Month>Feb</Month></PubDate></JournalIssue><Title>The Journal of clinical endocrinology and metabolism</Title><ISOAbbreviation>J. Clin. Endocrinol. Metab.</ISOAbbreviation></Journal><ArticleTitle>Common polymorphisms in the glucocorticoid receptor gene are associated with adrenocortical responses to psychosocial stress.</ArticleTitle><Pagination><MedlinePgn>565-73</MedlinePgn></Pagination><Abstract><AbstractText>Chronic dysregulation of hypothalamus-pituitary-adrenal axis activity is related to several stress-related disorders. Evidence suggests that polymorphisms in the glucocorticoid receptor (GR) gene may have an impact on this neuroendocrine system. In the present investigation, 112 healthy males were studied to estimate the impact of three GR gene polymorphisms (BclI RFLP, N363S, ER22/23EK) on cortisol and ACTH responses to psychosocial stress (Trier Social Stress Test) and pharmacological stimulation (1 microg ACTH(1-24), 0.5 mg dexamethasone). Because only four ER22/23EK heterozygotes were identified, these subjects were not statistically analyzed. Compared with subjects with the wild-type GR genotype (n = 36), 363S allele carriers (n = 10) showed significantly increased salivary cortisol responses to stress, whereas the BclI genotype GG (n = 18) was associated with a diminished cortisol response. BclI heterozygotes and homozygotes (GG) exhibited a trend toward lower ACTH responses, compared with wild-type subjects and 363S carriers. The cortisol response to ACTH(1-24) administration was not significantly different between genotypes. After dexamethasone ingestion, 363S carriers showed a trend toward an enhanced cortisol suppression. This is the first report documenting an impact of GR gene polymorphisms on cortisol (and perhaps ACTH) responses to psychosocial stress. 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