Document Detail

Fetal glucocorticoid synthesis is required for development of fetal adrenal medulla and hypothalamus feedback suppression.
MedLine Citation:
PMID:  22962254     Owner:  NLM     Status:  MEDLINE    
During pregnancy, fetal glucocorticoid is derived from both maternal supply and fetal secretion. We have created mice with a disruption of the Cyp11a1 gene resulting in loss of fetal steroid secretion but preserving the maternal supply. Cyp11a1null embryos have appreciable although lower amounts of circulating corticosterone, the major mouse glucocorticoid, suggesting that transplacental corticosterone is a major source of corticosterone in fetal circulation. These embryos thus provide a means to examine the effect of fetal glucocorticoids. The adrenal in Cyp11a1 null embryos was disorganized with abnormal mitochondria and oil accumulation. The adrenal medullary cells did not express phenylethanolamine N-methyltransferase and synthesized no epinephrine. Cyp11a1 null embryos had decreased diencephalon Hsd11b1, increased diencephalon Crh, and increased pituitary Pomc expression, leading to higher adrenocorticotropin level in the plasma. These data indicate blunted feedback suppression despite reasonable amounts of circulating corticosterone. Thus, the corticosterone synthesized in situ by the fetus is required for negative feedback suppression of the hypothalamus-pituitary-adrenal axis and for catecholamine synthesis in adrenal medulla.
Chen-Che Jeff Huang; Meng-Chun Monica Shih; Nai-Chi Hsu; Yu Chien; Bon-chu Chung
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-09-07
Journal Detail:
Title:  Endocrinology     Volume:  153     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-09-24     Completed Date:  2012-12-11     Revised Date:  2013-10-09    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4749-56     Citation Subset:  AIM; IM    
Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan.
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MeSH Terms
11-beta-Hydroxysteroid Dehydrogenase Type 1 / genetics,  metabolism
Adrenal Medulla / growth & development,  metabolism*
Adrenocorticotropic Hormone / biosynthesis*,  blood
Cholesterol Side-Chain Cleavage Enzyme / genetics*,  metabolism
Corticosterone / biosynthesis*,  blood
Corticotropin-Releasing Hormone / genetics,  metabolism
Epinephrine / biosynthesis
Feedback, Physiological / physiology*
Hypothalamo-Hypophyseal System / metabolism
Hypothalamus / metabolism*
Maternal-Fetal Exchange
Mice, Knockout
Mitochondria / metabolism
Phenylethanolamine N-Methyltransferase / genetics,  metabolism
Pituitary Gland / metabolism
Pituitary-Adrenal System / metabolism
Pro-Opiomelanocortin / genetics,  metabolism
Reg. No./Substance:
50-22-6/Corticosterone; 51-43-4/Epinephrine; 66796-54-1/Pro-Opiomelanocortin; 9002-60-2/Adrenocorticotropic Hormone; 9015-71-8/Corticotropin-Releasing Hormone; EC Dehydrogenase Type 1; EC Side-Chain Cleavage Enzyme; EC N-Methyltransferase

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