Document Detail

Association of 11β-hydroxysteroid dehydrogenase type I expression and activity with estrogen receptor β in adipose tissue from postmenopausal women.
MedLine Citation:
PMID:  23190557     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: 11β-Hydroxysteroid dehydrogenase type I (11βHSD1) regenerates active cortisol from inert cortisone in adipose tissue. Elevated adipose tissue 11βHSD1 activity is observed in obese humans and rodents, where it is linked to obesity and its metabolic consequences. Menopause is also associated with increased abdominal fat accumulation, suggesting that estrogen is also important in adipose tissue metabolism. The purpose of this current study was to establish whether estrogen signaling through estrogen receptor α (ER-α) and estrogen receptor β (ER-β) could influence 11βHSD1 in premenopausal and postmenopausal adipose tissues.
METHODS: Nineteen premenopausal (aged 26 ± 5 y; body mass index, 23.6 ± 1.6 kg/m) and 23 postmenopausal (aged 63 ± 4 y; body mass index, 23.4 ± 1.9 kg/m) healthy women were studied. Subcutaneous adipose tissue biopsies and fasting venous blood samples were taken. Body composition was measured by bioelectrical impedance analysis. Human Simpson-Golabi-Behmel syndrome adipocyte cells were treated with ER-α- and ER-β-specific agonists for 24 hours. Basic anthropometric data, serum 17β-estradiol and progesterone concentrations, ER-α and ER-β messenger RNA (mRNA) levels, and 11βHSD1 mRNA, protein, and activity levels were assessed.
RESULTS: ER-β and 11βHSD1, but not ER-α, mRNAs were significantly increased in adipose tissue from postmenopausal women compared with premenopausal women. ER-β had a significant positive correlation with the mRNA level of 11βHSD1 in adipose tissue from premenopausal and postmenopausal women. This association between ER-β and 11βHSD1 was greatest in adipose tissue from postmenopausal women. In human Simpson-Golabi-Behmel syndrome adipocytes, diarylpropiolnitrile, a selective ER-β agonist, increased 11βHSD1 mRNA, protein, and activity levels.
CONCLUSIONS: We conclude that, in adipose tissue, ER-β-mediated estrogen signaling can up-regulate 11βHSD1 and that this may be of particular importance in postmenopausal women.
Kerry J McInnes; Therése C Andersson; Kotryna Simonytė; Ingegerd Söderström; Cecilia Mattsson; Jonathan R Seckl; Tommy Olsson
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Menopause (New York, N.Y.)     Volume:  19     ISSN:  1530-0374     ISO Abbreviation:  Menopause     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-11-29     Completed Date:  2013-05-29     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  9433353     Medline TA:  Menopause     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1347-52     Citation Subset:  IM    
Endocrinology Unit, Center for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
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MeSH Terms
11-beta-Hydroxysteroid Dehydrogenases / genetics*,  metabolism*
Adipose Tissue / chemistry*,  enzymology*
Body Composition
Estradiol / blood
Estrogen Receptor alpha / analysis,  genetics
Estrogen Receptor beta / analysis*,  genetics,  physiology
Estrogens / physiology
Middle Aged
Postmenopause / metabolism*
Premenopause / metabolism
Progesterone / blood
RNA, Messenger / analysis
Signal Transduction / physiology
Grant Support
065998//Wellcome Trust
Reg. No./Substance:
0/Estrogen Receptor alpha; 0/Estrogen Receptor beta; 0/Estrogens; 0/RNA, Messenger; 50-28-2/Estradiol; 57-83-0/Progesterone; EC Dehydrogenases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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