Abstract | OBJECTIVE: RESEARCH DESIGN AND METHODS: RESULTS: CONCLUSIONS: These data suggest that long-term upregulation of 11beta-HSD1 in metabolically active tissues may follow prenatal "stress" hormone exposure and indicates a novel mechanism for fetal origins of adult obesity and the metabolic syndrome.
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Authors | Moffat J Nyirenda, Roderick Carter, Justin I Tang, Annick de Vries, Christina Schlumbohm, Stephen G Hillier, Frank Streit, Michael Oellerich, Victor W Armstrong, Eberhard Fuchs, Jonathan R Seckl |
Journal | Diabetes
(Diabetes)
Vol. 58
Issue 12
Pg. 2873-9
(Dec 2009)
ISSN: 1939-327X [Electronic] United States |
PMID | 19720800
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Blood Glucose
- Glucocorticoids
- Triglycerides
- Dexamethasone
- 11-beta-Hydroxysteroid Dehydrogenase Type 1
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Topics |
- 11-beta-Hydroxysteroid Dehydrogenase Type 1
(genetics, metabolism)
- Adipose Tissue
(enzymology)
- Aging
(metabolism)
- Animals
- Blood Glucose
(metabolism)
- Callithrix
- Dexamethasone
- Female
- Gene Expression Regulation, Enzymologic
- Glucocorticoids
- Metabolic Syndrome
(chemically induced, enzymology)
- Polymerase Chain Reaction
- Pregnancy
- Prenatal Exposure Delayed Effects
- Time Factors
- Triglycerides
(blood)
- Up-Regulation
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