Differential estrogenic 17beta-hydroxysteroid dehydrogenase activity and type 12 17beta-hydroxysteroid dehydrogenase expression levels in preadipocytes and differentiated adipocytes.
Bellemare V., Laberge P., Noël S., Tchernof A., Luu-The V.
Laboratory Study, published in J Steroid Biochem Mol Biol (2009) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- J Steroid Biochem Mol Biol (2009)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 19429442
- DOI
- 10.1016/j.jsbmb.2009.01.002
Abstract (original English)
Estradiol (E2) is produced locally in adipose tissue and could play an important role in fat distribution and accumulation, especially in women. It is well recognized that aromatase is expressed in adipose tissue; however the identity of its estrogenic 17beta-hydroxysteroid dehydrogenase (17beta-HSD) partner is not identified. To gain a better knowledge about the enzyme responsible for the conversion of estrone into estradiol, we determined the activity and expression levels of known estrogenic 17beta-HSDs, namely types 1, 7 and 12 17beta-HSD in preadipocytes before and after differentiation into mature adipocytes using an adipogenic media. Estrogenic 17beta-HSD activity was assessed using [(14)C]-labelled estrone, while mRNA expression levels of types 1, 7 and 12 17beta-HSD were quantified using real-time PCR and protein expression levels of type 12 17beta-HSD was determined using immunoblot analysis. The data indicate that there is a low conversion of E1 into E2 in preadipocytes; however this activity is increased approximately 5-fold (p<0.0001) in differentiated adipocytes. The increased estrogenic 17beta-HSD activity is consistent with the increase in protein expression levels of 17beta-HSD12.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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