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Estrogen sulfotransferase/SULT1E1 promotes human adipogenesis
Chibueze A Ihunnah1, Taira Wada, Brian J Philips
1Center for Pharmacogenetics, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Molecular and Cellular Biology
|February 26, 2014
Summary
Estrogen sulfotransferase (EST) promotes human fat cell (adipocyte) formation by deactivating estrogens. This enzyme, EST, may be a therapeutic target for obesity treatment.
Area of Science:
- Endocrinology
- Cell Biology
- Metabolic Research
Background:
- Estrogen sulfotransferase (EST/SULT1E1) deactivates estrogens.
- The role of EST in human adipogenesis is not well understood.
Purpose of the Study:
- To investigate the function of EST in human adipogenesis.
- To elucidate the molecular mechanisms by which EST influences fat cell development.
Main Methods:
- Utilized human primary adipose-derived stem cells (ASCs) and abdominal subcutaneous fat tissues.
- Performed gene overexpression and knockdown experiments.
- Analyzed estrogen receptor (ER) activity and PPARγ recruitment.
Main Results:
- EST expression increased during human ASC differentiation.
- EST overexpression promoted, while knockdown inhibited, adipogenesis.
- EST promoted adipogenesis by deactivating estrogens, opposing its effect in rodents.
- ER antagonism enhanced PPARγ recruitment, promoting adipogenesis.
Conclusions:
- EST acts as a proadipogenic factor in humans.
- EST may be a druggable target to regulate adipocyte turnover and accumulation in obesity.
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