Estrogen production and action.
Level 5 - mechanism / opinion, no new human data
Narrative review of biological mechanisms and tissue physiology without systematic review methodology or new human clinical data
PubMed 11511861 · doi:10.1067/mjd.2001.117432
What was done
This narrative review summarizes the physiological and pathophysiological mechanisms of extraglandular estrogen biosynthesis via the enzyme aromatase in various human tissues, including adipose tissue, skin fibroblasts, bone, placenta, and brain, as well as the regulation of aromatase by alternative promoters.
What was found
The abstract provides a qualitative mechanistic overview and reports no numerical data or effect sizes. Extraglandular aromatase converts C19 androgens to estrogens, with expression in adipose tissue and skin increasing with age and body weight. In obese anovulatory or postmenopausal women, this peripheral conversion can generate sufficient estradiol to drive uterine bleeding, endometrial hyperplasia, and endometrial cancer, while also acting to reduce postmenopausal bone loss. In breast carcinoma and endometriosis-derived stroma, aromatase expression is inappropriately elevated. Expression is regulated by tissue-specific alternative promoters (e.g., promoter II in ovary, I.1 in placenta, I.4 in skin, and I.3/I.4/II in adipose tissue), with promoter switching observed in response to PGE2, cytokines, glucocorticoids, and the presence of breast tumors.
Why it matters
Understanding local and extraglandular aromatase regulation explains how tissue-specific estrogen production influences estrogen-responsive diseases and postmenopausal bone health independently of circulating ovarian hormones.
Limits
The abstract contains no quantitative data, sample sizes, or statistical comparisons. As a narrative review, it lacks systematic search criteria, methodological quality assessments, and primary clinical trial outcomes.
Cited by
- supports When ovaries stop producing estradiol, adipose tissue produces estrone.