Estrogenic fat most likely refers to adipose tissue that develops under the direct influence of estrogens, particularly estradiol. The term, albeit not very common, specifically pertains to subcutaneous adipose tissue (also known as subcutaneous fat)
Estrogenic fat mainly refers to the feminine secondary sex characteristic that develops at puberty and is maintained by estradiol throughout the premenopausal years, while estradiol production levels are maintained. It results from estrogenic contributions to the accumulation of fatty acids in the hips, thighs, and buttocks rather than the abdomen promoting a gynoid body shape.[1][2] Estrogenic fat typically refers to subcutaneous adipose deposits as they are more sensitive to estrogen signaling than visceral adipose deposits due to higher concentrations of estrogen receptors than the latter.[3] Studies have shown that not only does body fat distribution vary by sex,[4] but is also modulated by sex hormones.[3][5][6]
Both estrogen receptors (ERα and ERβ) have been identified in adipose tissue and direct action of estrogen signaling in adipose tissue has been shown in humans, mice, and rats.[7][8] Direct effects of estrogen in adipose cells(adipocytes) includes modulation of cellular differentiation and proliferation, lipolysis, adipose tissue hyperplasia, cellular protein profile.[9][10]
Estrogen Levels Pre- and Post-Menopause
Pre-menopausal women have higher levels of hormones including estrogen. After menopause, estrogenic fat diminishes, and lower levels of both estradiol and estrone are found in breast adipocytes, with a more pronounced decrease in estradiol levels.[11]
1 2 Lu, Shi-fang; McKenna, Suzanne E.; Cologer-Clifford, Athena; Nau, Eugene A.; Simon, Neal G. (April 1998). "Androgen Receptor in Mouse Brain: Sex Differences and Similarities in Autoregulation 1". Endocrinology. 139 (4): 1594–1601. doi:10.1210/endo.139.4.5863.
↑ Bjorntorp, P. (1 October 1997). "Hormonal control of regional fat distribution". Human Reproduction. 12 (suppl 1): 21–25. doi:10.1093/humrep/12.suppl_1.21.
↑ Clegg, Deborah J.; Brown, Lynda M.; Woods, Stephen C.; Benoit, Stephen C. (1 April 2006). "Gonadal Hormones Determine Sensitivity to Central Leptin and Insulin". Diabetes. 55 (4): 978–987. doi:10.2337/diabetes.55.04.06.db05-1339.
↑ Haarbo, J; Marslew, U; Gotfredsen, A; Christiansen, C (December 1991). "Postmenopausal hormone replacement therapy prevents central distribution of body fat after menopause". Metabolism: clinical and experimental. 40 (12): 1323–6. doi:10.1016/0026-0495(91)90037-w. PMID1961129.
↑ Crandall, David L.; Busler, Dennis E.; Novak, Thomas J.; Weber, Renata V.; Kral, John G. (July 1998). "Identification of Estrogen Receptor β RNA in Human Breast and Abdominal Subcutaneous Adipose Tissue". Biochemical and Biophysical Research Communications. 248 (3): 523–526. doi:10.1006/bbrc.1998.8997.
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