Latest research on Estradiol

Generally refers to the 17-beta-isomer of estradiol, an aromatized C18 steroid with hydroxyl group at 3-beta- and 17-beta-position. Estradiol-17-beta is the most potent form of mammalian estrogenic steroids. In humans, it is produced primarily by the cyclic ovaries and the placenta. It is also produced by the adipose tissue of men and postmenopausal women. The 17-alpha-isomer of estradiol binds weakly to estrogen receptors (receptors, estrogen) and exhibits little estrogenic activity in estrogen-responsive tissues. Various isomers can be synthesized. [PubChem]

Latest findings

Gender has been revealed to alter dopaminergic neurotransmission, and recently Estradiol was shown to modulate dopamine baseline dependent cognitive functioning in humans (Haaxma et al., 2007; Jacobs and D'Esposito, 2011) and cost-benefit decision-making in rodents (Uban et al., 2012). [source, 2016]
In rodents, modification of Estradiol levels was previously related to alterations in cost-benefit decision-making (Uban et al., 2012). [source, 2016]
Free Estradiol was measured using routine clinical assays (detection limit, 0.15 ng/mL) as described previously [26]. [source, 2016]
There was a marked difference in Estradiol levels between the two conditions with a more than 25-fold increase in the stimulated stage. [source, 2016]
Thus, high levels of Estradiol induced by gonadotropin stimulation resulted in suppressed serum levels of hepcidin-25. [source, 2016]
In a recent study, a novel mechanism by which Estradiol could increase iron absorption and iron release from storage cells was proposed [18]. [source, 2016]
In brief, the authors described a functional ERE half-site in the human hepcidin promoter, and they observed that 24 h after Estradiol treatment, hepcidin mRNA decreased both in vitro in human liver cells and in vivo in mice. [source, 2016]
The small increase in the CRP level during initiation of IVF did not correlate with Estrogens levels (data not shown), supporting previous studies [37, 38] concluding that Estradiol does not correlate with CRP levels. [source, 2016]
In our study there was a small but significant increase of CRP during Estradiol suppression but no significant increase of ferritin or significant decrease of transferring during stimulation. [source, 2016]
This supports the concept that Estradiol per se, and not reduced inflammatory activity, decreased hepcidin levels. [source, 2016]