In rodents, 8β-VE2 stimulates follicular growth and to a comparable extent as estradiol, whereas the highly ERα-selective agonist 16α-LE2 has no effect on ovarian follicle development, indicating that the ERβ and not the ERα is involved in the effects of estrogen on ovarian follicles.[2][3] In contrast, 16α-LE2 stimulates uterine weight, whereas 8β-VE2 has no effect, indicating that the ERα and not the ERβ is involved in the effects of estrogen on the uterus.[2]
Research has determined through experimental rodent studies with estradiol, 16α-LE2, and 8β-VE2 that the positive, protective effects of estrogens on bone formationresorption and bone mineral density are mediated via the ERα, whereas the ERβ does not appear to be involved.[4] On the other hand, while both ERα and ERβ are expressed in skeletal muscle, it was found that ERβ is the predominant ER subtype that is responsible for estrogen stimulation of skeletal muscle growth and regeneration.[5] Moreover, similarly to testosterone, 8β-VE2 has anabolic effects in skeletal muscle and significantly increases muscle mass as well as produces muscle hypertrophy in rats.[5] In contrast to testosterone however, 8β-VE2 shows no androgenic effects.[5] The effects of 8β-VE2 and ERβ may be mediated, in part, by local stimulation of insulin-like growth factor 1 (IGF-1)-induced myogenicprotein synthesis, as 8β-VE2 has been found to strongly induce expression of IGF-1 in the rat levator ani muscle.[5]
^Binder K, Winuthayanon W, Hewitt SC, Couse JF, Korach KS (15 November 2014). "Steroid Receptors in the Uterus and Ovary". In Plant TM, Zeleznik AJ (eds.). Knobil and Neill's Physiology of Reproduction. Academic Press. pp. 1150–. ISBN 978-0-12-397769-4.