Estrogen receptor beta is involved in skeletal muscle hypertrophy induced by the phytoecdysteroid ecdysterone.
Parr, Maria Kristina 1,2; Zhao, Piwen 3; Haupt, Oliver 1,4; Ngueu, Sandrine Tchoukouegno 1; Hengevoss, Jonas 1; Fritzemeier, Karl Heinrich 5; Piechotta, Marion 6; Schlorer, Nils 7; Muhn, Peter 5; Zheng, Wen-Ya 1,8; Xie, Ming-Yong 8; Diel, Patrick 1
[Article] Molecular Nutrition & Food Research. 58(9):1861-1872, September 2014.

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Scope: The phytoectysteroid ecdysterone (Ecdy) was reported to stimulate protein synthesis and enhance physical performance. The aim of this study was to investigate underlying molecular mechanisms particularly the role of ER beta (ER[beta]).

Results: In male rats, Ecdy treatment increased muscle fiber size, serum IGF-1 increased, and corticosteron and 17[beta]-estradiol (E2) decreased. In differentiated C2C12 myoblastoma cells, treatment with Ecdy, dihydrotestosterone, IGF-1 but also E2 results in hypertrophy. Hypertrophy induced by E2 and Ecdy could be antagonized with an antiestrogen but not by an antiandrogen. In HEK293 cells transfected with ER alpha (ER[alpha]) or ER[beta], Ecdy treatment transactivated a reporter gene. To elucidate the role of ER[beta] in Ecdy-mediated muscle hypertrophy, C2C12 myotubes were treated with ER[alpha] (ALPHA) and ER[beta] (BETA) selective ligands. Ecdy and BETA treatment but not ALPHA induced hypertrophy. The effect of Ecdy, E2, and BETA could be antagonized by an ER[beta]-selective antagonist (ANTIBETA). In summary, our results indicate that ER[beta] is involved in the mediation of the anabolic activity of the Ecdy.

Conclusion: These findings provide new therapeutic perspectives for the treatment of muscle injuries, sarcopenia, and cachectic disease, but also imply that such a substance could be abused for doping purposes.

(C) 2014 John Wiley & Sons, Inc.