Citation
Parr, Maria Kristina, et al. "Estrogen Receptor Beta Is Involved in Skeletal Muscle Hypertrophy Induced By the Phytoecdysteroid Ecdysterone." Molecular Nutrition & Food Research, vol. 58, no. 9, 2014, pp. 1861-72.
Parr MK, Zhao P, Haupt O, et al. Estrogen receptor beta is involved in skeletal muscle hypertrophy induced by the phytoecdysteroid ecdysterone. Mol Nutr Food Res. 2014;58(9):1861-72.
Parr, M. K., Zhao, P., Haupt, O., Ngueu, S. T., Hengevoss, J., Fritzemeier, K. H., Piechotta, M., Schlörer, N., Muhn, P., Zheng, W. Y., Xie, M. Y., & Diel, P. (2014). Estrogen receptor beta is involved in skeletal muscle hypertrophy induced by the phytoecdysteroid ecdysterone. Molecular Nutrition & Food Research, 58(9), 1861-72. https://doi.org/10.1002/mnfr.201300806
Parr MK, et al. Estrogen Receptor Beta Is Involved in Skeletal Muscle Hypertrophy Induced By the Phytoecdysteroid Ecdysterone. Mol Nutr Food Res. 2014;58(9):1861-72. PubMed PMID: 24974955.
TY - JOUR
T1 - Estrogen receptor beta is involved in skeletal muscle hypertrophy induced by the phytoecdysteroid ecdysterone.
AU - Parr,Maria Kristina,
AU - Zhao,Piwen,
AU - Haupt,Oliver,
AU - Ngueu,Sandrine Tchoukouegno,
AU - Hengevoss,Jonas,
AU - Fritzemeier,Karl Heinrich,
AU - Piechotta,Marion,
AU - Schlörer,Nils,
AU - Muhn,Peter,
AU - Zheng,Wen-Ya,
AU - Xie,Ming-Yong,
AU - Diel,Patrick,
Y1 - 2014/06/27/
PY - 2013/11/04/received
PY - 2014/04/28/revised
PY - 2014/04/30/accepted
PY - 2014/7/1/entrez
PY - 2014/7/1/pubmed
PY - 2015/7/30/medline
KW - Dietary supplement
KW - Ecdysterone
KW - Estrogen receptor beta
KW - Skeletal muscle
KW - Traditional Chinese medicine
SP - 1861
EP - 72
JF - Molecular nutrition & food research
JO - Mol Nutr Food Res
VL - 58
IS - 9
N2 - 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 (ERβ). RESULTS: In male rats, Ecdy treatment increased muscle fiber size, serum IGF-1 increased, and corticosteron and 17β-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 (ERα) or ERβ, Ecdy treatment transactivated a reporter gene. To elucidate the role of ERβ in Ecdy-mediated muscle hypertrophy, C2C12 myotubes were treated with ERα (ALPHA) and ERβ (BETA) selective ligands. Ecdy and BETA treatment but not ALPHA induced hypertrophy. The effect of Ecdy, E2, and BETA could be antagonized by an ERβ-selective antagonist (ANTIBETA). In summary, our results indicate that ERβ 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.
SN - 1613-4133
UR - https://www.unboundmedicine.com/medline/citation/24974955/
DB - PRIME
DP - Unbound Medicine
ER -