Fiche publication
Date publication
mars 2017
Journal
American journal of physiology. Endocrinology and metabolism
Auteurs
Membres identifiés du Cancéropôle Est :
Dr METZGER Daniel
Tous les auteurs :
Ueberschlag-Pitiot V, Stantzou A, Messéant J, Lemaitre M, Owens DJ, Noirez P, Roy P, Agbulut O, Metzger D, Ferry A
Lien Pubmed
Résumé
In order to better define the role of male and female gonad-related factors (MGRF, presumably testosterone, and FGRF, presumably estradiol, respectively) on mouse hindlimb skeletal muscle contractile performance/function gain during postnatal development, we analysed the effect of castration initiated before puberty in male and female mice. We found that muscle absolute and specific (normalized to muscle weight) maximal forces were decreased in 6-month old male and female castrated mice, as compared to age- and sex-matched intact mice, without alteration in neuromuscular transmission. Moreover, castration decreased absolute and specific maximal powers, another important aspect of muscle performance, in 6-month old males, but not in females. Absolute maximal force was similarly reduced by castration in 3-month old muscle fibre androgen receptor (AR) -deficient and wild-type male mice, indicating that the effect of MGRF was muscle fibre AR independent. Castration reduced the muscle weight gain in 3-month mice of both sexes and in 6-month females but not in males. We also found that bone morphogenetic protein signaling through Smad1/5/9 was not altered by castration in atrophic muscle of 3-month old mice of both sexes. Moreover, castration decreased the sexual dimorphism regarding muscle performance. Together these results demonstrated that in the long-term MGRF and FGRF promote muscle performance gain in mice during postnatal development, independently of muscle growth in males, largely via improving muscle contractile quality (force and power normalized) and that MGFR and FGRF also contribute to sexual dimorphism. However, the mechanisms underlying MGFR and FGRF actions remain to be determined.
Mots clés
androgen deficiency, estrogen deficiency, maximal force, maximal power, muscle contractile quality, muscle fiber androgen receptor, postnatal development, skeletal muscle
Référence
Am. J. Physiol. Endocrinol. Metab.. 2017 Mar;:ajpendo.00446.2016
