FOLLISTATIN CONCENTRATIONS IN MALE SHEEP INCREASE FOLLOWING SHAM CASTRATION CASTRATION OR INJECTION OF INTERLEUKIN-1-BETA/

Citation
Dj. Phillips et al., FOLLISTATIN CONCENTRATIONS IN MALE SHEEP INCREASE FOLLOWING SHAM CASTRATION CASTRATION OR INJECTION OF INTERLEUKIN-1-BETA/, Journal of Endocrinology, 151(1), 1996, pp. 119-124
Citations number
30
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00220795
Volume
151
Issue
1
Year of publication
1996
Pages
119 - 124
Database
ISI
SICI code
0022-0795(1996)151:1<119:FCIMSI>2.0.ZU;2-H
Abstract
Plasma follistatin (FS) concentrations were determined after castratio n (n=5) or sham castration (n=4) of mature rams. Both treatments resul ted in a prolonged increase in FS between 7 and 19 h after surgery, wh ich returned to pretreatment concentrations by 24 h. Tumour necrosis f actor-alpha (TNF-alpha), a sensitive marker of an acute-phase response , was undetectable in plasma, indicating that the FS response was not induced by trauma due to surgery. In a second experiment, injection of castrated rams (n=4) with ovine recombinant interleukin-1 beta, an ac ute-phase mediator, resulted in a sustained rise in FS concentrations within 4 h of injection. Plasma TNF-alpha concentrations increased tra nsiently within 1 h of interleukin-1 beta injection, indicating that a n acute-phase response had been initiated. Plasma follicle-stimulating hormone (FSH) concentrations were significantly decreased at 8 and 24 h after interleukin-1 beta injection, strongly suggestive of an inhib itory effect of increased FS concentrations on the secretion of FSH. I njection of castrated rams (n=2) with a control preparation of recombi nant interleukin-2 did not induce an acute-phase response, and plasma FS and FSH concentrations were unaffected. These data show that the te stis is not a major source of circulating FS, that the increase in cir culating FS following sham castration/castration is not due to an acut e-phase response, but that conversely FS concentrations are modulated by the acute-phase mediator, interleukin-1 beta.