Abstract
The mechanisms by which the sex hormones achieve their bone-sparing effects remains unresolved. Interleukin-1β (IL-1β) is an autocrine/paracrine regulator of bone that may be produced in an estrogen-sensitive manner. The regulation of IL-1β production by the gonadal steroids was tested in the human osteoblastic HOBIT cell model. Dose-dependent 4–8-fold increases ( P < 0.05) in IL-1β mRNA levels followed a 6–48 h treatment with 17β-estradiol or testosterone. Receptor mediation of these responses was indicated by experiments using 17α-estradiol or flutamide. Tumor necrosis factor-α (TNF) dependent increases in IL-1β mRNA levels were additive to the effects of the steroids. Testosterone and TNF increased IL-1β protein release ( P < 0.05) while 17β-estradiol had little effect on release. The bone-sparing effects of the gonadal steroids may be accomplished, in part, through their mediation of local IL-1β production.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
