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Submitted on June 22, 2006
Accepted on December 18, 2006
Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR 72205; Department of Orthopaedic Surgery, Center for Orthopaedic Research, University of Arkansas for Medical Sciences, Little Rock, AR 72205; Department of Molecular Cellular Biology, Baylor College of Medicine, Houston, TX 77030
* To whom correspondence should be addressed. E-mail: gaddydana{at}uams.edu.
Gonadal function plays a major role in bone homeostasis. It is widely held that the skeletal consequences of hypogonadism are solely due to a loss of sex steroids; however, increases in bone turnover begin during perimenopause prior to decreases in serum estradiol levels. These data and our demonstration that Inhibins acutely regulate bone cell differentiation in vitro led us to test whether Inhibin A (InhA) regulates bone mass in vivo. Using a transgenic model of inducible human InhA expression, InhA increased total body BMD, increased bone volume, and improved biomechanical properties at the proximal tibia in intact mice, and also prevented the loss of BMD, and bone volume and strength associated with gonadectomy at both the spine and proximal tibia. In addition, InhA increased mineral apposition rate, double labeled surface, and serum osteocalcin levels in vivo and osteoblastogenesis ex vivo, without affecting osteoclast number or activity. Together these results demonstrate novel stimulatory effects of InhA on the skeleton in vivo. These studies provide in vivo evidence demonstrating that gonadal factors other than sex steroids play an important role in regulating bone mass and strength, and, combined with our previous clinical data, suggest that gonadal InhA may be a component of the normal endocrine repertoire that regulates bone quality in both the axial and appendicular skeleton.
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