Miami Lakes, FL -- (SBWIRE) -- 01/19/2015 -- Abstract: Growth hormone (GH) deficiency causes decreased bone mineral density and osteoporosis, predisposing to fractures. We investigated the mechanism of action of GH on bone modeling and remodeling in hypophysectomized (HX) female rats. Thirty female Sprague–Dawley rats at age 2 months were divided into three groups with 10 rats each: control (CON) group, HX group, and HX GH (3 mg/kg daily SC) group, for a 4-week study. Hypophysectomy resulted in cessation of bone growth and decrease in cancellous bone mass. Periosteal bone formation decreased and bone turnover rate of endocortical and trabecular surfaces increased as compared to the CON group. GH administration for 4 weeks restored weight gain and bone growth and mitigated decrease in bone density after hypophysectomy.
However, trabecular bone mass in the proximal tibial metaphysis remained.
Lower in group HX GH than in group CON. Dynamic histomorphometric analysis showed that bone modeling of periosteal bone formation and growth plate elongation was significantly higher in group HX GH than in group HX. New bone formed beneath the growth plate was predominately woven bone in group CON and group HX GH. Bone remodeling and modeling–remodeling mixed modes in the endocortical and PTM sites were enhanced by GH administration; both bone formation and resorption activities were significantly higher than in group HX.
In conclusion, GH administration to HX rats reactivated modeling activities in modeling predominant sites and increased new bone formation. GH administration also increases remodeling activities in remodeling predominant sites, giving limited net gain in the bone mass.
Resource:
The Japanese Society for Bone and Mineral Research and Springer.
Resource:
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