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The hypophysectomized rat has been used as a model to study the effects of growth hormone deficiency on bone. Here, we have investigated the influence of growth hormone administration to hypophysectomized rats (HX) for 6 wk on accumulation of triglycerides in bone marrow and on the differentiation of primary marrow stromal cells into adipocytes under in vitro conditions. We found that hypophysectomy significantly increased triglyceride concentration in bone marrow, which was attenuated by growth hormone administration. Primary bone marrow stromal cells derived from HX rats also had more adipocytes at confluence compared with growth hormone-treated hypophysectomized (GH) rats. When stimulated with 3-isobutyl-1-methylxanthine plus dexamethasone (IBMX-Dex), preadipocyte colony counts increased more significantly in GH rats. Markers of adipocyte differentiation were higher in HX than in control or GH rats at confluence. However, after stimulation with IBMX-Dex, increased expression of markers was seen in GH compared with HX rats. In conclusion, growth hormone administration to hypophysectomized rats attenuated triglyceride accumulation in bone marrow and inhibited the differentiation of stromal cells into adipocytes in vitro. hypophysectomy; triglycerides; adipocytes

A study was conducted to analyze the influence of pituitary hormone deficiency on the proliferation and differentiation of osteoprogenitor cells. The hypophysectomized rat was utilized as a model to carry out the analysis. Results indicated that osteoprogenitor cells exposed to pituitary hormone-deficient conditions in vivo support an improved proliferative capacity and an augmented expression of differentiation markers during exposure to an optimal environment in vitro.

The role of the growth hormone (GH) and 17beta-estradiol (E2) on bone mass and turnover was examined in ovariectomized rats. Administration of GH to the rats resulted in increased cortical bone formation, serum levels of osteocalcin and systemic growth. High or low doses of GH or E2 alone partially prevented cancellous bone loss but combined treatment of GH and E2 increased cancellous bone mass. These results suggested that the effect of GH and E2 on cancellous bone may be due to the anabolic effect of GH on bone formation and the suppressive impact of E2 on bone resorption.

Insulin-like growth factor I (IGF-I) mediates bone response to exercise. This is revealed in an analysis of IGF-I levels in serum, long bone, vertebrae and bone formation rate to explore the influence of treadmill exercise and ovine growth hormone administration. IGF-I is one of the growth factors determining bone formation. Long bone exhibits higher IGF-I concentration and periosteal bone formation only in exercised rats.

Three groups of6-week-old female rats were utilized in an investigation of the effeect of exercise on bone formation and resorption. Isotopic calcium was administered and the rate of excretion and retention as well as bone volume, calcium contentand resorption were monitored. Results reveal that physical activity is associated with an initial enhancement followed by a reduction of resorption asbone is actively formed. Immobilization is associated with poor bone formation and elevated resorption rate.

Osteoblast-like cells of the hypophysectomized rat: a model of aberrant osteoblast development. Am J Physiol Endocrinol Metab 278: E832-E838, 2000.--In a previous work, we demonstrated that the osteoprogenitors derived from the marrow stroma of the hypophysectomized (HX) rat demonstrate enhanced proliferative and differentiation capacities when placed in an optimal microenvironment. In this study, we sought to investigate the potential of the trabecular osteoblast-like cells of the HX rat. These cells represent a more mature pool of osteoblasts than the progenitors derived from the marrow stroma. We examined all three stages of osteoblast development using trabecular osteoblast-like cells derived from age-matched intact rats as a control. Using thymidine incorporation and cell number as indicators of proliferation, we found that these cells, like the osteoprogenitors derived from the HX rat, demonstrate augmented proliferation when placed in culture. Additionally, type I collagen expression remained at significant levels past the end stages of proliferation, at which point it is expected to be downregulated. Matrix maturation markers, such as alkaline phosphatase activity and bone sialoprotein expression, however, were significantly lower than in the controls. Mineralization potential, as measured by mineralized nodule formation, [Ca.sup.2+] content, and OPN and OCN expression, was also significantly reduced. Our results have uncovered an aberrant model of osteoblast development in which proliferation is deregulated, resulting in a minimal capacity of these cells to develop into fully differentiated mineralizing osteoblasts. alkaline phosphatase; mineralization potential; proliferation; differentiation