Publications (2)4.29 Total impact
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Article: Treadmill training regulates β-catenin signaling through phosphorylation of GSK-3β in lumbar vertebrae of ovariectomized rats.
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ABSTRACT: Postmenopausal osteoporosis is associated with high level of adipogenesis within the bone marrow at the expense of osteoblast population. The mechanical effect on β-catenin through phosphorylation of glycogen synthase kinase-3β (GSK-3β) is critical for inhibition of adipogenesis in mesenchymal stem cells in vitro. In present study, we hypothesized that treadmill training could regulate the β-catenin signaling through phosphorylation of GSK-3β in the lumbar vertebrae of ovariectomized (OVX) rats. 3-month-old female Sprague-Dawley rats were divided randomly into the following four groups: (a) Sham, (b) OVX, (c) OVX exercised (EX), and (d) OVX estrogen replacement (E(2)). At the end of the experiment, the serum levels of estradiol (E(2)) and luteinizing hormone (LH), the ultimate lumbar vertebra strength, as well as the protein expression for peroxisome proliferators-activated receptor γ (PPARγ), β-catenin, P-GSK-3β, and osterix (Osx) in lumbar vertebrae were analyzed. Moreover, the protein expression for β-catenin and P-GSK-3β were also examined in the uterus. The EX group had lower protein level of PPARγ, higher ultimate lumbar vertebral strength, and higher protein levels of β-catenin, and P-GSK-3β in lumbar vertebral bodies compared with sedentary OVX group. The effects of EX treatment on the protein levels of β-catenin and P-GSK-3β in bones were not reproducible in the uterus. Moreover, exercise treatment produced no estrogenic effect as evidenced by serum level of LH. In conclusion, this study suggested that treadmill training could activate the GSK-3β/β-catenin signaling and inhibit the production of PPARγ in lumbar vertebrae of OVX rats, which may contribute to the prevention of bone loss in OVX rats.Arbeitsphysiologie 01/2012; 112(9):3295-304. · 2.15 Impact Factor -
Article: Treadmill training prevents bone loss by inhibition of PPARγ expression but not promoting of Runx2 expression in ovariectomized rats.
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ABSTRACT: Exercise training has been reported to prevent bone loss in ovariectomized (OVX) rats and postmenopausal women. We hypothesized that treadmill training inhibited adipogenesis and enhanced osteogenesis through the regulation of adipocyte differentiation factor peroxisome proliferators-activated receptor gamma (PPARγ) and the osteogenic factor runt-related transcription factor 2 (Runx2) in a model of OVX-induced osteoporosis. To test this hypothesis, 3-month-old female Sprague-Dawley rats were divided randomly into the following groups: Sham, OVX, OVX exercised (EX), and OVX estrogen replacement (E(2)). At the end of the experiment, the bone mineral density (BMD) was detected using DEXA and the morphology change of bone tissues and uterus was observed by HE staining. The protein expression for PPARγ and Runx2 were measured by immunohistochemistry and western blot and the bone triacylglycerol (TG) was extracted by methanol/chloroform. OVX dramatically increased the number of fat vacuoles, protein levels for PPARγ and Runx2 as well as the TG level in tibiae and lumbar vertebrate. In contrast, the serum level of E(2), the lumbar vertebrate BMD as well as the proximal and distal femur BMD was significantly decreased in the OVX group. All changes induced by OVX were significantly reversed by exercise treatment except for the protein expression level of Runx2. Moreover, exercise treatment produced no estrogenic effects on uterus as evidenced by the uterus wet weight and histology. Treadmill training could prevent bone loss induced by OVX through the inhibition of adipocyte differentiation factor PPARγ rather than promoting osteogenic factor Runx2.Arbeitsphysiologie 01/2011; 111(8):1759-67. · 2.15 Impact Factor
