Abstract
Purpose : To determine the effect of dietary soy isoflavone supplementation on bone loss in ovariectomized (OVX) rats. Methods : Forty-eight rats were assigned randomly to groups of OVX rats receiving soy isoflavones (20, 30, or 40 mg/kg of body weight daily), untreated OVX rats, or untreated intact rats. After 8 weeks, bone mineral density (BMD), mineral (Ca, P, Mn, Mg, and Zn) concentrations, and the expression of osteoblast-related genes were measured in femur tissue samples. Results : Eight weeks after OVX, there was a significant decrease in body weight, serum levels of osteocalcin, alkaline phosphatase, and oestradiol, BMD and mineral elements, as well as the expressions of Ctnnb1, Runx2, and Sp7 (all p < 0.05). These decreases were accompanied by reduced maximum load capacity of lumbar vertebrae. Daily supplementation with soy isoflavones dosedependently ameliorated these effects (all p < 0.05). Western blotting revealed that these effects were likely due to the reversal of the OVX-induced decrease in Notch1 proteins in bone and muscle. Conclusion : Soy isoflavone treatment represents a potential therapy for preventing postmenopausal bone loss by stimulating the Notch signalling. Keywords : Mineral elements, Alkaline phosphatase, Isoflavones, Bone loss, Notch pathway
Highlights
Postmenopausal osteoporosis is a common condition in which reduced levels of oestrogen alter the mineral composition of bone, leading to a loss of mineralized bone tissue and structural failure [1,2,3,4]
We examined whether the intake of dietary soy isoflavones impacts bone mineral density (BMD) to prevent bone loss in animals with oestrogen deficiencies
The results demonstrate that soy isoflavones inhibit bone loss and alleviate osteoporosis in rats, in part, via upregulation of Notch signalling
Summary
Postmenopausal osteoporosis is a common condition in which reduced levels of oestrogen alter the mineral composition of bone, leading to a loss of mineralized bone tissue and structural failure (fracture) [1,2,3,4]. To delay the loss of bone minerals and thereby prevent bone fractures, treatment strategies have included oestrogen replacement or the administration of selective oestrogen receptor modulators, such as raloxifene, bisphosphonates, and calcitonin. These therapies increase the risk of hypercalcemia, hypercalciuria, hot flushes, and endometrial cancer [5,6,7]. There is evidence that isoflavones reduce the risk of endometrial cancer by interfering with oestrogen hormone production and signalling. The dietary intake of these compounds may influence the deposition of minerals in bone tissue in individuals with low levels of oestrogen
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