Location: Arkansas Children's Nutrition CenterTitle: The soy-associated phytoestrogen, genistein, does not protect against alcohol induced osteoporosis in male mice) Author
Submitted to: Toxicologist
Publication Type: Abstract only
Publication Acceptance Date: 11/30/2012
Publication Date: 3/1/2013
Citation: Yang, C., Mercer, K.E., Suva, L.J., Badger, T.M., Ronis, M.J. 2013. The soy-associated phytoestrogen, genistein, does not protect against alcohol induced osteoporosis in male mice [abstract]. Toxicologist. 132(1):Abstract 1302, p. 279-280. Interpretive Summary:
Technical Abstract: Alcohol abuse acts as a risk factor for osteoporosis by increasing osteoclast activity and decreasing osteoblast activity in bone. These effects can be reversed by estradiol. Soy diets are also suggested to have protective effects on bone loss in men and women, as a result of the presence of soy protein-associated phytoestrogens such as genistein and daidzein. In this study, male mice were pair fed (PF) a control diet, an EtOH diet, or EtOH diet supplemented with genistein (250 mg/kg) for 8 weeks. Ex vivo microCT analyses of formalin-fixed tibias from each group revealed a significant decrease in trabecular bone in the EtOH group in comparison with the pair-fed control in regards to bone volume (BV/TV), trabecular number (Tb.N), and trabecular separation (Tb.Sp), (p<0.05). No protective effect by genistein was observed in the EtOH+genistein group compared to the EtOH group in BV/TV, Tb.N, and Tb.Sp. Interestingly, there was an increase in trabecular thickness (Tb.Th) in the PF+genistein group compared to the PF (P<0.05), suggesting genistein can affect bone remodeling. In ex vivo bone marrow cultures, EtOH exposure decreased the number of pre-osteoblasts compared to PF controls. In contrast, exposure to EtOH+genistein increased pre-osteoblast numbers compared to the EtOH-treated group, (p<0.05). These findings suggest that genistein has a partial protective effect on bone formation. In conclusion, genestein does not protect against ethanol-induced bone loss despite increasing osteoblastogenesis.