Synergistic Phytochemicals Fail to Protect Against Ovariectomy Induced Bone Loss in Rats.

Menopause induces a loss of bone as a result of estrogen deficiency. Despite pharmaceutical options for the treatment of osteopenia and osteoporosis, many aging women use dietary supplements with estrogenic activity to prevent bone loss and other menopausal-related symptoms. Such supplements are yet to be tested for efficacy against a Food and Drug Administration (FDA) approved medication for menopausal bone loss such as zoledronic acid (ZA). The postmenopausal rat model was used to investigate the efficacy of various synergistic phytochemical blends mixed into the diet for 16 weeks. Retired-breeder, Fischer 344 rats were randomly assigned to sham or ovariectomy surgery and 4 treatment groups: ZA; genistein supplementation; and a low dose and high dose blend of genistein, resveratrol, and quercetin. Ovariectomy resulted in a loss of both trabecular and cortical bone which was prevented with ZA. The phytochemical blends tested were unable to reverse these losses. Despite the lack of effectiveness in preventing bone loss, a significant dose-response trend was observed in the phytochemical-rich diets in bone adipocyte number compared to ovariectomized control rats. Data from this study indicate that estrogenic phytochemicals are not as efficacious as ZA in preventing menopausal-related bone loss but may have beneficial effects on bone marrow adiposity in rats.

Bone quality and strength are greater in growing male rats fed fructose compared with glucose.

Optimization of peak bone mass during adolescence is important for osteoporosis prevention. Studies in rodents and humans have demonstrated the harmful effects of sugar intake on bone health. With the high levels of sucrose in the diets of adolescents, it is necessary to understand the influence of glucose and fructose on growing bones. This study compared the effects of dietary glucose and fructose on bone formation, microarchitecture, and strength. Because of the different metabolic effects of glucose and fructose, we hypothesized that their individual effects on bone would be different. Eighteen male Sprague-Dawley rats (age, 60 days) were randomly assigned to high-fructose (n = 9; 40% fructose, 10% glucose) or high-glucose diet (n = 9; 50% glucose) for 12 weeks. Bone measurements included histology and histomorphometry of trabecular bone in the distal femur and a 3-point bending test of the whole tibia. Whole liver mass and postprandial serum glucose, insulin, and triglycerides were used to assess differences in energy metabolism between the diets. There were no differences in food intake, body weight, or visceral adiposity between groups, but fructose consumption led to heavier livers (P = .001) and elevated serum triglycerides (P = .00). The distal femurs of fructose-fed rats had greater bone volume (bone volume/total volume; P = .03), lower bone surface (bone surface/bone volume; P = .02), and thicker trabeculae (trabecular thickness; P = .01). The tibias of the fructose-fed rats also withstood a greater maximum flexure load (P = .032). These results indicate that consumption of the high-fructose diet resulted in stronger bones with enhanced microarchitecture than consumption of the high-glucose diet.