Naringin prevents bone damage in the experimental metabolic syndrome induced by a fructose-rich diet.

We analyzed the effect of naringin (NAR), a flavonoid from citric fruits, on bone quality and biomechanical properties, as well as the redox state of bone marrow in rats fed a fructose-rich diet (FRD), an experimental model to mimic human metabolic syndrome. NAR blocked the increase in the number of osteoclasts and adipocytes and the decrease in the number of osteocytes and osteocalcin (+) cells caused by FRD. Trabecular number was significantly higher in the FRD+NAR group. FRD induced a decrease in the femoral trabecular and cortical bone mineral density, which was blocked by NAR. The fracture and ultimate loads were also decreased in the FRD and FRD+NAR groups. NAR increased the number of nodes to terminal trabecula, the number of nodes to node trabecula, the number of nodes, and the number of nodes with 2 terminals and decreased the Dist (mean size of branches) value. FRD decreased bone marrow catalase activity, an effect that was prevented by NAR. In conclusion, FRD has detrimental effects on the long bones, which are associated with oxidative stress in the bone marrow. Most of these changes are prevented by NAR through its antioxidant properties and promotion of bone formation. Fructose-rich diets have detrimental effects on long bones, which are associated with oxidative stress in the bone marrow. Most of these changes are prevented by naringin through its antioxidant properties and promotion of bone formation.