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

CORBALL L; RIGALLI A; RODRIGUEZ V; RIVOIRA M; TOLOSA DE TALAMONI N

APPLIED PHYSIOLOGY, NUTRITION AND METABOLISM

NATL RESEARCH COUNCIL CANADA-N R C RESEARCH PRESS

Lugar: Otawa; Año: 2022 vol. 47 p. 395 - 404

1715-5312

We have analyzed the effect of naringin (NAR), a flavonoid from citric fruits, on bone quality and bone 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 enhancement in the number of osteoclasts and adipocytes and the decrease in the number of osteocytes and osteocalcin (+) cells caused by FRD. The trabecular number was significantly higher in the FRD+NAR group. FRD induced a decrease in femoral trabecular and cortical bone mineral density, which was completely blocked by NAR. The fracture and ultimate loads were also decreased by 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 two terminals, and decreased the Dist (mean size of branches) value. Bone marrow catalase activity was decreased by the FRD, an effect prevented by NAR. In conclusion, FRD produces detrimental effects on long bones, which are associated with oxidative stress in bone marrow. Most of these changes are avoided by NAR through its antioxidant properties and promotion of bone formation.