Naringin, natural flavonoid, prevents bone alterations induced by a fructose rich diet

RODRÍGUEZ V; GUIZZARDI S; RIVOIRA M; TOLOSA DE TALAMONI N; CORBALL L

Mar del Plata

Congreso; Reunión Anual SAIC-SAI-SAFIS; 2018

There is a considerable evidence that fructose rich diet (FRD) causesadverse metabolic perturbations. Recently, we have demonstrated that FRD inhibits the intestinal Ca2+ absorption, which was avoid naringin (NAR). The aim of this study was to know the effect of NAR on bone alterations in FRD rats. Male Wistar rats were used: 1) controls, 2) treated with FRD, 3) FRD treated with 40 mg NAR/kg b.w. for 30 days. Histomorphometric parameters were measured in distal femur and proximal tibiae. Parameters of oxidative stress were measured in bone marrow from femur. Adipocytes and osteocytes were counted in tibiae histological sections. Osteocalcin (OCN) was determined in bone and serum. The data showed that serum OCN levels were reduced by FRD, and NAR treatment returned them to the control values. FRD rats presented reduced bone volume, thickness and intertrabecular spaces in proximal tibiae. All these changes were normalized with NAR. There are no differences in the histomorphometric parameters from distal femur. An increase in the number of adipocytes in tibiae from FRD rats was blocked by NAR. In the proximal tibiae from FRD rats, the number of OCN(+) cells and osteocytes decreased as compared to that of control rats. NAR treatment significantly increased the number of OCN(+) cells and osteocytes. In FRD rats, the GSH content was similar to the control, but NAR treatment increased total GSH in comparison with that from the control and FRD rats. .O2- levels were highly augmented by the FRD and NAR could not normalize them. CAT activity decreased in FRD and NAR administration avoided this response. In summary, NAR protects the bone alterations triggered by FRD. The OCN normalization, the reduction in the number of adipocytes and the increase in the number of osteocytes suggest that NAR is acting as a possible bone protector in FRD rats.