Bone alterations in the experimental metabolic syndrome: effect of a natural antioxidant

RIGALLI A; RODRÍGUEZ VA; CORBALL L; RIVOIRA MA; TOLOSA DE TALAMONI NG

Buenos Aires

Otro; XXXVI Reunión anual AAOMM; 2019

There is considerable evidence that a fructose rich diet (FRD) causesadverse metabolic perturbations. The aim of this study was to know the effect of naringin (NAR) on bone alterations in FRD rats. Wistar male rats were used: 1) controls, 2) FRD: the same control diet plus 10% fructose, 3) FRD treated with 40 mg NAR/kg b.w. for 30 days. The data showed that serum osteocalcin (OCN) levels were reduced by FRD, and NAR treatment normalized them. FRD rats presented reduced bone mineral density (BMD), bone volume, thickness and intertrabecular spaces. All these changes were blocked by NAR. In distal femur, NAR increased the number of trabeculae. An increase in the number of adipocytes in tibiae from FRD rats was avoided 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 increased the number of OCN(+) cells and osteocytes. The GSH content in bone marrow of femur from FRD rats was similar to that of the control rats, 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 rats and NAR administration blocked this response. NAR increased the BMD from cortical and trabecular femur of FRD. In summary, NAR avoids the bone alterations triggered by FRD. The BMD and 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 metabolic syndrome.