Naringin: A possible bone protector for experimental type I diabetes mellitus

RIVOIRA M; RODRÍGUEZ V; PICOTTO G; BATTAGLINO R; TOLOSA DE TALAMONI N

Buenos Aires

Congreso; Meeting 2016- Argentine Association of Osteology; 2016

Asociación Argentina de Osteología y Metabolismo Mineral

There is a relationship between Diabetes mellitus (D.m.) and low boneremodeling that cannot be improved by insulin administration. As D.m. also produces oxidative stress, our hypothesis is that bone alterations may be associated with redox changes and if so, this could be avoided by an antioxidant therapy like naringin. Adult male Wistar rats were used: 1) controls, 2) diabetic rats treated with 60 mg/kg/bw of streptozotocin (STZ), 3?4) STZ rats treated with 40 or 80 mg/kg/bw/day of naringin for 30 days. Histomorphometry, bone mineral density (BMD) and content (BMC) and microcomputarized tomography were analyzed (μCT). We also determined vitamin D status and other systemic parameters of calcium metabolism. Bone marrow was studied for glutathione content (GSH), catalase activity (CAT), while adipocyte and osteoclast (OC) numbers were counted from histological sections. Calcitriol and osteocalcin levels were reduced by STZ. Naringin returned osteocalcin values to control ones. STZ rats presented low BMD and BMC in distal femur and proximal tibiae, and the highest dose of naringin avoided this effect. STZ group presented reduced bone volume, thickness, trabecular number and intertrabecular spaces. All these changes were overcome with naringin-80. Diabetic rats had increased adipocytes and OC numbers and low GSH concentration and high CAT activity. All these changes were prevented with naringin. In summary, our results suggest that naringin protects the bone osteolytic effects triggered by insulin deficiency. Osteocalcin normalization and the reduction in the number of adipocytes and OC suggest that naringin acts as an anabolic agent for the diabetic bone.