The natural antioxidant naringin improves bone metabolism in experimental type I diabetes mellitus

PICOTTO G; RODRIGUEZ V; RIVOIRA MA; BATTAGLINO R; TOLOSA DE TALAMONI N

Mar del Plata

Congreso; LXI Reunión Científica Anual de la Sociedad Argentina de Investigación Clínica; 2016

SAIC

Diabetes mellitus (D.m.) is usually related to a reduced bone mineral density (BMD) and low bone remodeling 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, 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 gluthatione 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 activitity. All these changes were prevented with naringin. In summary, our results suggest that naringin, a low cost antioxidant, protects the bone osteolytic effects triggered by insulin deficiency. Osteocalcin and redox status normalization and the reduction in the number of adipocytes and OC suggest that naringin is acting as a possible bone protector for experimental type 1 D.m.