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

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

Mar del Plata

Congreso; Reunión conjunta de SAIC, SAI y SAFE; 2016

Diabetes mellitus (D.m.) isusually related to a reduced bone mineral density (BMD) and low bone remodelingthat cannot be improved by insulin administration. As D.m. also producesoxidative stress, our hypothesis is that bone alterations may be associated withredox changes and if so, this could be avoided by an antioxidant therapy likenaringin. Adult male Wistar rats were used: 1) controls, 2) diabetic rats treatedwith 60 mg/kg/bw of streptozotocin (STZ), 3-4) STZ rats treated with 40 or 80 mg/kg/bw/dayof naringin for 30 days. Histomorphometry, BMD and content (BMC) andmicrocomputarized tomography were analyzed (µCT). We also determined vitamin Dstatus and other systemic parameters of calcium metabolism. Bone marrow wasstudied for gluthatione content (GSH), catalase activity (CAT), while adipocyteand osteoclast (OC) numbers were counted from histological sections. Calcitrioland osteocalcin levels were reduced by STZ. Naringin returned osteocalcinvalues to control ones.  STZ ratspresented low BMD and BMC in distal femur and proximal tibiae, and the highestdose of naringin avoided this effect.  STZgroup presented reduced bone volume, thickness, trabecular number andintertrabecular spaces.  All thesechanges were overcome with naringin-80.  Diabeticrats had increased adipocytes and OC numbers and low GSH concentration and highCAT activitity. All these changes were prevented with naringin. In summary, ourresults suggest that naringin, a low cost antioxidant, protects the boneosteolytic effects triggered by insulin deficiency. Osteocalcin and redox status normalization and thereduction in the number of adipocytes and OC suggest that naringin is acting asa possible bone protector for experimental type 1 D.m.