Naringin prevents bone loss in a rat model of type I Diabetes mellitus

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

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2018 p. 56 - 63

0003-9861

Bone disease is associated with the type 1 Diabetes mellitus (D.m.). The aim of this work was to know whether the bone complications of the experimental type 1 D.m. could be prevented by chronic administration of naringin (NA), an antioxidant agent, in a model of streptozotocin (STZ) induced diabetes in rats. Male Wistar rats were employed: 1) controls, 2) STZ-rats, 3) STZ- rats treated with 40 mg NA/kg of b.w., and 4) STZ-rats treated with 80 mg NA/kg of b.w. BMD and BMC were performed by dual-energy X-ray absorptiometry. Bone histomorphometry and histology as well as TRAP staining were done in long bones. Osteocalcin (OCN) was determined in bone by immunohistochemistry and in serum by ELISA. Glutathione (GSH) content and catalase (CAT) activity were assayed in bone marrow from femur. The data showed that NA80 increased the BMD and BMC from the long bones of STZ-rats. Both NA40 and NA80 normalized the trabecular number and the trabecular separations. An increase in the number of adipocytes and TRAP (+) cells in tibia from STZ-rats was blocked by NA. NA40 treatment increased the number of OCN (+) cells, but only the NA80 treatment allowed to reach the control values. NA did not affect the GSH content but normalized the CAT activity in bone marrow of femur from STZ-rats. In conclusion, NA avoids alterations in the physical properties and microstructure of bone from STZ-rats probably by stimulation of osteoblastogenesis, inhibition of the osteoclastogenesis and adipogenesis via blocking the oxidative stress.