4.6 Article

Naringin prevents bone loss in a rat model of type 1 Diabetes mellitus

Journal

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
Volume 637, Issue -, Pages 56-63

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2017.12.001

Keywords

Type 1 D.m.; Naringin; Oxidative stress; Bone mineral density; TRAP(+) cells; Adipocytes

Funding

  1. Bilateral Cooperation CONICET (Argentina)-National Science Foundation (USA)
  2. CONICET (PIP), Argentina
  3. SECYT (UNC), Argentina
  4. NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR064793] Funding Source: NIH RePORTER

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The aim of this work was to know whether naringin (NA) could prevent the bone complications in a model of streptozotocin (STZ) induced diabetes. Rats were divided in: 1) controls, 2) STZ-rats, 3) STZ-rats treated with 40 mg NA/kg, and 4) STZ-rats treated with 80 mg NA/kg. BMD and BMC were performed by DEXA. Bone histomorphometry and histology as well as TRAP staining were done in tibia. Osteocalcin (OCN) was determined in bone and serum. Glutathione content and SOD and catalase activities 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 normalized the SOD and catalase activities 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.

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