Osteopenia, an important complication of diabetes mellitus, is responsible of an increase in bone fracture and of a delay in fracture healing. The pathogenesis of this complication is unclear, however decreased availability and synthesis of nitric oxide (NO) may be regarded as a possible cause of disregulation of bone turnover. The aim of our study was to evaluate the effect of streptozotocin (STZ)-induced diabetes in the rat on bone mineral density (BMD) and bone turnover. We also examined whether supplementation of L-arginine (which acts as a NO substrate) could be beneficial for bone. After 6 weeks of STZ treatment, diabetic rats showed a significant decrease of BMD in the whole body, at the spine, at the pelvis, and at the femur. Bone turnover evaluation revealed a significant decrease in the serum levels of osteocalcin (a marker of bone formation), and an increase of the serum levels of the C-terminal telopeptide of type I collagen (RatLaps; a marker of bone resorption). L-arginine supplementation prevented the diabetes-induced reduction of BMD and osteocalcin, and the increase of RatLaps. These pharmacological actions of L-arginine produce a new suggestion that increase of NO synthesis and availability is potentially useful for effective prevention and treatment of osteopenia associated with diabetes. (J. Endocrinol. Invest. 32: 546-551, 2009) (C) 2009, Editrice Kurtis

L-arginine supplementation normalizes bone turnover and preserves bone mass in streptozotocin-induced diabetic rats

Clementi G.;Luca T.;Martinez G.;Muratore F.;Fiore C. E.
2009-01-01

Abstract

Osteopenia, an important complication of diabetes mellitus, is responsible of an increase in bone fracture and of a delay in fracture healing. The pathogenesis of this complication is unclear, however decreased availability and synthesis of nitric oxide (NO) may be regarded as a possible cause of disregulation of bone turnover. The aim of our study was to evaluate the effect of streptozotocin (STZ)-induced diabetes in the rat on bone mineral density (BMD) and bone turnover. We also examined whether supplementation of L-arginine (which acts as a NO substrate) could be beneficial for bone. After 6 weeks of STZ treatment, diabetic rats showed a significant decrease of BMD in the whole body, at the spine, at the pelvis, and at the femur. Bone turnover evaluation revealed a significant decrease in the serum levels of osteocalcin (a marker of bone formation), and an increase of the serum levels of the C-terminal telopeptide of type I collagen (RatLaps; a marker of bone resorption). L-arginine supplementation prevented the diabetes-induced reduction of BMD and osteocalcin, and the increase of RatLaps. These pharmacological actions of L-arginine produce a new suggestion that increase of NO synthesis and availability is potentially useful for effective prevention and treatment of osteopenia associated with diabetes. (J. Endocrinol. Invest. 32: 546-551, 2009) (C) 2009, Editrice Kurtis
Diabetes mellitus
L-arginine
osteopenia
streptozotocin
Alkaline Phosphatase
Animals
Arginine
Bone Density
Bone Diseases, Metabolic
Bone Remodeling
Calcium
Collagen Type I
Creatinine
Diabetes Mellitus, Experimental
Diabetes Mellitus, Type 1
Male
Nitric Oxide Donors
Osteocalcin
Peptides
Rats
Rats, Sprague-Dawley
Statistics, Nonparametric
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11769/542399
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