title: L-arginine supplementation normalizes bone turnover and preserves bone mass in streptozotocin-induced diabetic rats.
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.
authors.affiliation: Department of Internal Medicine, University of Catania, Catania, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Pennisi
authors.forename: G
authors.initials: G
authors.lastname: Clementi
authors.forename: A
authors.initials: A
authors.lastname: Prato
authors.forename: T
authors.initials: T
authors.lastname: Luca
authors.forename: G
authors.initials: G
authors.lastname: Martinez
authors.forename: R A
authors.initials: RA
authors.lastname: Mangiafico
authors.forename: I
authors.initials: I
authors.lastname: Pulvirenti
authors.forename: F
authors.initials: F
authors.lastname: Muratore
authors.forename: C E
authors.initials: CE
authors.lastname: Fiore
mesh_terms: D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D001120:Arginine / Q000008:administration & dosage*; D015519:Bone Density / Q000502:physiology; D001851:Bone Diseases, Metabolic / Q000097:blood / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control*; D016723:Bone Remodeling / Q000187:drug effects*; D002118:Calcium / Q000097:blood; D024042:Collagen Type I / Q000097:blood; D003404:Creatinine / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D008297:Male; D020030:Nitric Oxide Donors / Q000008:administration & dosage*; D015675:Osteocalcin / Q000097:blood; D010455:Peptides / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D018709:Statistics, Nonparametric
chemical_list: D024042:Collagen Type I; D020030:Nitric Oxide Donors; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide; D015675:Osteocalcin; D001120:Arginine; D003404:Creatinine; D000469:Alkaline Phosphatase; D002118:Calcium