L-arginine supplementation normalizes bone turnover and preserves bone mass in streptozotocin-induced diabetic rats
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.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2009 |
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| Erschienen: |
2009 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:32 |
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| Enthalten in: |
Journal of endocrinological investigation - 32(2009), 6 vom: 07. Juni, Seite 546-51 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Pennisi, P [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 17.02.2010 Date Revised 20.10.2021 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1007/BF03346505 |
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| Förderinstitution / Projekttitel: |
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| 245 | 1 | 0 | |a L-arginine supplementation normalizes bone turnover and preserves bone mass in streptozotocin-induced diabetic rats |
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| 520 | |a 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 | ||
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| 700 | 1 | |a Luca, T |e verfasserin |4 aut | |
| 700 | 1 | |a Martinez, G |e verfasserin |4 aut | |
| 700 | 1 | |a Mangiafico, R A |e verfasserin |4 aut | |
| 700 | 1 | |a Pulvirenti, I |e verfasserin |4 aut | |
| 700 | 1 | |a Muratore, F |e verfasserin |4 aut | |
| 700 | 1 | |a Fiore, C E |e verfasserin |4 aut | |
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