L-Carnitine and Isovaleryl L-Carnitine Fumarate Positively Affect Human Osteoblast Proliferation and Differentiation In Vitro |
| |
Authors: | S. Colucci G. Mori S. Vaira G. Brunetti G. Greco L. Mancini G. M. Simone F. Sardelli A. Koverech A. Zallone M. Grano |
| |
Affiliation: | (1) Department of Human Anatomy and Histology, University of Bari, Bari, Italy;(2) Department Unit Carnitine, Sigma-tau, Roma, Italy |
| |
Abstract: | Age-related bone loss is characterized by decreased osteoblast activity, possibly related to the reduction of energy production. Carnitine promotes energy availability and its concentration declines with age; Therefore, two Carnitine derivatives, L-carnitine fumarate (LC) and isovaleryl L-carnitine fumarate (Iso-V-LC), have been tested on several parameters of human osteoblasts in vitro. Both compounds significantly increased osteoblast activity, but the new compound Iso-V-LC was more efficient than LC at lower concentrations. They both significantly enhanced cell proliferation, [3H]-proline incorporation and the expression of collagen type I (COLLI), and the bone sialoproteins (BSPs) and osteopontin (OPN). The percentage of alkaline phosphatase (ALP)–positive cells and the secretion of osteocalcin were not modified by LC and Iso-V-LC. Both molecules increased the formation of mineralized nodules, but Iso-V-LC reached the maximum effect at a concentration 10-fold lower than that of LC. Furthermore, we showed that insulin-like growth factor (IGF)-I and IGF-II mRNA levels were not modified by the treatment. However, the two compounds induced an increase of insulin-like growth factor binding protein (IGFBP)-3 and a decrease of IGFBP-5 in both osteoblast lysates and the extracellular matrix (ECM). In conclusion these data suggest that carnitine and, in particular, its new derivative, Iso-V-LC supplementation in the elderly may stimulate osteoblast activity and decrease age-related bone loss. |
| |
Keywords: | Carnitine Carnitine derivatives Osteoblast Proliferation Differentiation |
本文献已被 PubMed SpringerLink 等数据库收录! |
|