Osteoblasts have a high rate of energy consumption during bone formation and bone protein synthesis. Therefore, it is likely that decreased energy production that accompanies aging, could contribute to reduced osteoblast activity, a critical feature of senile osteoporosis, and that this reduction might be counteracted by favoring energy availability. Cells of the osteoblastic lineage generate 4080% of the requested energy through fatty acid degradation, thus the modulation of lipid oxidation could be involved in the availability of energy required for protein synthesis. L-Carnitine (LC) promotes energy availability, as it is an essential cofactor for the transport of fatty acid into the mitochondrial matrix where β-oxidation occurs. Based on these evidences, we studied the possible stimulatory effects of L-Carnitine on cells of the osteogenic lineage. For this purpose we treated human osteoblasts (hOb) derived from trabecular bone waste material of orthopaedic surgery (Ethics Committee approved), with 5 mM LC at different times,3,6 and 24 h.
After 24 h treatment LC induced an increase in mitochondrial activity, as shown by Mito Tracker Dye assay. This effect was accompanied by a significant increase of SOD2 protein levels, which plays an important role in neutralizing oxidative stress, and an increase in Calcium-Calmodulin Kinase II protein (CaMKII). Since CaMKII is able to favour synthesis and transcriptional activity of osterix (OSX), we evaluated the effect of LC on osteogenesis-related genes. LC increased significantly (P<0.01) OSX and bone sialo-protein mRNA expression. Moreover, LC stimulated osteopontin mRNA and protein expression. Altogether these results suggest that LC, exerts a stimulatory effect on bone by favouring osteoblast differentiation. Considering its safety profile, LC could be a useful supplement to support bone health in the elderly.
14 - 17 May 2016
European Calcified Tissue Society