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The RANKL protein may play a role in a relationship between oxidized lipids and immune-mediated bone loss.
The RANKL protein may play a role in a relationship between oxidized lipids and immune-mediated bone loss, according to research published online Aug. 22 in Clinical Immunology.
Lucia S. Graham, of the David Geffen School of Medicine at the University of California in Los Angeles, and colleagues write that hyperlipidemia has repeatedly been associated with osteoporosis. The authors exposed human T lymphocytes to minimally oxidized low density lipoprotein-which is highly inflammatory-and noted that production of the receptor activator NFκB ligand (RANKL) was significantly increased.
In addition, the authors found that mice rendered hyperlipidemic by a high-fat diet showed reduced femoral bone mineral content compared to chow-fed mice, and their T lymphocytes expressed significantly greater RANKL mRNA than T lymphocytes from controls. The human and mouse studies suggest that exposure to oxidized lipids encourages T lymphocyte RANKL production.
Graham LS, Parhami F, Tintut Y, et al. Oxidized lipids enhance RANKL production by T lymphocytes: implications for lipid-induced bone loss. Clin Immunol. 2009 Aug 20. [Epub ahead of print]