An increasing amount of scientific evidence suggests that western diet is a risk factor for osteopenia and osteoporosis. Indeed, metabolic acidosis, occurring after high levels of protein intake, may adversely impact on the skeleton by disrupting calcium metabolism, and leads to a decrease of bone mineral density (BMD). Currently, the prevention and treatment of osteopenia and osteoporosis are mainly based on lifestyle modifications (i.e. exercise, quitting smoking and ensuring an adequate daily intake of calcium and vitamin D) and medical therapies (e.g. bisphosphonates, denosumab, and proton pump inhibitors).
Recent studies have demonstrated that potassium citrate supplementation results in BMD increase, sustained improvement of calcium balance, and decrease of bone resorption markers in both postmenopausal women and healthy young adults. Despite promising clinical data on the efficacy of alkaline citrates on calcium metabolism, it is still not clear whether potassium citrate acts only as a buffer or has a direct effect on bone cells.
In this study, we investigated the role of potassium citrate on human primary osteoclasts differentiation and activity in the presence of an acidic microenvironment.
We analyzed the effect of different potassium citrate concentrations on murine osteoclast precursor cells of Raw 264.7 monocyte-macrophage cell line, cultured in pH 6.8 media, in order to mimic a sub-acidosis condition. In particular, we examined Raw 264.7 viability in the presence of increasing concentrations of potassium citrate (0, 5, 7.5, 10, 12.5, 15 and 30 g/l), every 24 h, for a total period of 96 h, using Alamar blue assay. Moreover, we measured pH variation at the same time points.
Our preliminary results demonstrated that only 5 and 7.5 g/l potassium citrate have a alkaline effect at non-cytotoxic doses. These two concentrations will be used to investigate citrate potassium effects on human OC and other bone cells.
14 May 2016 - 17 May 2016