Vitamin D treatment of senescence accelerated mice (SAM-P/6) induces several regulators of stromal cell plasticity.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

In an attempt to understand the regulation of bone marrow multipotential cells plasticity in vivo, we treated 4-month-old SAM-P/6 mice with a constant infusion of either 18 pmol/24 h of 1,25(OH)2D3 or vehicle alone for 6 weeks. In vehicle treated animals 78% +/- 4 adipose volume vs. total volume was stained positive with oil red O as compared to only 32 +/- 3% in 1,25(OH)2D3 treated animals (P < 0.001). Furthermore, we aimed to identify the changes in gene expression induced by 1,25(OH)2D3 in bone marrow cells by analyzing a set of 5440 genes in the NIA 15K Mouse cDNA microarray. Overall, a coordinated regulation of genes which both stimulate osteoblastogenesis and inhibit adipogenesis was observed in 1,25(OH)2D3-treated mice when compared to vehicle treated mice. In summary, this study illustrates the anti-adipogenic effect of 1,25(OH)2D3 in bone cells and identifies some of the possible key signals involved in bone cell plasticity.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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