Retinoid/vitamin A metabolites such as all- trans retinoic acid and 9- cis retinoic acid affect several steps of metabolism in vertebrates. Several studies have shown that retinoids regulate target genes through nuclear retinoid receptors (RARs and RXRs) in order to play their roles. The nuclear receptors are ligand-modulated transcription factors that respond to retinoids, steroids, and thyroid hormones, to control development and body physiology. The 9- cis retinoic acid receptor, RXR, acts as a common heterodimeric partner with several receptors, such as all- trans retinoic acid receptors (RARs), vitamin D₃ receptor, and thyroid hormone receptors. In this study, the author investigated the gene regulation of nuclear retinoid receptors (RARα, -β, -γ and RXRα, -β, -γ) by nutritional status in vivo , and a retinoid-inducible gene in a retinoid target cell in vitro . Retinoid up-regulates the gene expression of only RARβ at the transcriptional level. This suggests specific ligand regulation of RARβ gene expression in the intact animal, and that the altered levels of RARβ according to retinoid status may affect retinoid-inducible gene expression. Moreover, thyroid hormone up-regulates the gene expression of RXRβ but down-regulates the level of RXRγ mRNA in rat tissues. These findings suggest that RXR-mediated signal transduction through molecules such as retinoid, vitamin D and thyroid hormone, may be modulated in part through thyroid hormone. We investigated the molecular mechanisms of retinoid-modulated bone-resorption in vitro , and clearly demonstrated the gene expression of RARα and RXRβ in mature osteoclasts, i.e. bone-resorbing cells. Retinoids up-regulate the bone-resorbing activity and the gene expression of cathepsin K in osteoclasts. These results suggest that osteoclasts are the target cells for retinoids, and that retinoids partly regulate bone metabolism through these cells.