Effects of High Phosphorus Diet on Bone Metabolism-Related Gene Expression in Young and Aged Mice

In this study, the effects of high phosphorus (P) diet on bone metabolism-related gene expression were investigated in young and aged mice. Twelve- and 80-week-old ddY male mice were divided into two groups, respectively, and fed a control diet containing 0.3% P or a high P diet containing 1.2% P. After 4 weeks of treatment, serum parathyroid hormone (PTH) concentration was significantly higher in the high P groups than in the control groups in both young and aged mice and was significantly higher in aged mice than in young mice fed the high P diet. High P diet significantly increased receptor activator of NF-κB ligand (RANKL) mRNA in the femur of both young and aged mice and significantly increased the RANKL/osteoprotegerin (OPG) mRNA ratio only in aged mice. High P diet significantly increased mRNA expression of transient receptor potential vanilloid type 6, calbindin-D9k, and plasma membrane Ca2+-ATPase 1b in the duodenum of both young and aged mice. These results suggest that high P diet increased RANKL mRNA expression in the femur and calcium absorption-related gene expression in the duodenum regardless of age. Furthermore, the high P diet-induced increase in PTH secretion might increase the RANKL/OPG mRNA ratio in aged mice

Iron deficiency decreases renal 25-hydroxyvitamin D3-1α-hydroxylase activity and bone formation in rats

BACKGROUND: Dietary iron intake is associated with bone metabolism in human and animals. Previous studies have suggested that iron deficiency diminishes bone formation and causes bone loss in rats, however, the detailed mechanisms remain unclear. To clarify the mechanism of the diminishing bone formation in iron deficiency, we examined the renal 25-hydroxyvitamin D3-1α-hydroxylase (1α-hydroxylase) activity and femoral expression of bone formation-related genes in iron-deficient rats. METHODS: Male Wistar rats (n = 18) at 3 weeks of age were divided into three groups of six rats each. Two groups of rats were given free access to a control diet or an iron-deficient diet for 4 weeks. Rats in the third group were pair-fed the control diet, calculated as the mean food intake of the iron-deficient group. RESULTS: Following the treatment, compared with the control and pair-fed groups, hemoglobin and liver iron concentrations were significantly lower and heart weight was significantly higher in the iron-deficient group. Serum 1,25-dihydroxyvitamin D3 concentration and renal 1α-hydroxylase activity were significantly lower in the iron-deficient group compared with the control and pair-fed groups. Serum osteocalcin concentration and bone mineral density of the femur were also significantly lower in the iron-deficient group compared with the control and pair-fed groups. Furthermore, iron-deficient diet decreased runt-related transcription factor 2, osteocalcin, and type I collagen mRNA expression in the femur. CONCLUSIONS: Our findings indicate that iron deficiency reduces renal 1α-hydroxylase activity, leading to a decreased bone formation in rats

Additional file 1: Table S1. of Iron deficiency decreases renal 25-hydroxyvitamin D3-1Îą-hydroxylase activity and bone formation in rats

Composition of the experimental diets. Table S2. Body weight, food intake, hemoglobin, heart weight, and liver iron concentration. Table S3. Bone turnover markers and BMC, area, and BMD of the femur. (DOC 32 kb

Sulforaphene attenuates multinucleation of pre-osteoclasts by suppressing expression of cell–cell fusion-associated genes <i>DC</i>-<i>STAMP</i>, <i>OC</i>-<i>STAMP,</i> and <i>Atp6v0d2</i>

<p>We assessed the effect of sulforaphene (SFE) on osteoclast differentiation. SFE significantly decreased the number of RANKL-induced tartrate-resistant acid phosphatase-positive cells and suppressed pre-osteoclast multinucleation. Furthermore, SFE downregulated mRNA expression of <i>DC</i>-<i>STAMP</i>, <i>OC</i>-<i>STAMP,</i> and <i>Atp6v0d2</i>, which encode cell–cell fusion molecules. Our data suggest that SFE attenuates pre-osteoclast multinucleation via suppression of cell–cell fusion.</p