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

• Published in: BMC nutrition 2016-01, Vol.2
• Main Authors: Katsumata, Shinichi, Katsumata, Rie, Matsumoto, Naoki, Inoue, Hirofumi, Takahashi, Nobuyuki, Uehara, Mariko
• Format: Article
• Language: English
• Subjects: Nutrition
• ISSN: 2055-0928
• DOI: 10.1186/s40795-016-0072-8

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.