Maternal excess dietary phosphate intake in the periconceptional period is a potential risk for mineral disorders in offspring mice

Growing consumption of processed foods may cause a greater risk of excessive dietary phosphate intake. The increased dietary phosphate intake as a food additive in the periconceptional period may affect the children's future health. Here, we investigated the effects of maternal excess dietary phosphate intake on offspring in C57BL/6J mice. Female mice were fed a control diet (CP, 0.8% phosphate) or a high-phosphate diet (HP, 1.5% phosphate) for either 21 days during pre-pregnancy or almost 20 days during pregnancy. After weaning, offspring were raised on the CP diet. Relative to the CP groups, offspring from dams fed HP during pre-pregnancy or pregnancy showed decreased urinary phosphate excretion without significant changes in either plasma phosphate level or renal sodium-dependent phosphate transporter mRNA expression at 3 or 10 weeks. However, mRNA expression of intestinal sodium-dependent phosphate transporter was decreased, suggesting that the reduced urinary phosphate excretion was due to decreased absorption of intestinal phosphate. Interestingly, offspring in the HP groups also demonstrated significant differences in plasma levels of parathyroid hormone, fibroblast growth factor 23, and vitamin D. To our knowledge, this is the first report to show that maternal excess intake of dietary phosphate in the periconceptional period disturbs phosphate metabolism in offspring.