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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Increased dietary phosphate, primarily from additives in processed foods, is a growing public health concern. While it has been reported that high phosphate intake is a risk factor for renal injury, its effects on body fluid and electrolyte balance remain to be clarified. In this study, we aimed to investigate the changes in body fluid and electrolyte balance in mice fed a high-phosphate diet.
Male 8-week-old C57BL/6J mice were fed a control diet (0.35% phosphate), a high-phosphate diet (HPD, 2% phosphate), or a cation-matched diet supplemented with NaCl and KCl to match the sodium and potassium content of the HPD for 10 days. Throughout the feeding period, daily water intake, food intake, urine volume, and body weight were monitored. On day 10, tissues were harvested to measure water and electrolyte content using the ashing-flamephotometry method, and the liver samples were subjected to metabolome and RNA-sequence analyses.
The HPD group did not alter food and water intake but significantly increased urine volume associated with a decrease in urinary osmolality compared with the control group. The HPD-induced renal water loss significantly decreased total body water, sodium, and potassium. These effects were phosphate-specific, as they were not observed in the cation-matched NaCl/KCl group. We have previously reported the compensatory increase in urea accumulation at the tissue level that conserves water during high salt intake; however, the HPD significantly reduced urea levels in the liver and muscle and tended to reduce in plasma and renal inner medulla. Metabolome analysis confirmed the HPD-induced suppression of hepatic ureagenesis, showing decreased levels of urea cycle intermediates and their precursor amino acids/nitrogen-associated metabolites. Furthermore, liver RNA-sequencing revealed an increase in fatty acid oxidation in the HPD group, leading to a relative reduction in the substrate from amino acid catabolism available for urea production.
These findings suggest that excessive phosphate intake affects body fluid homeostasis by inducing osmotic diuresis, leading to water loss and a catabolic state. The phosphate-induced water loss is associated with the suppression of the compensatory urea-driven water conservation, which is activated by high salt intake but not a high-phosphate diet. These findings reveal a novel link between dietary phosphate, hepatic metabolism, and body fluid balance, highlighting the need for further investigation into this axis, particularly in humans.
