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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.
Modern diets contain abundant phosphorus, resulting in chronic exposure across the human lifespan. Prior animal studies show that acute, high-dose (2–3%) phosphorus loading induces hyperphosphatemia and consequent organ damage, including renal injury and vascular calcification. In contrast, the long-term effects of low-dose phosphorus loading that does not cause hyperphosphatemia—a common real-world exposure pattern in humans—remain incompletely understood. This study investigates the systemic effects of long-term and low-dose dietary phosphorus loading in the absence of hyperphosphatemia.
We employed male and female C57BL/6J mice to conduct a long-term animal study. Mice were randomly assigned to two dietary groups: Control group receiving a normal diet (0.84% phosphorus) and Pi group receiving a mildly high phosphorus diet (1% phosphorus). The study involved intraperitoneal glucose tolerance test and insulin tolerance test at 6 months. Histological findings of kidney, liver and pancreas were evaluated at 6 months. Survival rates were accessed at 24 months, alongside regular evaluating of serum phosphorus levels, renal function, and body weight throughout the study period.
Both dietary groups maintained comparable food intake, serum phosphorus levels, and renal function throughout the intervention period, regardless of sex. However, significant sex-specific differences were observed in metabolic outcomes and survival. Male mice in the Pi group demonstrated significantly reduced survival rates over the 24-month observation period and exhibited increased body weight at 4 months. They developed impaired glucose tolerance, hepatic lipid accumulation and pancreatic islet enlargement at 6 months. In contrast, female mice showed no difference in survival between dietary groups, although mice in Pi group exhibited increased body weight at 4 months. Pi-fed female mice maintained normal glucose tolerance and showed no hepatic lipid accumulation. Real-time PCR analysis of hepatic metabolism-related gene revealed upregulation of beta-oxidation related genes in the Pi fed female mice, whereas no such differences were observed in male mice. Furthermore, to investigate the role of sex hormones in phosphorus-induced mortality, mice underwent gonadectomy with or without hormone replacement therapy, followed by 6 months of Pi loading. Notably, castrated male mice receiving testosterone supplementation exhibited significantly decreased survival rates compared to all other experimental groups.
Long-term, low-dose phosphorus loading induces significant metabolic alterations and reduced lifespan without hyperphosphatemia, with sex-specific manner likely influenced by sex hormones. Our experimental models provide new insights into the sex-specific outcomes observed in chronic kidney disease patients, who are particularly susceptible to phosphorus dysregulation.
