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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.
The organ-protective effects of dietary restriction and SGLT2 inhibitors observed in large clinical trials have highlighted ketone bodies as potential mechanistic mediators. Although the liver is the main site of ketone body production, emerging evidence indicates that the kidney also has this capability. However, the physiological role of renal ketogenesis remains poorly understood. In this study, we investigated the functional significance of renal ketone bodies.
Single-cell RNA sequencing (scRNA-seq) was conducted on renal tissues from mice subjected to both fasting and non-fasting conditions. Immunostaining for Hmgcs2, the key enzyme involved in ketone body synthesis, was carried out to ascertain its localization. Mice with proximal tubule-specific knockout of Hmgcs2 (Hmgcs2ΔPT) were generated via crossing SLC34a1-CreER mice with Hmgcs2-flox mice. Both wild-type and Hmgcs2ΔPT mice underwent fasting protocols. Renal tissue ketone concentrations were analyzed through mass spectrometry imaging (MSI). Additionally, measurements of urine volume, osmolality, and electrolyte concentrations were performed.
scRNA-seq and immunostaining showed that Hmgcs2 expression was mainly localized to the proximal tubules during fasting. In Hmgcs2ΔPT mice, Hmgcs2 expression was blunted in the proximal tubules. Although blood ketone levels did not change significantly, renal tissue ketone levels during fasting determined by MSI were notably lower in Hmgcs2-PTCKO mice. These mice also had increased urine volume and higher urinary sodium excretion compared to WT controls only under fasting conditions.
These findings indicate that ketone bodies are physiologically produced in the kidneys during fasting and play a role in urine concentration. Impaired renal ketogenesis may lead to a decreased ability to concentrate urine during fasting.
