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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.
In patients with heart failure, renal dysfunction can lead to diuretic resistance, complicating fluid management. Compared with hemodialysis, peritoneal dialysis (PD) enables gradual ultrafiltration and better hemodynamic stability, providing an effective strategy for treating volume overload. In PD, ultrafiltration largely depends on the glucose concentration of the dialysis solution; however, the mechanisms underlying glucose transport across the peritoneal membrane remain incompletely understood. This study aimed to investigate the glucose uptake capacity of peritoneal mesothelial cells isolated from gene-modified rats lacking sodium-glucose cotransporters (SGLTs).
Genome editing of Sglt1 and Sglt2 was performed in Sprague-Dawley rats using the rat genome-editing via oviductal nucleic acids delivery (rGONAD) technique, an in vivo clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-based genome editing method. Peritoneal mesothelial cells were isolated and cultured from Sglt1-deficient rats and their wild-type littermates, as well as from Sglt2-deficient rats and their wild-type littermates. Cellular glucose uptake was examined using flow cytometry under incubation with 2-NBDG [2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose], a fluorescently labeled glucose analog. Cell viability was assessed using the WST-8 assay.
Glucose uptake, indicated by 2-NBDG fluorescence intensity, was partially reduced in peritoneal mesothelial cells derived from Sglt1-deficient rats compared with wild-type controls, whereas Sglt2 deficiency had no effect. Neither Sglt1 nor Sglt2 deletion altered cell viability or morphology under standard culture conditions.
SGLT1, but not SGLT2, contributes to glucose uptake in peritoneal mesothelial cells. These findings suggest that SGLT1 plays a key role in glucose transport across the peritoneal membrane. A better understanding of glucose handling in peritoneal mesothelial cells may provide new insights for optimizing PD therapy and improving osmotic ultrafiltration efficiency in patients with heart failure and volume overload.
