Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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 high prevalence of cardiovascular-kidney-metabolic (CKM) syndrome in the population requires novel therapeutics to reduce cardiovascular death, and to this aim, predictive animal models are needed. Here we evaluated the effects of the GLP-1 receptor agonist semaglutide on kidney dysfunction and heart failure with preserved ejection fraction (HFpEF) in the Spontaneously Diabetic Torii (SDT) fatty, as a type 2 diabetic rat model of CKM syndrome.
Male, 6-week-old SDT fatty rats were treated with vehicle or semaglutide 15 nmol/kg s.c. Q3D for 6 weeks. At the end of the treatment, glomerular filtration rate (GFR) was measured using transdermal fluorescence measurement after FITC-sinistrin i.v. injection and cardiac function was investigated by echocardiography.
Compared to vehicle, semaglutide for 6 weeks significantly reduced body weight and body weight gain with a concomitant reduction in food intake. Semaglutide also reduced blood glucose levels in fed and fasting conditions (-22% and -44%, respectively, both p<0.05 vs. vehicle). As expected, vehicle treated SDT fatty rats showed hyperfiltration with high GFR values at treatment start and end. After 6 weeks of treatment, semaglutide significantly improved hyperfiltration with a 25 % reduction in GFR (p<0.05 vs. vehicle).
Echocardiography demonstrated that semaglutide did not alter left ventricle ejection fraction but improved diastolic dysfunction of SDT fatty rats. Semaglutide reduced left ventricle dilation with lower left ventricle internal diameter and significantly reduced end-diastole volume. Additionally, semaglutide significantly lowered the E/E’ ratio, increased E’/A’ ratio, and reduced isovolumic relaxation time.
Our data indicate that a 6-week treatment with semaglutide improved both kidney dysfunction and HFpEF in the SDT fatty rat. This preclinical model will be useful to evaluate novel therapies targeting CKM syndrome versus the standard of care semaglutide.