PR002324 (Project)

Description:Trans-fatty acids, prevalent in Western diets, contribute to the onset and progression of renal damage. This study investigates the effects of trans-fat consumption on kidney health using a comprehensive approach encompassing metabolomics, lipidomics, molecular, and cellular analyses. We analyzed both wild-type mice and mice with partial transforming growth factor beta 3 (Tgfβ3) deletion, a model for pre-existing renal damage. In control animals, the trans-fat diet induced significant dysregulation in renal lipid metabolism. Omic analyses revealed a reduction in triglycerides and an increase in plasmalogens, which are associated with cellular protection and signaling. Furthermore, upregulation of Tricarboxylic acid cycle (TCA) metabolites, malic and fumaric acids, indicated mitochondrial dysfunction. In mice with partial Tgfβ3 deletion, trans-fat consumption exacerbated renal fibrosis, and further depleted triglycerides and plasmalogens. Despite similar lipid profiles in both groups, Tgfβ3-deleted mice exhibited larger lipid droplets and worsened renal damage, including a notable reduction in taurine levels. This study underscores the value of detailed metabolic profiling to uncover mechanisms driving renal dysfunction linked to harmful dietary habits and genetic mutations.