Background /Objectives
Lipedema is a chronic, progressive fat distribution disorder almost exclusively affecting women, with underlying mechanisms still unknown. Given the suspected involvement of inflammation, lymphatic impairment, and stromal remodeling, EVs have gained attention as potential mediators and biomarkers of these processes. This study aims to isolate and characterize EVs from lipoaspirates of both healthy individuals and lipedema patients to investigate potential cell-type and disease-specific EV release patterns.
Methods
Lipoaspirates were collected from healthy female donors and female patients diagnosed with lipedema. After processing, three major components were isolated: (1) stromal vascular fraction (SVF), (2) adipocytes, (3) a mixture of blood and lymph fluid from liposuction. EVs were isolated through a combination of differential centrifugation and ultracentrifugation. The concentration and size distribution of isolated EVs were analyzed using Nanoparticle Tracking Analysis (NTA), allowing for quantitative and qualitative comparison between fractions and donor groups. Using high-resolution mass spectrometry, the metabolomic profile of each cell fraction was analyzed to identify and quantify a wide range of metabolites.
Results
Preliminary results show that EVs could be successfully isolated from all groups examined. In addition, the data indicates differences in particle number and size between the different cell types. Metabolomic analysis uncovered distinct metabolic profiles between the cell fractions, with several pathways related to lipid metabolism, oxidative stress, and inflammation differentially regulated in lipedema samples.
Conclusion
These initial results indicate that there are discrepancies in both EV release and metabolic profiles across diverse cell types and between healthy and lipedema-derived lipoaspirate fractions. The correlation between altered metabolic pathways, especially those related to lipid processing, inflammation and oxidative stress, suggests a functional link between cellular metabolism and EV-mediated intercellular communication. These findings provide novel insights into the pathophysiology of lipedema and support the hypothesis that EVs may function not only as biomarkers but also as active participants in disease progression.
Keywords
Lipedema, EV-Disease specific Marker, Research in Human Model, Metabolomics
Funding/Acknowledgments
This research was funded by core funding of the Health and Medical University Potsdam and the Klinikum Ernst von Bergmann. We thank all patients for providing samples with informed consent, in accordance with institutional ethical guidelines. Their contributions were essential to this study.
