Note from BEF: The following Metabolon press release details a newly published research paper. The paper’s findings “reveal novel metabolic abnormalities associated with the CF pathological process and identify a panel of potential biomarkers for therapeutic development using this model system,” according to Metabolon. The company’s metabolomics-driven approach enables the identification of biomarkers useful for the development of a wide range of diagnostics and provides insight into complex biochemical processes such as drug action, toxicology and bioprocess optimization.
Metabolon, Inc., leaders in global metabolomics, biomarker discovery and biochemical analysis, announces the publication of “Metabolomic Profiling Reveals Biochemical Pathways and Biomarkers Associated with Pathogenesis in Cystic Fibrosis Cells”, in the Journal of Biological Chemistry (2010, Vol. 285, No. 40, Pages 30516-30522). The article describes the application of non-targeted biochemical profiling (metabolomics) to study the biochemical changes in human lung epithelial cell lines of cystic fibrosis (CF) patients. The study was carried out in collaboration with the Cystic Fibrosis Foundation Therapeutics, Inc. (CFFT), a nonprofit subsidiary of the Cystic Fibrosis Foundation, and CF researchers from the University of Pittsburgh funded by CFFT.
The identification of the cystic fibrosis transmembrane conductance regulator (CFTR) gene has lead to many genetic and molecular biology studies which have aided our understanding of the effects of gene mutations on the CFTR protein. Yet, how the CFTR defects lead to downstream biological changes and the resulting CF clinical symptoms remains unclear. In the JBC report, the investigators used metabolomics to gain an initial understanding of the global biochemical alterations in CF primary lung epithelial cells. The authors measured changes in glucose, sorbitol and pentose phosphate metabolism that could serve to exacerbate CF-associated oxidative stress as well as other metabolic changes that suggest altered purinergic signaling.