Nikolaos Psychogios1,2, Yiorgos Apidianakis3,
Valeria Righi1,2, Hazel Szeto4, Ronald G. Tompkins,
Laurence G. Rahme3, Aria A. Tzika1,2
1NMR Surgical Laboratory,
Department of Surgery, Massachusetts General Hospital & Shriners Burn
Institute, Harvard Medical School, Boston, MA, United States; 2Department
of Radiology, Athinoula A. Martinos Center for Biomedical Imaging,
Massachusetts General Hospital, Charlestown, MA, United States; 3Molecular
Surgery Laboratory, Massachusetts General Hospital & Shriners Burn
Institute, Harvard Medical School, Boston, MA, United States; 4Department
of Pharmacology, Joan & Sanford I. Weill Medical College of Cornell
University, New Yor, Joan & Sanford I. Weill Medical College of Cornell
University, New York, NY, United States
Using high-resolution MAS proton NMR spectroscopy in vivo, we evaluated in a Drosophila melanogaster fly trauma model the effects of a novel (Szeto-Schiller) SS-31 peptide known to be targeted to mammalian mitochondria. In old flies, our results showed that SS-31 peptide reduced both insulin resistance and apoptosis biomarkers. We thus provide evidence for the hypothesis that trauma in aging is linked to insulin signaling and thus mitochondrial dysfunction. Our approach advances the development of novel in vivo non-destructive research approaches in the model host D. melanogaster, and suggests biomarkers for investigation of biomedical paradigms that may contribute to the development of novel therapeutics.