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Proton NMR spectroscopy shows lipids accumulate in skeletal muscle in response to burn trauma-induced apoptosis

Loukas G. Astrakas^*,, Igor Goljer, Shingo Yasuhara, Katie E. Padfield^*, Qunhao Zhang^*, Suresh Gopalan^*, Michael N. Mindrinos, George Dai, Yong-Ming Yu^*, J. A. Jeevendra Martyn, Ronald G. Tompkins^*, Laurence G. Rahme^* and A. Aria Tzika^*,,1

^* Department of Surgery, Massachusetts General Hospital, Shriners Burns Institute and Harvard Medical School, Boston, Massachusetts, USA;
Athinoula A. Martinos Center of Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Boston, Massachusetts, USA;
Varian NMR Systems, Columbia, Maryland, USA;
Departments of Anesthesiology and Critical Care, Massachusetts General Hospital, Shriners Burns Institute and Harvard Medical School, Massachusetts; and
Department of Biochemistry, Stanford University School of Medicine, Stanford, California, USA

¹ Correspondence: NMR Surgical Laboratory, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, 51 Blossom St., Room 261, Boston, MA 02114, USA. E-mail:atzika{at}partners.org

Burn trauma triggers hypermetabolism and muscle wasting via increased cellular protein degradation and apoptosis. Proton nuclear magnetic resonance (¹H NMR) spectroscopy can detect mobile lipids in vivo. To examine the local effects of burn in skeletal muscle, we performed in vivo ¹H NMR on mice 3 days after burn trauma; and ex vivo, high-resolution, magic angle spinning ¹H NMR on intact excised mouse muscle samples before and 1 and 3 days after burn. These samples were then analyzed for apoptotic nuclei using a terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay. To confirm our NMR and cell biology results, we used transcriptome analysis to demonstrate that burn trauma alters the expression of genes involved in lipid metabolism and apoptosis. Our results demonstrate that burn injury results in a localized intramyocellular lipid accumulation, which in turn is accompanied by burn-induced apoptosis and mitochondrial dysfunction, as seen by the up-regulation of apoptotic genes and down-regulation of genes that encode lipid oxidation and the peroxisomal proliferator activator receptor coactivator PGC-1ß. Moreover, the increased levels of bisallylic methylene fatty acyl protons (2.8 ppm) and vinyl protons (5.4 ppm), in conjunction with the TUNEL assay results, further suggest that burn trauma results in apoptosis. Together, our results provide new insight into the local physiological changes that occur in skeletal muscle after severe burn trauma.—Astrakas, L. G., Goljer, I., Yasuhara, S., Padfield, K. E., Zhang, Q., Gopalan, S., Mindrinos, M. N., Dai, G., Yu, Y.-M., Jeevendra Martyn, J. A., Tompkins, R. G., Rahme, L. G., Tzika, A. A. Proton NMR spectroscopy shows lipids accumulate in skeletal muscle in response to burn trauma induced apoptosis.

Key Words: magnetic resonance spectroscopy • high-resolution magic angle spinning skeletal muscle • burn trauma • mitochondria • intramyocellular lipids

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				M. G. Cree and R. R. Wolfe Postburn trauma insulin resistance and fat metabolism Am J Physiol Endocrinol Metab, January 1, 2008; 294(1): E1 - E9. [Abstract] [Full Text] [PDF]