The Burn Research Center at the Massachusetts General Hospital serves as the focal point within MGH for research on burn injury. As the first-in-the-nation P50 award (GM-21700) from the National Institute of General Medical Sciences, the MGH Center has sought to advance our understanding of post-burn injury alterations of metabolic patterns and nutritional requirements from immediately after injury through recovery. Since its first year of funding in 1974, the Center has successfully integrated basic laboratory observations and principles into the clinical setting and has fostered multidisciplinary interactions within the MGH research and clinical communities and beyond. In association with the Center, there has been a NIGMS T32 Burn Research Training Grant (GM-07035) funded since 1975, which currently has six positions available for postdoctoral training in burn and trauma research.

Through the years, the studies from the Center grant have contributed novel insights into our understanding of the metabolic dysregulation that occurs in response to burn injury, in large part from the interactive and synergistic nature of the projects and cores. The Center has recruited and retained a truly outstanding multidisciplinary investigative team of scientists and clinicians that is collectively much stronger than the sum of its parts.

The Projects and Cores

We have organized our research program into four projects that focus on the interrelated aspects of specific amino acid, glucose, and fatty acid metabolism and more recently, muscle protein catabolism and apoptosis. Within our ongoing research over the past thirty years, our evaluation of the roles of amino acids in the post-injury state have identified glutamine, arginine, and the sulfur-containing amino acids (methionine and cysteine) as critical in the regulation of nitrogen and energy metabolism. The projects can be summarized in the following statements.

1. Alterations in the regulation of energy and amino acid metabolism are of etiological importance in morbidity and mortality of burn patients. (Amino Acid Interrelations and Metabolism - Project 1)



2. Regional quantitative measurements of metabolism after burn injury can be undertaken using the metabolic imaging techniques of PET. (Tissue-Specific Metabolic Response to Injury - Project 2)



3. Altered IRS-1 function and/or degradation may contribute to the metabolic etiology of impaired glucose tolerance and the insulin resistance associated with severe burn injury. (Molecular Mechanisms of Burn-Induced Insulin Resistance - Project 3)



4. Decreased Akt/PKB activity and insulin resistance may be responsible for loss of muscle mass by apoptosis following severe burn injury. (Muscle Wasting in Burns: the Pivotal Role of Akt/PKB - Project 4)