Gut Ischemia/Reperfusion Injury: Modulation by Nutrients

Summary

Principal Investigator: Rosemary Kozar
Abstract: DESCRIPTION (provided by applicant): Candidate: Dr. Kozar is a new faculty member at the University of Texas-Houston Medical School (UTHMS), where she is a member of the Department of Surgery. She first acquired basic research skills as a NRSA Fellow while obtaining her PhD at Baylor College of Medicine. Following completion of her general surgery training, the candidate accepted a faculty position in Trauma and Critical Care at MCP-Hahnemann University School of Medicine under the direction of Dr. Joel Rosyln. During this time she began to develop research experience in the field of Trauma and Critical Care by investigating the activity of antioxidant enzymes in an acute lung injury model, funded by a private grant for which she was the principal investigator. Since becoming a faculty member in the Department of Surgery at UTHMS she has become very active in the NIGMS-sponsored Trauma Research Center, focusing on the role of the gut in multiple organ failure. A Career Development Award, in conjunction with the support of two highly respected mentors, would enhance the acquisition of the necessary skills and talents crucial to becoming a future independent investigator. Research: The proposed research project is an extension of the Trauma Research Center?s interest in the link between gut dysfunction and multiple organ failure. As proposed in this application, the candidate wilt test the hypothesis that specific enterat nutrients during gut ischemia/reperfusion impair gut function and enhance gut injury. The goal of the proposed project is to understand how enterat nutrients during times of metabolic stress can be detrimental to gut function. The results obtained will facilitate a better understanding of postinjury gut dysfunction and aide in future strategies to achieve enteral tolerance in patients at high risk for multiple organ failure. Environment: The UTHMS in the center of the Texas Medical Center is comprised of 42 member institutions dedicated not only to outstanding patient care but also to the highest standards and quality of research. As part of the Department of Surgery's Trauma Research Center, the candidate has the guidance and support of numerous researchers in the Department of Surgery as well as in Integrative Biology, and Medicine. The sponsors are an integral part of this arrangement and are especially suited to ensure success of the proposed project.
Funding Period: 2002-08-10 - 2007-10-31
more information: NIH RePORT

Top Publications

  1. ncbi Immune-enhancing enteral nutrients differentially modulate the early proinflammatory transcription factors mediating gut ischemia/reperfusion
    Norio Sato
    Department of Surgery, University of Texas Houston, Houston, Texas 77030, USA
    J Trauma 58:455-61; discussion 461. 2005
  2. ncbi Differential induction of PPAR-gamma by luminal glutamine and iNOS by luminal arginine in the rodent postischemic small bowel
    N Sato
    Department of Surgery, Houston School of Medicine, University of Texas, 77030, USA
    Am J Physiol Gastrointest Liver Physiol 290:G616-23. 2006

Detail Information

Publications2

  1. ncbi Immune-enhancing enteral nutrients differentially modulate the early proinflammatory transcription factors mediating gut ischemia/reperfusion
    Norio Sato
    Department of Surgery, University of Texas Houston, Houston, Texas 77030, USA
    J Trauma 58:455-61; discussion 461. 2005
    ..We now hypothesize that arginine and glutamine differentially modulate the early proinflammatory transcription factors activated by gut I/R...
  2. ncbi Differential induction of PPAR-gamma by luminal glutamine and iNOS by luminal arginine in the rodent postischemic small bowel
    N Sato
    Department of Surgery, Houston School of Medicine, University of Texas, 77030, USA
    Am J Physiol Gastrointest Liver Physiol 290:G616-23. 2006
    ..The induction of PPAR-gamma by luminal glutamine is a novel protective mechanism, whereas luminal arginine appears harmful to the postischemic gut due to enhanced expression of iNOS...