John A. Corbett, PhD
Chairman and Professor
John A. Corbett received his Bachelor of Science degree in Chemistry from Saint Norbert in 1985 and his Doctorate in Biochemistry from Utah State University in 1990. He performed postdoctoral studies at Washington University School of Medicine in the Department of Pathology from 1990-94. In 1995 Dr. Corbett joined Saint Louis University as an Assistant Professor in Biochemistry and rose to the rank of Professor in 2005. In 2007, Dr. Corbett joined the University of Alabama at Birmingham as the Nancy R. and Eugene C. Gwaltney Family Endowed Chair in Juvenile Diabetes Research, Professor in Medicine, and Director of The Comprehensive Diabetes Center. Dr. Corbett joined the faculty of the Medical College of Wisconsin in 2010.
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Our laboratory is focused on determining the factors that influence the function and survival of pancreatic beta cells in the context of both type 1 and type 2 diabetes mellitus. We currently have three ongoing research programs. The broad goals of the first project are to elucidate the cellular mechanisms that are responsible for pancreatic beta cell death and to identify mechanisms by which beta cells protect themselves against cytokine- and free radical-mediated damage. Nitric oxide, the primary mediator of the inhibitory actions of interleukin-1 (IL-1) and interferon-g (IFN-g) on beta cell function, also activates a "recovery" pathway that protects beta cells from cytokine-mediated damage. It is the delicate balance between the toxic and protective actions of nitric oxide that ultimately determine the susceptibility of beta cells to cytokine-mediated damage. The broad goals of the second research program are to elucidate the biochemical mechanisms by which virus infection regulates macrophage activation and to determine the virus-activated pathways that contribute to the loss of beta cell function and viability. Using a virus known to induce diabetes in susceptible mice, we have recently identified three novel antiviral signaling pathways that regulate inflammatory gene expression in macrophages. The third major research program tests the hypotheses that increased levels of random mutations in beta cell mtDNA lead to the loss of beta cell function and the inability to maintain normal glycemic control, and increase the vulnerability of beta cells to a secondary stress such as insulin resistance induced by a high fat diet. To examine these hypotheses, transgenic (Tg) mice that accumulate mtDNA mutations in beta cells due to the expression of an error-prone mtDNA polymerase under control of the rat insulin promoter have been generated.