Graduate ThesisMy thesis focuses on orphan nuclear receptor Nr4a1 deletion combined with maternal overnutriton and how this genetic alteration and diet affects the onset of diabetes in offspring. It has been suggested that early lifestyle factors, such as diet, play a significant role in the maturation of beta-cells and the onset of type 2 diabetes. Researchers have studied how maternal diet can play a role in early development of diabetes in offspring. The mechanism by which early onset of diabetes develops may be related to altered beta-cell development and beta-cell mitochondrial dysfunction. We understand the Nr4a1 is involved in beta-cell development and therefore the purpose of this project is to determine if Nr4a1 is necessary for development of beta-cell mass and to determine how maternal overnutrition affects this mechanism. Attached is a copy of my thesis prospectus which explains in detail the methods for my project.
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Presentations |
The role of HDAC1 in increasing function beta-cell mass and protecting against apoptosis. Environmental Biology, San Diego. April 2016.
The role of CDK5r1 in increasing functional beta-cell mass. Utah Conference of Undergraduate Research, Dixie State University. February 2015. |
Publications |
Draney C, Hobson AE, Grocer SG, Jack BO, Tessem JS. Cdk5r1 overexpression induces primary beta-cell proliferation. J Diabetes Res. 2016:1-15.
Hobson A, Draney C, Stratford A, Becker TC, Lu D, Arlotto M, Tessem JS. Aurora Kinase A is critical for the Nkx6.1 mediated beta-cell proliferation pathway. Islets. 2015;7(1). |