Diabetes is a disease, characterized by the failure of the body to make or use insulin, resulting in improper glucose homeostasis. Insulin, a hormone that regulates glucose uptake, metabolism and storage in various cells of the body, is produced by pancreatic beta cells, located in the islets of Langerhans. Diabetes can be characterized as one of two types, type 1, also known as autoimmune or insulin-dependent diabetes, and type 2, also known as adult onset, or insulin resistance.
Type 1, or insulin-dependent diabetes mellitus (IDDM) is characterized by the selective destruction of insulin-secreting pancreatic beta cells. Proinflammatory cytokines, such as interleukin (IL)-1 beta and interferon (IFN)-gamma, are believed to participate in the death of beta cells during the development of autoimmune diabetes. In the first part of this application, the activation of endoplasmic reticulum stress by salicylates will be examined as a mechanism by which to attenuate cytokine signaling, and consequently, cytokine-mediated beta-cell damage.
Type 2 diabetes is characterized by the inability of the body to either produce enough, or respond to the hormone insulin, also known as insulin resistance. Many factors, such as blood glucose levels, hormones and autonomic innervations can all modulate islet secretory function. In the second part of this application, the regulation of pancreatic function by a novel peptide hormone, neuronostatin, which shares the same precursor hormone as somatostatin, will be examined. In addition, the signaling cascades activated by, and potential receptors for, neuronostatin will be examined using basic biochemical and molecular biology techniques.
|Advisor:||Samson, Willis K.|
|School:||Saint Louis University|
|School Location:||United States -- Missouri|
|Source:||DAI-B 71/04, Dissertation Abstracts International|
|Subjects:||Molecular biology, Biochemistry, Physiology|
|Keywords:||Diabetes, Insulin, Islet cells, Neuronostatin, Pancreatic beta cells|
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