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Impact of a UCP2 Inhibitor on Amylin in Pancreatic beta cells

Faculty #25
Discipline: Chemistry & Chemical Sciences
Subcategory: STEM Research

Tameka Clemons - Spelman College


Uncoupling protein 2 (UCP2) has been shown to be present on pancreatic alpha and beta cells. A function of UCP2 on pancreatic beta cells is to serve as a protector, which has been demonstrated by increasing UCP2 and seeing a decrease in cytokine-induced production of ROS in pancreatic beta cells. Pancreatic beta-cells are well known for insulin secretion. However, amylin is co-secreted alongside insulin and is responsible for sending satiety signals to the brain. The role of amylin in metabolism is suggested to be significant because of its ability to contribute to glucose homeostasis. Likewise, UCP2 contributes to metabolism traditionally by impacting ATP release during cellular respiration. However, a new role for UCP2 that is specific to cell signaling on pancreatic beta cells may involve UCP2 influencing amylin’s function. The objective of this study is to analyze the relationship between UCP2 and amylin. This analysis includes employing methods such as ELISA in order to analyze the activity levels of amylin, as well as Western blot analysis in order to understand if UCP2 influences change in amylin protein expression. An understanding of the activity level and protein expression level of amylin when UCP2 has been inhibited will elucidate whether the two proteins communicate with one another. The experiments conducted center around the hypothesis that inhibiting UCP2 increases the activity level and protein expression level of amylin. The studies were conducted in pancreatic beta cells stimulated with either 11mM or 30 mM glucose and compared to control.

Funder Acknowledgement(s): National Science Foundation

Faculty Advisor: None Listed,

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This material is based upon work supported by the National Science Foundation (NSF) under Grant No. DUE-1930047. Any opinions, findings, interpretations, conclusions or recommendations expressed in this material are those of its authors and do not represent the views of the AAAS Board of Directors, the Council of AAAS, AAAS’ membership or the National Science Foundation.

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