UCP2 Expression Is Increased in Pancreas From Brain-Dead Donors and Involved in Cytokine-Induced [beta] Cells Apoptosis.

Background: Systemic inflammation associated with brain death (BD) decreases islet yield and quality, negatively affecting outcomes of human islet transplantation. A recent study from our group showed an increased expression of uncoupling protein-2 (UCP2) in pancreas from rats with BD as compared with controls. UCP2 is located in the mitochondrial inner membrane and regulates production of reactive oxygen species and glucose-stimulated insulin secretion. It has been suggested that UCP2 also plays a role in [beta] cell apoptosis, but these findings remain controversial. Methods: We have presently performed a case-control study to assess UCP2 expression in pancreas from BD donors (cases) and subjects who underwent pancreatectomy (controls). We next investigated the role of Ucp2 in cytokine-induced apoptosis of rat insulin-producing INS-1E cells. Results: UCP2 gene expression was higher in pancreas from BD donors compared with controls (1.73 +/- 0.93 vs 0.75 +/- 0.66; fold change, P

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