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desumoylation controls insulin exocytosis in response to metabolic signalsdesumoylation控制胰岛素胞外分泌针对代谢信号
Biomolecules 2012, 2, 269-281; doi:10.3390/biom2020269 OPEN ACCESS biomolecules ISSN 2218-273X /journal/biomolecules/ Article DeSUMOylation Controls Insulin Exocytosis in Response to Metabolic Signals Elisa Vergari 1, Gregory Plummer 2, Xiaoqing Dai 2 and Patrick E. MacDonald 2,* 1 BIOTEC TU-Dresden, Tatzberg 47/49 01307, Germany; E-Mail: elisa.vergari@ocdem.ox.ac.uk (E.V.) 2 Alberta Diabetes Institute and Department of Pharmacology, University of Alberta, Edmonton T6G 2E1, AB, Canada; E-Mails: gplummer@ualberta.ca (G.P.); xdai@ualberta.ca (X.Q.D.) * Author to whom correspondence should be addressed; E-Mail: pmacdonald@ualberta.ca; Tel.: +1-780-492-8063. Received: 3 May 2012; in revised form: 14 May 2012 / Accepted: 16 May 2012 / Published: 24 May 2012 Abstract: The secretion of insulin by pancreatic islet β-cells plays a pivotal role in glucose homeostasis and diabetes. Recent work suggests an important role for SUMOylation in the control of insulin secretion from β-cells. In this paper we discuss mechanisms whereby (de)SUMOylation may control insulin release by modulating β-cell function at one or more key points; and particularly through the acute and reversible regulation of the exocytotic machinery. Furthermore, we postulate that the SUMO-specific protease SENP1 is an important mediator of insulin exocytosis in response to NADPH, a metabolic secretory signal and major determinant of β-cell redox state. Dialysis of mouse β-cells with NADPH efficiently amplifies β-cell exocytosis ev
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