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Diabetes 54:2132-2142, 2005
© 2005 by the American Diabetes Association, Inc.

Redox Control of Exocytosis

Regulatory Role of NADPH, Thioredoxin, and Glutaredoxin

Rosita Ivarsson1, Roel Quintens2, Sandra Dejonghe3, Katsura Tsukamoto2, Peter in ’t Veld3, Erik Renström1, and Frans C. Schuit2

1 Department of Physiological Sciences, Lund University, Lund, Sweden
2 Department of Molecular Cell Biology, Gene Expression Unit, Katholieke Universiteit Leuven, Leuven, Belgium
3 Diabetes Research Center, Vrije Universiteit Brussels, Brussels, Belgium

Cellular redox state is an important metabolic variable, influencing many aspects of cell function like growth, apoptosis, and reductive biosynthesis. In this report, we identify NADPH as a candidate signaling molecule for exocytosis in neuroendocrine cells. In pancreatic ß-cells, glucose acutely raised the NADPH-to-NADP+ ratio and stimulated insulin release in parallel. Furthermore, intracellular addition of NADPH directly stimulated exocytosis of insulin granules. Effects of NADPH on exocytosis are proposed to be mediated by the redox proteins glutaredoxin (GRX) and thioredoxin (TRX) on the basis of the following evidence: 1) Expression of GRX mRNA is very high in ß-cells compared with other studied tissues, and GRX protein expression is high in islets and in brain; 2) GRX and TRX are localized in distinct microdomains in the cytosol of ß-cells; and 3) microinjection of recombinant GRX potentiated effects of NADPH on exocytosis, whereas TRX antagonized the NADPH effect. We propose that the NADPH/GRX/TRX redox regulation mediates a novel signaling pathway of nutrient-induced insulin secretion.

Address correspondence and reprint requests to Frans C. Schuit, Department of Molecular Cell Biology, Katholieke Universiteit Leuven, Herestraat 49, B-3000 Leuven, Belgium. E-mail: frans.schuit{at}med.kuleuven.ac.be or Erik Renström, Department of Physiological Sciences, Lund University, BMC B11, SE 22184 Lund, Sweden. E-mail: erik.renstrom{at}mphy.lu.se

Abbreviations: GRX, glutaredoxin; KATP channel, ATP-sensitive K+ channel; TRX, thioredoxin


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