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Originally published In Press as doi:10.1074/jbc.M205401200 on August 6, 2002

J. Biol. Chem., Vol. 277, Issue 40, 37446-37455, October 4, 2002
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Important Role of Phosphodiesterase 3B for the Stimulatory Action of cAMP on Pancreatic beta -Cell Exocytosis and Release of Insulin*

Linda HärndahlDagger §, Xing-Jun Jing, Rosita Ivarsson, Eva DegermanDagger , Bo Ahrén||, Vincent C. Manganiello**, Erik Renström, and Lena Stenson HolstDagger

From the Dagger  Department of Cell and Molecular Biology, Biomedical Centre, C11, Lund University, SE-221 84 Lund, Sweden, the ** Pulmonary/Critical-Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, the || Department of Medicine, Biomedical Centre, B11, Lund University, SE-221 84 Lund, Sweden, and the  Department of Physiological Sciences, Biomedical Centre, F11, Lund University, SE-221 84 Lund, Sweden

Cyclic AMP potentiates glucose-stimulated insulin release and mediates the stimulatory effects of hormones such as glucagon-like peptide 1 (GLP-1) on pancreatic beta -cells. By inhibition of cAMP-degrading phosphodiesterase (PDE) and, in particular, selective inhibition of PDE3 activity, stimulatory effects on insulin secretion have been observed. Molecular and functional information on beta -cell PDE3 is, however, scarce. To provide such information, we have studied the specific effects of the PDE3B isoform by adenovirus-mediated overexpression. In rat islets and rat insulinoma cells, approximate 10-fold overexpression of PDE3B was accompanied by a 6-8-fold increase in membrane-associated PDE3B activity. The cAMP concentration was significantly lowered in transduced cells (INS-1(832/13)), and insulin secretion in response to stimulation with high glucose (11.1 mM) was reduced by 40% (islets) and 50% (INS-1). Further, the ability of GLP-1 (100 nM) to augment glucose-stimulated insulin secretion was inhibited by ~30% (islets) and 70% (INS-1). Accordingly, when stimulating with cAMP, a substantial decrease (65%) in exocytotic capacity was demonstrated in patch-clamped single beta -cells. In untransduced insulinoma cells, application of the PDE3-selective inhibitor OPC3911 (10 µM) was shown to increase glucose-stimulated insulin release as well as cAMP-enhanced exocytosis. The findings suggest a significant role of PDE3B as an important regulator of insulin secretory processes.

* This work was supported by Swedish Research Council Grants 3362 (to E. D.), 6834 (to B. A.), and 12234 (to E. R.); a Center of Excellence grant from the Juvenile Diabetes Foundation and the Knut and Alice Wallenberg Foundation, Sweden; the Swedish Society of Medicine; the Swedish Diabetes Association; the A. Påhlsson, M. Bergwall, F. and I. Thuring, and Crafoord Foundations, Sweden; and by Novo Nordisk, Denmark.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ To whom correspondence should be addressed. Tel.: 46-46-222-85-87; Fax: 46-46-222-40-22; E-mail: Linda.Harndahl@medkem.lu.se.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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