AKAP 18 α and γ have opposing effects on insulin release in INS-1E cells

Josefsen, Knud; Lee, Ying C.; Thams, Peter; Efendic, Suad; Nielsen, Jens H.

doi:10.1016/j.febslet.2009.10.086

« Previous Next »FEBS Letters
Volume 584, Issue 1 , Pages 81-85, 4 January 2010

AKAP 18 α and γ have opposing effects on insulin release in INS-1E cells

Edited by Laszlo Nagy

Knud Josefsen
- Bartholin Institute, Rigshospitalet, Copenhagen, Denmark
- Corresponding author. Bartholin Institute, Rigshospitalet, Københavns Biocenter, Ole Maaløes Vej 5, 2200 Copenhagen N, Denmark. Fax: +45 3545 6088.
- K.J. and Y.C.L. contributed equally to this work.
Ying C. Lee
- Department of Biomedical Sciences, Panum Institute, University of Copenhagen, Copenhagen, Denmark
- K.J. and Y.C.L. contributed equally to this work.
Peter Thams
- Department of Biomedical Sciences, Panum Institute, University of Copenhagen, Copenhagen, Denmark
Suad Efendic
- Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden
Jens H. Nielsen
- Department of Biomedical Sciences, Panum Institute, University of Copenhagen, Copenhagen, Denmark

Received 13 August 2009; received in revised form 28 October 2009; accepted 31 October 2009. published online 06 November 2009.

Abstract

A-kinase anchoring proteins (AKAPs) are known to compartmentalise protein kinase(s) to discrete cellular locations. Here we show that silencing of AKAP 18 α or γ expression results in decreased or increased glucose-stimulated insulin secretion in INS-1E cells. Glucose stimulates AKAP 18 α and inhibits AKAP 18 γ mRNA expressions while palmitate markedly reduces AKAP 18 α expression. Human growth hormone (GH) stimulates AKAP 18 α expression and attenuates palmitate-induced suppression of AKAP 18 α mRNA level. The roles of AKAP 18 α and γ in mediating insulin release are consistent with their respective regulations by glucose.

Keywords: AKAP 18 transcript variant, INS-1E cell, siRNA silencing, Insulin secretion, Expression regulation