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

• Published in: FEBS letters Vol. 584; no. 1; pp. 81 - 85
• Main Authors: Josefsen, Knud, Lee, Ying C., Thams, Peter, Efendic, Suad, Nielsen, Jens H.
• Format: Journal Article
• Language: English
• Published: England Elsevier B.V 04-01-2010
• Subjects: Adaptor Proteins, Signal Transducing; AKAP 18 transcript variant; Animals; Carrier Proteins - biosynthesis; Carrier Proteins - genetics; Cell Line, Tumor; Expression regulation; Glucose - metabolism; Glucose - pharmacology; Growth Hormone - pharmacology; INS-1E cell; Insulin - metabolism; Insulin Secretion; Insulin-Secreting Cells - drug effects; Insulin-Secreting Cells - metabolism; Medicin och hälsovetenskap; Rats; siRNA silencing; Transcription, Genetic; INS-1E cell; siRNA silencing; AKAP 18 transcript variant; Expression regulation; Insulin secretion
• ISSN: 0014-5793; 1873-3468; 1873-3468
• DOI: 10.1016/j.febslet.2009.10.086

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.