Kim Cheng, Kenneth Ho, Rebecca Stokes, Christopher Scott, Sue Mei Lau, Wayne J. Hawthorne, Philip J. O’Connell, Thomas Loudovaris, Thomas W. Kay, Rohit N. Kulkarni, Terumasa Okada, Xiaohui L. Wang, Sun Hee Yim, Yatrik Shah, Shane T. Grey, Andrew V. Biankin, James G. Kench, D. Ross Laybutt, Frank J. Gonzalez, C. Ronald Kahn, Jenny E. Gunton
Decreasing Hif1a by RNAi-impaired β cell function, gene expression, and ATP generation.
(A) RNAi decreased Hif1a mRNA. (B) Hif1a RNAi decreased GSIS in Min6 cells and caused a small decrease in KCl-stimulated insulin release. (C) Combination RNAi treatment caused slightly more severe impairment in insulin release. (D) Hif1a RNAi decreased expression of genes from the MODY family and (E) glucose-uptake and glycolysis genes. (F) Hif1a RNAi decreased basal and glucose-stimulated ATP concentrations. *P < 0.05, **P < 0.01, and ***P < 0.001.