期刊
ISLETS
卷 4, 期 3, 页码 199-206出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/isl.19982
关键词
beta-cells; insulin; glucose tolerance; transcription factor; Islet-1
资金
- [NIH-DK078606]
- [JDRF-2-2007-730]
A decrease in the expression of Islet-1 (Isl-1), an islet transcription factor, has been reported in several physiological settings of reduced beta-cell function. Here, we investigate whether an increased level of Isl-1 in islet cells can enhance beta-cell function and/or mass. We demonstrate that transgenic mice with Isl-1 overexpression display improved glucose tolerance and enhanced insulin secretion without significant changes in beta-cell mass. From our microarray study, we identify approximately 135 differentially expressed genes in the islets of Isl-1 overexpressing mice that have been implicated to function in numerous biological processes including protein trafficking, metabolism and differentiation. Using real-time PCR we have confirmed upregulation of Caps2, Sec14l4, Slc2a10, P2rx7, Afamin and Neurogenin 3 that may in part mediate the observed improved insulin secretion in Isl-1 overexpressing mice. These findings show for the first time that Isl-1 is a key factor in regulating adult beta-cell function in vivo, and suggest that Isl-1 elevation could be beneficial to improve glucose homeostasis.
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