<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>The authors have derived a new <italic>β</italic>-cell line (βIns2<sup>−/−lacZ</sup>) from Ins2<sup>−/−</sup> mice that carry the <italic>lacZ</italic> reporter gene under control of the <italic>Ins2</italic> promoter. βIns2<sup>−/−lacZ</sup> cells stained positively using anti-insulin antibody, expressed <italic>β</italic>-cell–specific genes encoding the transcription factor PDX-1, glucokinase, and Glut-2, retained glucose-responsiveness for insulin secretion, and expressed the <italic>lacZ</italic> gene. Analysis of <italic>Ins1</italic> expression by reverse transcriptase–polymerase chain reaction (RT-PCR) showed that <italic>Ins1</italic> transcripts were significantly raised to compensate for the lack of <italic>Ins2</italic> transcripts in βIns2<sup>−/−lacZ</sup> cells, as compared to those found in <italic>β</italic>TC1 cells expressing both <italic>Ins1/Ins2</italic>. Thus, transcriptional up-regulation of the remaining functional insulin gene in Ins2<sup>−/−</sup> mice could potentially contribute to the <italic>β</italic>-cell adaptation exhibited by these mutants, in addition to the increase in <italic>β</italic>-cell mass that we previously reported.We have also shown that <italic>lacZ</italic> expression, as analyzed by determining <italic>β</italic>-galactosidase activity, was up-regulated by incubating βIns2<sup>−/−lacZ</sup> cells with GLP-1 and/or IBMX, 2 known stimulators of insulin gene expression. These cells thus represent a new tool for testing of molecules capable of stimulating <italic>Ins2</italic> promoter activity</p>
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Int J Exp Diabesity Res. 2003; 4(1):7-12