<i><span style="font-family:Verdana;"><i>Diabetes mellitus</i></span><i></i></i><span style="font-family:Verdana;"> is a chronic disease that i...<i><span style="font-family:Verdana;"><i>Diabetes mellitus</i></span><i></i></i><span style="font-family:Verdana;"> is a chronic disease that impacts the homeostasis of blood sugar levels caused by loss or defect of insulin-producing β-cells in the Islets of Langerhans.</span> <i><span color:black;"=""><span style="font-family:Verdana;"><i>Type 1 diabetes</i></span><i></i></span></i><span style="font-family:Verdana;"> (</span><i><i></i><i><span style="font-family:Verdana;">T1D</span></i><i></i></i><span style="font-family:Verdana;">)</span><i><span color:black;"=""> </span></i><span style="font-family:Verdana;">is caused by auto-immune mediated destruction of β-cells,</span> <span color:black;"=""><span style="font-family:Verdana;">whereas in </span><i><i></i><i><span style="font-family:Verdana;">T2D</span></i><i></i></i></span><span style="font-family:Verdana;">, insulin is produced but used inefficiently.</span><span color:black;"=""> <i><i></i><i><span style="font-family:Verdana;">T2D</span></i><i></i></i></span><span style="font-family:Verdana;"> accounts for 90% of people with diabetes worldwide (</span><i><i></i><i><span style="font-family:Verdana;">WHO</span></i><i></i></i><i> </i><span style="font-family:Verdana;">1999)</span><span style="font-family:Verdana;"> and is</span> <span style="font-family:Verdana;">the fastest increasing disease worldwide (</span><span style="font-family:Verdana;"><a href="https://diabetesatlas.org/en/" target="_blank">https://diabetesatlas.org/en/</a></span><span style="font-family:Verdana;">)</span><span color:black;"=""><span style="font-family:Verdana;">. For an improved understanding of the pathomechanism of diabetes, profound knowledge of pancreas organogenesis and the associated gene regulatory networks is required. Therefore, we dissected and profiled the pancreatic endodermal and non-endodermal compartment between the embryonic stages (E) 12.5 and E 15.5 when progenitor cells commit to their different pancreatic lineages. Our associated study mined the global mRNA expression profile to increase the understanding of the secondary transition, endodermal-non-endodermal tissue interaction, and diabetic-related gene regulation. Furthermore, we validated 635 regulated pancreatic genes using the publicly available </span><i><i></i><i><span style="font-family:Verdana;">GenePaint.org</span></i><span color:black;"=""><span style="font-family:Verdana;">, respective </span><i><span style="font-family:Verdana;">gp3.mpg.de</span></i></span><i></i></i></span><span style="font-family:Verdana;"> to evaluate genes associated with genetic variants in Single-nucleotide polymorphism (SNP) related to </span><i><i></i><i><span style="font-family:Verdana;">T2D</span></i><i></i></i><span style="font-family:Verdana;">.</span>展开更多
文摘<i><span style="font-family:Verdana;"><i>Diabetes mellitus</i></span><i></i></i><span style="font-family:Verdana;"> is a chronic disease that impacts the homeostasis of blood sugar levels caused by loss or defect of insulin-producing β-cells in the Islets of Langerhans.</span> <i><span color:black;"=""><span style="font-family:Verdana;"><i>Type 1 diabetes</i></span><i></i></span></i><span style="font-family:Verdana;"> (</span><i><i></i><i><span style="font-family:Verdana;">T1D</span></i><i></i></i><span style="font-family:Verdana;">)</span><i><span color:black;"=""> </span></i><span style="font-family:Verdana;">is caused by auto-immune mediated destruction of β-cells,</span> <span color:black;"=""><span style="font-family:Verdana;">whereas in </span><i><i></i><i><span style="font-family:Verdana;">T2D</span></i><i></i></i></span><span style="font-family:Verdana;">, insulin is produced but used inefficiently.</span><span color:black;"=""> <i><i></i><i><span style="font-family:Verdana;">T2D</span></i><i></i></i></span><span style="font-family:Verdana;"> accounts for 90% of people with diabetes worldwide (</span><i><i></i><i><span style="font-family:Verdana;">WHO</span></i><i></i></i><i> </i><span style="font-family:Verdana;">1999)</span><span style="font-family:Verdana;"> and is</span> <span style="font-family:Verdana;">the fastest increasing disease worldwide (</span><span style="font-family:Verdana;"><a href="https://diabetesatlas.org/en/" target="_blank">https://diabetesatlas.org/en/</a></span><span style="font-family:Verdana;">)</span><span color:black;"=""><span style="font-family:Verdana;">. For an improved understanding of the pathomechanism of diabetes, profound knowledge of pancreas organogenesis and the associated gene regulatory networks is required. Therefore, we dissected and profiled the pancreatic endodermal and non-endodermal compartment between the embryonic stages (E) 12.5 and E 15.5 when progenitor cells commit to their different pancreatic lineages. Our associated study mined the global mRNA expression profile to increase the understanding of the secondary transition, endodermal-non-endodermal tissue interaction, and diabetic-related gene regulation. Furthermore, we validated 635 regulated pancreatic genes using the publicly available </span><i><i></i><i><span style="font-family:Verdana;">GenePaint.org</span></i><span color:black;"=""><span style="font-family:Verdana;">, respective </span><i><span style="font-family:Verdana;">gp3.mpg.de</span></i></span><i></i></i></span><span style="font-family:Verdana;"> to evaluate genes associated with genetic variants in Single-nucleotide polymorphism (SNP) related to </span><i><i></i><i><span style="font-family:Verdana;">T2D</span></i><i></i></i><span style="font-family:Verdana;">.</span>