Gene Expression Profiling of the Mouse Pancreas during the Secondary Transition in the Organogenesis of the Pancreatic Gland*

Diabetes mellitus 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. Type 1 diabetes (T1D) is caused by auto-immune mediated destruction of β-cells, whereas in T2D, insulin is produced but used inefficiently. T2D accounts for 90% of people with diabetes worldwide (WHO 1999) and is the fastest increasing disease worldwide (https://diabetesatlas.org/en/). 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 GenePaint.org, respective gp3.mpg.de to evaluate genes associated with genetic variants in Single-nucleotide polymorphism (SNP) related to T2D.