During aging, the pancreatic endocrine islets undergo chronic inflammation, which is associated with a reduced capacity for self-renewal of the insulin-producing beta-cells in zebrafish.

A previously undescribed protein produced by certain resident intestinal bacteria induces zebrafish pancreatic beta cell expansion.

Ribosome profiling and loss-of-function during human ESC pancreatic differentiation reveal abundant lncRNA translation and an essential role for translated LINC00261 in beta cell differentiation, likely through a trans-regulatory, microprotein-independent mechanism.

Analysis of epigenome maps from human pancreatic progenitors and functional validation in zebrafish identify LAMA1 and CRB2 as type 2 diabetes risk-associated genes with roles in pancreatic development.

Pancreatic α and β cells have different cell autonomous signatures; this explains why α but not β cells can clear infections by potentially diabetogenic viruses.

The regulation of beta cell induction requires combined hierarchical and combinatorial transcriptional networks.

Combinations of transcription factors can convert pancreatic acinar cells into endocrine α-, β- and δ-cells in vivo.

Combination of deep learning models trained on tissue-specific genomic data and fine-mapping approaches supports efforts to identify causal variants and mechanisms at GWAS loci.

Class 1 histone deacetylase (HDAC) inhibitor MS-275 enhances the efficacy of glucagon-like peptide 1 receptor (GLP-1R) therapy for glycemic control and reduction of obesity.

mTORC1 inhibition by perinatal ER stress induces beta-cell growth arrest with subsequent development of diabetes.