Human pancreatic islet high-resolution chromatin state maps generated from DNA methylation, open chromatin and ChIP-seq mark data facilitate the characterisation of regulatory mechanisms at type 2 diabetes genome-wide association study loci.

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.

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.

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.

Live human pancreatic α-cells can be purified effectively using zinc-based reaction probe diacetylated Zinpyr1 and cultured as pseudoislets without losing their viability and function.

Cells from the human pancreatic duct can be grown in culture and triggered to become insulin-producing cells, which could potentially be transplanted into patients with diabetes.

Synchronized β cell response to glucose is lost concomitant with loss of islet architecture in Robo-deficient islets of Langerhans in vivo.

The signaling requirements to decouple proliferation of pancreatic progenitors from differentiation were elucidated and employed for the reproducible expansion, under GMP-compliant conditions, of pancreatic progenitors derived from different human pluripotent stem cell lines.

Proinsulin misfolding, an established cause of diabetes in patients with INS gene mutations, is now observed in normal human pancreatic islets, and rodents with genetic predisposition to type 2 diabetes.

Analysis of islet calcium oscillation responses will provide the field with a resource with which to determine the strain of interest for their specific islet biology questions.