Endocrine Abstracts

Most genetic mechanisms that are currently known to underlie developmental processes and human diseases are based on the analysis of a very small portion of the genome that encodes for protein-coding sequences. Novel sequence-based technologies, however, have recently disclosed that a major portion of the noncoding genome contains functional regulatory elements. It is thus reasonable to presume that the analysis of such elements can shed new light into developmental and cellul...

Understanding how fate choices are made by multipotent progenitors during pancreas development is valuable information in the quest for regenerative medicine and cell therapy to treat diabetes mellitus. Pancreatic differentiation is well defined and understood in rodents however, human data are comparably scarce. Specifically, when human pancreatic progenitors are multipotent is unknown as are the epigenetic changes that these cells undergo during their differentiation to beta...

Genome-wide association studies have identified nearly 250 loci carrying genetic variants associated with type 2 diabetes (T2D) susceptibility, which are often located within pancreatic islet transcriptional enhancers. Due to the complex nature of transcriptional enhancers, assigning risk variants to true disease susceptibility effector genes has remained a challenge. In this study, we applied promoter capture Hi-C to create a genome-wide map of promoter-enhancer interactions ...

Introduction: Pancreatic β-cells control glucose homeostasis by secreting insulin in response to high glucose. MiRNAs regulate β-cell function and contribute to β-cell failure in type 2 diabetes. MiR-184 regulates β-cell compensatory expansion during pregnancy and obesity and its expression is reduced by glucose through unknown mechanisms. AMPK is a suggested target of antidiabetic drugs and an important energy sensor. Its β-cell-selective inactivation...