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.
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.
Systemic inflammation is greater in individuals with concurrent TB and diabetes than in euglycemic individuals with TB, and this disparity persists through the full 6-month course of anti-tubercular treatment.
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.
Integrating gene expression with genetic association data provided insights into the functional relevance of genetic risk for a complex disease, thus implicating folliculin as a putative diabetic retinopathy susceptibility gene.
Text mining of complete EHRs for 14,017 diabetes patients and subsequent clustering led to phenotypically deep clusters, showing distinct glycemic profiles, comorbidities, and SNP association patterns.