Eugenol has the ability to improve the type 1 diabetes mellitus through NRF2-mediated oxidative stress pathway.

Deep immunophenotyping characterizes the genetic factors influencing immune functionality in patients with type 1 diabetes.

Alteration of host gut microbiota by antibiotic exposure in early life remodeled host intestinal immune development and metabolism and enhanced the induction of type 1 diabetes in genetically predisposed animals.

A novel process by which counter-regulatory glucagon release is regulated in both mouse and human.

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.

A short treatment of the NOD mouse model of type-1 diabetes with I-BET151, a small molecule bromodomain blocker, provides long-term protection from disease by inducing macrophages to adapt an anti-inflammatory tenor whilst promoting islet β cell regeneration.

Insulin secreting cells harbor distinct subpopulations of insulin granules and loss of one or the other correlates strongly with secretory deficiencies characterizing type-1 or type-2 diabetes.

Loss of mature β cell identity in diabetes can be prevented and rescued by small molecule inhibitors of the TGFβ pathway.

Contrary to previous reports, a complete absence of glucagon signaling is not sufficient to prevent diabetes after near-total β-cell loss.