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.

The major protein disulfide isomerase family member, PDIA1, is essential in beta cells of mice fed a high-fat diet to maintain glucose homeostasis, proinsulin maturation and organelle integrity.

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.

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.

Thioredoxin-Interacting Protein binds directly to fructose transporters and regulates fructose metabolism, both acutely and chronically.

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.