Osteoblast glucose metabolism is impaired in a mouse model for type II diabetes and can be boosted pharmacologically or genetically to alleviate diabetic osteopenia.

Atomic structures of hIAPP fibrillar segments, determined using the cryo electron microscopy method MicroED, reveal that strong, stable intermolecular interactions are important features of cytotoxic amyloid proteins.

Patients with Type 2 diabetes show patterns of neurodegeneration consistent with accelerated brain aging, including impaired cognition and loss of brain volume, which are more severe in those with increased disease duration.

We are writing to comment on the study by Meyer et al., 2016 on disease-ameliorating autoantibodies.

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.

PDZ-RhoGEF controls adipose tissue abundance and whole body metabolism.

SWELL1 is required for basal, stretch, and flow-mediated endothelial AKT-eNOS signaling in vitro and protects against angiotensin-induced hypertension and diabetes-associated vascular dysfunction in vivo.

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

An integrative approach, combining genetic mouse and large-scale human genetics studies, was used to reveal a novel role for the Bcl-2 protein Bid in maintenance of mitochondrial function that alters susceptibility to myocardial infarction.

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