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3D light-sheet imaging identifies the location and metabolic sensitivity of β-cell subpopulations that lead and coordinate islet Ca²⁺ oscillations.

Primary cilia on endothelial cells are required for VEGF-A/ VEGFR2-dependent signaling, islet vascularization and, consequently, nutrient delivery and insulin disposal.

A genetically sensitized drug screen identifies a circadian diabetes target and establishes a novel discovery pathway to treat β-cell failure.

ATF4, the master regulator of transcription during the Integrated Stress Response (ISR), causes global changes in cysteine sulfhydration of proteins and this event causes cellular metabolic reprogramming.

Non-imprinted genes can contribute to parent-of-origin effects on phenotype through interactions with imprinted genes.

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

Tissue-resident macrophages sense environmental cues and regulate adaptive immunity via an immune checkpoint molecule CRIg.

Toxic IAPP intermediates have some molecular features that are similar to, and others that are distinct from, toxic species reported for other amyloidogenic polypeptides.

Most regenerated cells after β-cell damage in zebrafish are Insulin+ Somatostatin+ bihormonal cells that are functional and able to restore glucose control.

Synchronized β cell response to glucose is lost concomitant with loss of islet architecture in Robo-deficient islets of Langerhans in vivo.