Multi-omic profiling of gene expression in response to reduced insulin/IGF-like-signalling reveals tissue-specific regulation of DNA damage and lysosomal mannosidase regulation of tissue homeostasis as pro-longevity responses.

Drosophila HNF4 directs a developmental switch at the onset of adulthood that suppresses diabetes by promoting mitochondrial function and supporting glucose-stimulated insulin secretion.

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

The catalytic activity of a Drosophila neprilysin is critical to proper insulin expression and food intake by regulating homeostasis of distinct signaling peptides.

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

Feedback signaling between the synapse and nucleus via FGF22 and IGF2 directs the activity-dependent stabilization of presynaptic terminals in the mouse hippocampus.

Lower mitochondrial coenzyme Q was a consistent feature across multiple in vitro and in vivo models of insulin resistance and was sufficient to cause insulin resistance through increased mitochondrial oxidants.

Profiling the adipocyte secretome reveals LRG1 as a novel adipokine that promotes insulin sensitivity and modulates inflammation triggered by release of cytochrome c from dead/dying cells, describing a new pathway at the intersection of obesity and its systemic sequelae.

Mouse and tissue culture studies reveal that adipose DNA methyltransferase 3a mediates insulin resistance, partially through repressing the expression of FGF21.

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