Zebrafish insulin mutants serve as an innovative platform to identify novel mechanisms regulating glucose homeostasis.

Long-term physical exercise had a substantial effect on the plasma proteome, identifying novel exerkines and suggesting CD300LG as a potential link to insulin sensitivity.

Loss miRNA maturation in proopiomelanocortin (POMC) neurons causes metabolic dysregulation and favors the differentiation of Pomc progenitors into neuropeptide Y neurons, a developmental process that appears to specifically involve miR-103/107.

β2-adrenergic receptors control glucose metabolism by regulating cross-talk between pancreatic islet endocrine cells and vasculature during development.

A series of experiments at the molecular level reveal the underlying mechanism of how a gene activates liver glucose production to regulate the blood glucose metabolism in mice.

Hepatic TAZ coordinates the differential expression of gluconeogenic genes in the fasted and fed states by inhibiting glucocorticoid receptor.

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.

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

A proteomics screening in mouse adipose tissue shows that loss of adipose Hexokinase 2 is a mechanism of obesity-induced insulin insensitivity.

Use of a newly developed experimental model in fruit flies reveals that death following traumatic brain injury is largely due to a mechanism by which brain damage triggers disruption of the intestinal barrier, leading to elevated levels of glucose in the circulatory system with deleterious consequences.