Experiments on mice show that an enzyme called DNA methyltransferase 3a is involved in insulin resistance via an epigenetic mechanism.

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

Yeast specific lipids promote the transport of lipid transfer protein (LTP) across the blood brain barrier to the neurons that regulate systemic insulin signaling.

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

Utilizing a conserved mechanism, a ribosome can initiate translation from a site within the insulin receptor mRNA to maintain protein synthesis even when standard mechanisms of initiating translation have been inhibited by stress.

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

Cells from the human pancreatic duct can be grown in culture and triggered to become insulin-producing cells, which could potentially be transplanted into patients with diabetes.

By controlling the SUMOylation of the protein CAR-1, the aging-regulating pathways downstream of the Insulin/IGF signaling cascade and of the germ cells of the nematode Caenorhabditis elegans are integrated.

Feeding and fasting associated alterations in proopiomelanocortin neuronal responses to insulin coordinate glucose metabolism.

Hermaphroditic Caenorhabditis elegans slow the onset of mating-induced death through self-sperm-regulated insulin-like gene expression, which regulates the activity of the IIS/FOXO pathway, mTOR signaling, and the TFEB/HLH-30 transcription factor.