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

Direct insular recordings in humans reveal that contrary to several prominent models of speech production, it is not engaged in pre-articulatory planning, but in auditory and somatosensory components of speech.

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.

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

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.

An insulin-Myc feed-forward loop triggered by transient JNK boosts transcription of genes essential for mitochondrial respiration and biogenesis during early oogenesis to support massive mtDNA replication and inheritance in Drosophila.

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.

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