In Caenorhabditis elegans, an insulin-like signalling pathway culminates in
a transcription factor (TF) that is homologous to a subfamily of Tps respo
nsible for the regulation of a subset of insulin-responsive genes in humans
. Under harsh conditions, C. elegans reduces signalling through this pathwa
y and arrests developmentally in a manner that is similar to the metabolic
syndrome of humans. We propose that an understanding of this pathway could
lead to drugs with optimal potency and selectivity in the treatment of type
2 diabetes mellitus.