SREBP1c-CRY1 signalling represses hepatic glucose production by promoting FOXO1 degradation during refeeding

Abstract

The clock protein Cry regulates hepatic glucose metabolism. Here the authors show that SREBP1c, activated by insulin signalling after feeding, directly regulates Cry transcription at specific circadian time points, and that Cry represses hepatic glucose production by promoting proteasomal degradation of Foxo1.