FIGURE 7.

Proposed model of FOXP1-mediated repression of hepatic gluconeogenesis. Under pathophysiological conditions (left panel) FOXP1 expression levels were decreased, allowing FOXO1 binding to IRE of gluconeogenic genes, subsequently activating their expression. However, under the feeding condition (right panel), increased FOXP1 proteins directly bind to IRE in the promoters of gluconeogenesis genes occupied by FOXO1 or physically interacts with FOXO1, preventing FOXO1 binding, thereby inhibiting expression of hepatic gluconeogenic genes.