[HTML][HTML] Glucose regulates steady-state levels of PDX1 via the reciprocal actions of GSK3 and AKT kinases
The pancreatic beta cell is sensitive to even small changes in PDX1 protein levels;
consequently, Pdx1 haploinsufficiency can inhibit beta cell growth and decrease insulin
biosynthesis and gene expression, leading to compromised glucose-stimulated insulin
secretion. Using metabolic labeling of primary islets and a cultured β cell line, we show that
glucose levels modulate PDX1 protein phosphorylation at a novel C-terminal GSK3
consensus that maps to serines 268 and 272. A decrease in glucose levels triggers …
consequently, Pdx1 haploinsufficiency can inhibit beta cell growth and decrease insulin
biosynthesis and gene expression, leading to compromised glucose-stimulated insulin
secretion. Using metabolic labeling of primary islets and a cultured β cell line, we show that
glucose levels modulate PDX1 protein phosphorylation at a novel C-terminal GSK3
consensus that maps to serines 268 and 272. A decrease in glucose levels triggers …