“…In response to rising blood glucose, the ATP-sensitive potassium (K ATP ) channel in β cells is inhibited, leading to membrane depolarization, elevation of cytosolic calcium, and insulin secretion (Newgard and McGarry, 1995; Nichols, 2006). Previous studies have shown that O-GlcNAc transferase (OGT) (Bond and Hanover, 2015; Erickson et al, 2013; Hardiville and Hart, 2014; Ruan et al, 2013), and ChREBP and MondoA together with their binding partner Mlx (Havula and Hietakangas, 2012; Postic et al, 2007; Uyeda and Repa, 2006) contribute to the transcriptional effects of glucose in diverse cell types, including skeletal muscle (Ahn et al, 2016; Stoltzman et al, 2008). However, whether glucose directly engages nutrient sensing pathways in skeletal myocytes to regulate glucose disposal remains largely unknown.…”