To corroborate that dysregulation of FoxO1 signaling is directly involved in disruption of glycolytic processes, we cultured skeletal muscle EC in low (5 mmol/L) and high glucose (25 mmol/L) conditions, as previous in vitro studies have shown that hyperglycemia can both increase FoxO1 activity (Tanaka et al., 2009) and stall EC metabolism (Du et al., 2000; Zhang et al., 2000; Du et al., 2003). This evidence concerns the gene FOXO1 and Hyperglycemia.