In vitro and in vivo antioxidant, anti-hyperlipidemia, and antiglycation may have contributed to the reversal of the hypoactivation/malfunction of the IRS-PI3K-AKT-GLUT4 and PKC-α -insulin signaling pathways in high glucose and high insulin (in vitro and ex vivo) and STZ-induced diabetic rat model when compared to the insulin-resistant (diabetic) control group. This evidence concerns the gene AKT1 and diabetes mellitus.