Insulin is a peptide hormone produced in the beta cells of the islets of Langerhans of the pancreas. Insulin regulates glucose influx and lipid metabolism in the liver, while inhibiting fatty acid oxidation, glycogenolysis and gluconeogenesis. Insulin is composed of 2 polypeptides, 51 amino acids and a molecular weight of 5808 Da. These two chains are coupled together by disulfide bridges (Bell et al., 1980), chains A are composed of 21 amino acids and B of 30 amino acids in its chain. Insulin is made in β cells as pre-proinsulin. Immediately after synthesis, pre-proinsulin is released into the rough endoplasmic reticulum where it is cleaved by proteolytic enzymes to form proinsulin. Proinsulin, the A and B chains linked by the C chain, is then transported to the Golgi apparatus, where it is packaged into vesicles. Proinsulin is converted to insulin by a series of proteases, including the prohormones converatase 2 and 3 and carboxy-peptidase E (Hutton, 1994) (Rorsman et al, 2013). Insulin release occurs in two phases. The first phase is driven by changes in blood glucose and the second occurs independently of glucose. There are various substances that stimulate insulin, such as arginine, leucine, acetylcholine, sulfonylurea and cholecystokinin (CCK) (Rorsman et al, 2013). Glucose is taken up by beta cells via GLUT-2 receptors. Once glucose is absorbed by beta cells, it is oxidized by glucokinase, a major enzyme involved in glycolysis and which also acts as a glucose sensor. At low glucose levels, below 90 mg/dl, K+ enters the cell via open K+-ATP channels, which maintains the β cell membrane at a negative potential. As blood glucose increases, glucose absorption and metabolites decrease significantly (Romeo et al. 2012). Research has shown that insulin resistance is associated with a number of diseases, including non-alcoholic fatty liver disease, Alzheimer's disease, atherosclerosis and heart failure, and is a major factor in the pathogenesis type 2 diabetes (T2DM). (Liu et al., 2011) showed that cerebral glucose metabolism is suppressed in Alzheimer's disease (AD) patients, but the underlying mechanism is not understood. In the study, they investigated the brain insulin-PI3K-AKT signaling pathway in the autopsied frontal cortices of nine AD cases, 10 T2D cases, eight T2D-AD cases, and seven control cases. Research has revealed decreased levels and activities of several components of the insulin-PI3K-AKT signaling pathway in AD and T2D. Insulin-PI3K-AKT signaling deficiency was more severe in people with both T2D and AD.