Insulin is a peptide hormone produced by the beta cells of the islets of Langerhans in 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), the A chain is composed of 21 amino acids and the B with 30 amino acids in its chain. Insulin is produced in β cells in the form of 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 through a series of proteases including prohormone converatase 2 and 3 and carboxypeptidase E (Hutton, 1994) (Rorsman et al, 2013). The release of insulin occurs in two phases. The first phase is stimulated by changes in blood glucose levels, while the second occurs independently of glucose. There are several 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. After glucose is taken up by beta cells, it is oxidized by glucokinase, an important enzyme involved in glycolysis and which also serves as a glucose sensor. At low glucose levels, below 90 mg/dl, K+ enters the cell through open K+-ATP channels, which maintain the ß cell membrane at a negative potential. As blood glucose levels increase, glucose absorption and metabolism are significantly reduced (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 an important factor in the pathogenesis of type 2 diabetes (T2D). (Liu et al., 2011) demonstrated that glucose metabolism in the brain is suppressed in patients with Alzheimer's disease (AD), however, 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 T2DM, eight T2DM-AD, and seven control cases. Research has found decreases in the levels and activities of several components of the insulin-PI3K-AKT signaling pathway in cases of AD and T2DM. Insulin-PI3K-AKT signaling deficiency was more severe in subjects with both T2DM and AD.