The rough endoplasmic reticulum (ER) is the site of synthesis of many proteins in the cell. It also contributes to subsequent protein folding via numerous proteins housed in its lumen. However, the raw ER may be under stress and protein folding may not always be completed or properly executed. ER stress leading to an accumulation of both unfolded and misfolded proteins triggers the unfolded protein response, or UPR. The UPR is a mechanism by which the ED increases its protein folding capacity and decreases its caseload, thereby enabling it to cope with stress. However, prolonged periods of UPR activation due to extreme and prolonged ER stress harm the cell. Correlational and mechanistic research studies have shown that sustained OR contributes to the pathogenesis of type II diabetes, a disorder characterized by increased blood sugar levels due to insulin resistance. Obesity, the most common cause of type II diabetes, causes ER stress that triggers two UPR signal transduction pathways: inositol requiring protein 1 (IRE1) and protein kinase RNA-like ER kinase (PERK). IRE1 leads to insulin resistance by inactivating an adapter protein necessary for the interaction of insulin with its receptor. PERK boosts high blood sugar levels by activating an apoptotic agent that targets the insulin-producing beta cells of the pancreas. Currently, various medical treatments for type II diabetes are being carried out. This includes non-peptide activators of insulin action, incretins and glucokinase activators. Type II Diabetes Insulin is a hormone produced by the pancreas in response to high blood sugar levels (Vijan, 2010). It stimulates cells to take up glucose, where it can be metabolized for energy or stored as glycogen (e.g. ... middle of paper ...... activation of cokinase also lowers the glycemia by promoting glycogen synthesis in the liver (Pal, 2009).In conclusion, type II diabetes is mediated by the prolongation of the deployed endoplasmic reticulum protein response, or UPR (Ozcan and Tabas, 2012). Obesity subjects the ER to extreme stress which triggers excessive activation of IRE1 and PERK signaling pathways (Wu and Kaufman, 2006). death of pancreatic cells that produce insulin (Ozcan and Tabas, 2012). Various treatments are now used to treat type II diabetes. This includes TLK16998-based drugs that improve insulin action, incretins. intestinal GLP-1 which increases insulin and suppresses glucagon, and glucokinase activators which positively regulate insulin secretion and promote the storage of glucose as glycogen (Tahrani et al.., 2011).