Insulin characterized by abnormally high blood glucose concentrations, and generalized body wasting. In type 2 diabetes mellitus the destruction of beta cells is less pronounced than in type 1 diabetes, and is not due to an autoimmune process. Instead there is an accumulation of amyloid in the pancreatic islets, which likely disrupts their anatomy and physiology. The pathogenesis of type 2 diabetes is not well understood but patients exhibit a reduced population of islet beta-cells, reduced secretory function of islet beta-cells that survive, and peripheral tissue insulin resistance. Type 2 diabetes is characterized by high rates of glucagon secretion into the
Insulin analog required throughout the day representing about 50% of daily insulin requirement, the insulin amount needed at mealtime makes up for the remaining 50%. Non hexameric insulins (monomeric insulins) were developed to be faster acting and to replace the injection of normal unmodified insulin before a meal. There are phylogenetic examples for such monomeric insulins in animals. All insulin analogs must be tested for carcinogenicity, as insulin engages in cross-talk with IGF pathways, which can cause abnormal cell growth and tumorigenesis. Modifications to insulin always carry the risk of unintentionally enhancing IGF signalling in addition to the desired pharmacological properties. There