Insulin and Glucagon are the two principal hormones that participate in the glucose homeostasis. Insulin is synthesized and secreted by the beta cells of the pancreas that regulates the carbohydrate as well as fat metabolism (Cushman & Wardzala, 2001). Insulin functions through reducing the blood glucose level as it stores the excess glucose as muscle glycogen. Thereby insulin maintains a steady state level of glucose protecting the body either from hyperglycemia or hypoglycaemia. A rise in the blood glucose level signals the pancreatic beta cells to release insulin into the bloodstream, which in turn stimulates uptake of glucose from muscle glycogen. This in turn acts as a reservoir of energy for future use. The condition when the blood glucose level exceeds the normal range (80-120 mg/dl), diabetes ensues.

Destruction of pancreatic beta cells or increased resistance to insulin has been found to be primarily responsible for diabetes. Insulin binds to specific receptors on the cells, where the density of the receptors varies according to the cell-type. Insulin receptors are mainly a group of RTKs (Receptors Tyrosine Kinases), having two extracellular alpha subunits and two transmembrane beta subunits. Upon interaction with receptors, a signalling cascade gets activated. Glucose transporters (GLUT4) are transported to the cell surface, which assists the intake of glucose across the plasma membrane. Covalent modification (phosphorylation or dephosphorylation) of the enzymes regulate the glucose intake. Specific protein kinases functions through different second messengers (cyclic AMP and PIP3) and play critical roles in the transport of GLUT4 to the cell surface. Generally a combination of short as well as long acting insulin is typically prescribed to diabetes patients