Insulin signal transduction pathway signals the conversion of the glycogen already stored in the liver cells into glucose. This process is called glycogenolysis. Conversely, when the blood-glucose levels are too high, the pancreas is signaled to release insulin. Insulin is delivered to the liver and other tissues throughout the body (e.g., muscle, adipose). When the insulin is introduced to the liver, it connects to the insulin receptors already present, that is tyrosine kinase receptor. These receptors have two alpha subunits (extracellular) and two beta subunits (intercellular) which are connected through the cell membrane via disulfide bonds. When the insulin binds to these alpha subunits,
Insulin resistance with insulin resistance. It is hypothesized that increasing cell membrane fluidity by increasing PUFA concentration might result in an enhanced number of insulin receptors, an increased affinity of insulin to its receptors, and a reduced insulin resistance, and vice versa. Many stressing factors may lead to increased cortisol in the bloodstream. Cortisol counteracts insulin, contributes to hyperglycemia-causing hepatic gluconeogenesis, and inhibits the peripheral utilization of glucose, which eventually leads to insulin resistance. It does this by decreasing the translocation of glucose transporters (especially GLUT4) to the cell membrane. Inflammation by itself also seems to be implicated in causing insulin resistance.