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,
Pulsatile insulin factors. Continuous exposure to insulin and glucagon is known to decrease the hormones’ metabolic effectiveness on glucose production in humans due to the body developing an increased tolerance to the hormones. Down-regulation at the cellular level may partially explain the decreased action of steady-state levels of insulin, while pulsatile hormone secretion may allow recovery of receptor affinity and numbers for insulin. Intermittent intravenous insulin administration with peaks of insulin concentrations may enhance suppression of gluconeogenesis and reduce hepatic glucose production. Dr. Thomas Aoki, former Head of Metabolism Research at the Joslin Diabetes Center in Boston, Massachusetts, and a former Professor