blood sugar level. glucose enters the beta cells and goes through glycolysis to form atp that eventually causes depolarization of the beta cell membrane (as explained in insulin secretion section of this article). the depolarization process causes voltage-controlled calcium channels (ca2+) opening, allowing the calcium to flow into the cells. an increased calcium level activates phospholipase c, which cleaves the membrane phospholipid phosphatidylinositol 4,5-bisphosphate into inositol 1,4,5-trisphosphate (ip3) and diacylglycerol (dag). ip3 binds to receptor proteins in the membrane of the endoplasmic reticulum (er). this releases (ca2+) from the er via ip3 gated channels, and raises the cell concentration of calcium even more. the influx of ca2+ ions causes the secretion of insulin stored in vesicles through the cell membrane. the process of insulin secretion is an example of a trigger mechanism in a signal transduction pathway because insulin is secreted after glucose enters the beta cell and that triggers several other processes in a chain reaction. counter mechanism function of glucagon while insulin is secreted by the pancreas to lower blood glucose levels, glucagon is secreted to raise blood glucose levels. this is why glucagon has been known for decades as a counter-regulatory hormone. when blood glucose levels are low, the pancreas secretes glucagon, which in turn causes the liver to convert stored glycogen polymers into glucose monomers, which is then released into the blood. this process is called glycogenolysis. liver cells, or hepatocytes, have glucagon receptors which allow for glucagon to attach to them and thus stimulate glycogenolysis. contrary to insulin, which is produced by pancreatic β-cells, glucagon is produced by pancreatic α-cells. it is also known that an increase in insulin suppresses glucagon secretion, and a decrease in insulin, along with low glucose levels, stimulates the secretion of glucagon. oscillatory behavior when blood glucose levels are too low, the pancreas is signaled to release glucagon, which has essentially the opposite effect of insulin and therefore opposes the reduction of glucose in the blood. glucagon is delivered directly to the liver, where it connects to the glucagon receptors on the membranes of the liver cells, 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, 'glucose transport 4' (glut4) is released and transferred to the cell membrane to regulate glucose transport in and out of the cell. with the release of glut4, the allowance of glucose into cells is increased, and therefore the concentration of blood glucose might decrease. this, in other words, increases the utilization of the glucose already present in the liver. this is shown in the adjacent image. as glucose increases, the production of insulin increases, which thereby increases the utilization of the glucose, which maintains the glucose levels in an efficient manner and creates an oscillatory behavior.