Insulin signal transduction pathway is secreted after glucose enters the beta cell and that triggers several other processes in a chain reaction. 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
Adrenocortical hormone and increased blood potassium levels caused by a deficiency of aldosterone. These electrolyte imbalances induce nerve and muscle issues. Other symptoms include fatigue, salt cravings, weight loss, and increased skin pigmentation. Increased skin pigmentation is caused by a deficiency of the adrenocortical hormone hydrocortisone. Its normal behavior would be as negative feedback at the pituitary gland, stimulating the pituitary gland to decrease secretion of corticotropin. Because hydrocortisone is not able to be produced in Addison’s disease, the pituitary gland continues to secrete corticotropin which binds to the receptor for melanocyte-stimulating hormone. It then causes melanocytes to produce more pigment, thus