From wikipedia:
Glucose in the body increases after food consumption. This is primarily due to carbohydrate intake, but to much lesser degree protein intake ([1])([2]). Depending on the tissue type, the glucose enters the cell through facilitated or passive diffusion. In muscle and adipose tissue, glucose enters through GLUT 4 receptors via facilitated diffusion ([3]). In brain, kidney and retina, glucose enters passively. In the beta-cells of the pancreas, glucose enters through the GLUT 2 receptors (process described below).
Two aspects of this process are explained below: insulin secretion and insulin action on the cell.
Insulin Secretion process
Insulin secretion
The glucose that goes in the bloodstream after food consumption also enters the beta cells in the Islets of Langerhans in the pancreas. The glucose passively diffuses in the beta cell through a GLUT-2 vesicle. Inside the beta cell, the following process occurs:
Glucose gets converted to Glucose-6-Phosphate (G6P) through Glucokinase; and G6P is subsequently oxidized to form ATP. This process inhibits the ATP sensitive potassium ion channels of the cell causing the Potassium ion channel to close and not function anymore. The closure of the Potassium channels causes Depolarization of the cell membrane causing the cell membrane to stretch which causes the voltage-gated Calcium channel on the membrane to open causing an influx of Ca2+ ions. This influx then stimulates fusion of the insulin vesicles (bubble like structure with insulin in them) to the cell membrane and secretion of insulin in the extracellular fluid outside the beta cell; thus making it enter the bloodstream...
In addition:
Trigger mechanism
Insulin is secreted in the beta cells of the islets of Langerhans. Before secretion, insulin is synthesized. Once insulin is synthesized, the beta cells are ready to release it in two different phases. As for the first phase, insulin release is triggered rapidly when the blood glucose level is increased.
The second phase is a slow release of newly formed vesicles that are triggered regardless of the sugar level. Glucose enters the beta cells and goes through glycolysis to form ATP that eventually cause 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 and allowing the calcium to flow into the cells. An increased calcium level causes activation of phospholipase C, which cleaves the membrane phospholipid phosphtidyl inositol 4 into inositol 1 and diacylglycerol. Inositol 1,4,5-triphosphate (IP3) binds to receptor proteins in the membrane of endplasmic reticulum (ER). This allows the release of (Ca2+) from the ER via IP3 gated channels, and raises the cell concentration of calcium even more. The influx of Ca2+ ions push the Insulin molecules (that are inside their "bubble" surrounding) outside of the cell.
Therefore, 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.
http://en.wikipedia.org/wiki/Insulin..._blood_glucose
Unsure if this answers your question.
I recall a discussion concerning hypokalemic periodic paralysis; interestingly A calcium channel mutation causes hypokalemic periodic paralysis.