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Homeostasis Blood glucose level are at the pet point (roughly 90mg/100ml)…

- - - - In the Pancreas Beta cells in the isles of Langerhans detect the high blood glucose concentration, (as there will be an increased level o glucose entering the Beta cells via the glucose transporters)
        
        in response to the high blood glucose concentration the beta cells switch on a gene to begin the protein synthesis of insulin. along with this they release pre-made stores of insulin, that have been stored in vesicles.
        
        vesicles of insulin travel to the plasma membrane of the nervous, where they fuse together allowing the insulin to be secreted into the bloodstream - (this process in called Exocytosis)
        
        The insulin then travels through the bloodstream to insulin receptors located on the plasma membrane of the liver, muscle and fat cells
        
        Transduction in the Muscle cells
        
        The Insulin binds to the receptors along the plasma membrane , this causes the inter cellular portion of the receptor to change shape. this change in shape activates a an enzyme called Glycogen Synthase and a chain of enzyme controlled reactions that eventually turn Glucose monomers into Glycogen polymers. inside the Muscle cells there are vesicles containing GLUT4 (witch are glucose transporters). move towards the cell membrane and fuse with it (this is possible as the cell membrane is a phospholipid bilayer). Now the numbers of transporters along the cell membrane has increased witch enables more glucose to be transported into the cell at a faster rate (a greater rate of diffusion down the concentration gradient). Glucose monomers are converted into glycogen polymers at a faster rate.
        
        Transduction in the liver
        
        the insulin binds to the receptors along the plasma membrane, this causes the inter cellular portion of the receptor to change shape. The change in shape activates an enzyme called Glycogen Synthase, witch catalyses the reaction that turns Glucose monomers into glycogen polymers, through a chain of enzyme controlled reactions. as the concentration of Glucose inside the liver cells decreases it creates a a concentration gradient, allowing more glucose to diffuse fro the bloodstream, into the liver cells though the glucose transporters
        
        Transduction in the Fat cells
        
        The Insulin binds to the receptors along the plasma membrane , this causes the inter cellular portion of the receptor to change shape. this change in shape activates a chain of enzyme controlled reactions that eventually turns Glucose into glycerol. Inside the Fat cells there are vesicles containing GLUT4 (glucose transporters), through a series of enzyme controlled reactions these will move to the cell membrane and fuse with it. Now that there is an increased number of Glucose transporters along the membrane, glucose diffusion into the cell and conversion to Glycerol, happens at a faster rate.
- - - - Glucagon (Hormone) travels via the bloodstream, to the glucagon receptors on the liver cells, cell membrane
        
        Glucagon binds to the receptor causing the inter cellular portion of the receptor to change Shape. this change in shape activates an enzyme called glycogen Phosphorylase. A chain of enzyme reactions then go on to catalyse the reaction to break down Glycogen polymers into Glucose Monomers.
        
        the Increases concentration of Glucose inside the liver cells, causes the concentration gradient to flow from the inside of the cell to the outside. thus the glucose diffuses out of the liver cells into the bloodstream, via the glucose transporters. the glucose can then be taken around the body and used to make ATP (energy) for all life processes of the organism.
        
        Thus, the Blood glucose concentration will gradually increase back towards the set point.
        
        As soon as the in Glucagon receptors are activated, the cell begins a process to degrade the glucagon, in order to prevent the cell from the risk of producing to much glucose, and causing you to have a high blood glucose concentration. If you still require the more glucose in the bloodstream, the Alpha cells will continue to detect this and send more glucagon to the receptors, were it will bind and perform this whole process again, with 'new' Glucagon.
        So, once the glucagon receptors have been activated the membrane starts to bud off, creating a vesicle around the Glucagon receptors. Then, the contents inside the vesicle is acidified, and as the PH levels decrease , it creates an environment in witch the Glucagon (a protein structure) denatures, and can no longer bind to the receptor, so is essentially useless. so without the glucagon, the inter cellular portion of the receptor returns to its original shape and hence shits off the signal of the Glucagon, and the Glycogen stops being broken apart into glucose (the reason the Glucagon receptor is encapsulated n a vesicle before it is acidified, is to prevent any damage to other components of the cell)