When blood glucose concentration rises above its optimum level of 90mg/100cm3, it is detected by β-cells in the Islets of Langerhans in the pancreas. These β-cells release insulin into the bloodstream. Insulin binds to receptors on the target cells, mainly hepatocytes (liver cells) and muscle cells. This binding causes a range of responses that increase the rate of facilitated diffusion of glucose into cells, lowering blood glucose concentration: it stimulates a change in tertiary structure of glucose transport carrier proteins in the cell surface membrane of target cells, causing them to open; it stimulates vesicles in target cells containing glucose transport carrier proteins to fuse with the cell surface membrane, increasing the number of glucose transport channels; it activates enzymes in the target cells that convert glucose into GP then glycogen, increasing the rate of glycogenesis which helps to maintain a steep concentration gradient for glucose to enter the cell down; and it activates enzymes in fat storage (brown adipose) tissue that convert glucose to fat.