Carb 8

• GLUT 4 is located in adipose tissue and muscle and responds to the glucose concentration in peripheral blood.
• The rate of glucose transport in adipose tissue and muscle is increased by insulin, which stimulates the movement of additional GLUT 4 transporters to the membrane by a mechanism involving exocytosis.
• The K of GLUT 4 is close to the normal glucose levels in blood (~5 mM), meaning that the transporter is saturated when blood glucose levels are just a bit higher than normal.
• When a person has high blood sugar concentrations, these transporters will still permit only a constant rate of glucose influx because they will be saturated (zero-order kinetics).
• Cells with GLUT 4 transporters can increase their intake of glucose by increasing the number of GLUT 4 transporters on their surface.
• Although basal levels of transport occur in all cells independently of insulin, the transport rate increases in adipose tissue and muscle when insulin levels rise.
• Muscle stores excess glucose as glycogen, and adipose tissue requires glucose to form dihydroxyacetone phosphate (DHAP), which is converted to glycerol phosphate to store incoming fatty acids as triacylglycerols.
• Diabetes mellitus is caused by a disruption of the insulin/GLUT 4 mechanism.
• In type 1 diabetes, insulin is absent and cannot stimulate the insulin receptor.
• In type 2 diabetes, the receptor becomes insensitive to insulin and fails to bring GLUT 4 transporters to the cell surface.
• In both cases, blood glucose rises, leading to immediate symptoms (increased urination, increased thirst, ketoacidosis) and long-term symptoms (blindness, heart attacks, strokes, nerve damage).