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The mechanism for GLUT4 is an example of a cascade effect, where binding of a ligand to a membrane receptor amplifies the signal and causes a cellular response. In this case, insulin binds to the insulin receptor in its dimeric form and activates the receptor's tyrosine-kinase domain.
When insulin is secreted, glucose uptake of cells increase, since insulin stimulates GLUT4 to move from the intracellular surface to the outer surface. In a similar fashion, TUG retains GLUT4 within unstimulated cells, but when insulin is secreted it causes GLUT4 to dissociate and so GLUT4 moves to the cell surface. TUG binds directly and ...
GLUT3 is primarily expressed in neurons, specifically in cell processes (axons and dendrites), however, it is also found in many other cells throughout the body. [7] GLUT4 is an insulin-responsive glucose transporter located in the heart, skeletal muscle, brain, and adipose tissue. GLUT4 is generally in vesicles in the cytoplasm.
The influx of Ca 2+ ions causes the secretion of insulin stored in vesicles through the cell membrane. 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.
Levels in cell membranes are increased by reduced glucose levels and decreased by increased glucose levels. GLUT1 expression is upregulated in many tumors. GLUT2: Is a bidirectional transporter, allowing glucose to flow in 2 directions. Is expressed by renal tubular cells, liver cells and pancreatic beta cells.
This hormone, insulin, causes the liver to convert more glucose into glycogen (this process is called glycogenesis), and to force about 2/3 of body cells (primarily muscle and fat tissue cells) to take up glucose from the blood through the GLUT4 transporter, thus decreasing blood sugar.
This is possible because Insulin causes the insertion of the GLUT4 transporter in the cell membranes of muscle and fat tissues which allows glucose to enter the cell. [66] Increased fat synthesis – insulin forces fat cells to take in blood glucose, which is converted into triglycerides; decrease of insulin causes the reverse. [71]
Homozygous carriers of the p.Arg684Ter allele have lower concentrations of fasting plasma glucose and insulin. They also have a markedly increased risk of Type II Diabetes — individuals with two mutant genes have about 10 times the chance of contracting Type II diabetes ( odds ratio = 10.3) compared to noncarriers.