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Increased insulin levels cause the uptake of glucose into the cells. GLUT4 is stored in the cell in transport vesicles, and is quickly incorporated into the plasma membrane of the cell when insulin binds to membrane receptors. [24] Under conditions of low insulin, most GLUT4 is sequestered in intracellular vesicles in muscle and fat cells.
When the insulin binds to these alpha subunits, 'glucose transport 4' (GLUT4) is released and transferred to the cell membrane to regulate glucose transport in and out of the cell. With the release of GLUT4, the allowance of glucose into cells is increased, and therefore the concentration of blood glucose might decrease.
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 ...
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.
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 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]
David Ernest James FAA (born in Sydney in 1958) is a cell biologist who discovered the glucose transporter GLUT4.He has also been responsible for the molecular dissection of the intracellular trafficking pathways that regulate GLUT4 translocation to the cell surface, the topological mapping of the insulin signal transduction pathway, the creation of a method for studying in vivo metabolism in ...
The variant mainly affects individuals with two copies of the mutation, indicating recessive inheritance. Although the mutation does not effect the short isoform of the protein, it introduces a premature stop codon in the long isoform, resulting in the absence of the long isoform protein in muscle tissue.