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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.
The insulin receptor (IR) is a transmembrane receptor that is activated by insulin, IGF-I, IGF-II and belongs to the large class of receptor tyrosine kinase. [5] Metabolically, the insulin receptor plays a key role in the regulation of glucose homeostasis; a functional process that under degenerate conditions may result in a range of clinical manifestations including diabetes and cancer.
Through a series of kinase proteins, the proteins are constantly being phosphorylated and activated. At the end of the transduction process, the activated protein binds to the PIP 2 proteins embedded in the membrane. By doing so, the initial signal has successfully transmitted the extracellular signal.
The insulin signal transduction pathway begins when insulin binds to the insulin receptor proteins. Once the transduction pathway is completed, the GLUT-4 storage vesicles becomes one with the cellular membrane. As a result, the GLUT-4 protein channels become embedded into the membrane, allowing glucose to be transported into the cell.
Insulin appears to affect both glucokinase transcription and activity through multiple direct and indirect pathways. While rising portal vein glucose levels increase glucokinase activity, the concomitant rise of insulin amplifies this effect by induction of glucokinase synthesis.
The insulin signal transduction pathway begins when insulin binds to the insulin receptor proteins. Once the transduction pathway is completed, the GLUT-4 storage vesicles becomes one with the cellular membrane. As a result, the GLUT-4 protein channels become embedded into the membrane, allowing glucose to be transported into the cell.
Transcription of insulin is regulated by the binding of various transcription factors to the ~400 base pairs before the insulin transcription start site, called the "insulin regulatory sequence". [1] This sequence is made up of several distinct regions with different biochemical properties, each of which serve as binding sites for distinct ...
Type 2 diabetes, also known as non insulin dependent diabetes and as chronic hyperglycemia, is caused primarily by genetics and the development of metabolic syndrome. [2] [9] The beta cells can still secrete insulin but the body has developed a resistance and its response to insulin has declined. [4]