Search results
Results from the WOW.Com Content Network
The insulin transduction pathway is a biochemical pathway by which insulin increases the uptake of glucose into fat and muscle cells and reduces the synthesis of glucose in the liver and hence is involved in maintaining glucose homeostasis. This pathway is also influenced by fed versus fasting states, stress levels, and a variety of other ...
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.
It belongs to the class B family of G protein-coupled receptors, also known as secretin-like receptors. The N-terminus of the receptor is responsible for binding glucagon-like peptide-1 (GLP-1) ligands, while the intracellular C-terminus interacts with intracellular signaling proteins to initiate downstream signaling pathways.
In contrast, mice that do not have Akt2 but have normal Akt1 have mild growth deficiency and display a diabetic phenotype (insulin resistance), again consistent with the idea that Akt2 is more specific for the insulin receptor signaling pathway. [5] The role of Akt3 is less clear, though it appears to be expressed predominantly in brain.
The amount of glucokinase can be increased by synthesis of new protein. Insulin is the principal signal for increased transcription, operating mainly by way of a transcription factor called sterol regulatory element binding protein-1c (SREBP1c) in the liver. This occurs within an hour after a rise in insulin levels, as after a carbohydrate meal.
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.
The product of this gene is phosphorylated by the insulin receptor tyrosine kinase upon receptor stimulation, as well as by an interleukin 4 receptor-associated kinase in response to IL4 treatment. [6] Mice lacking IRS2 have a diabetic phenotype [7] as well as a 40% reduction in brain mass. [8]
An important role for PDPK1 is in the signaling pathways activated by several growth factors and hormones including insulin signaling. Mice lacking PDPK1 die during early embryonic development, indicating that this enzyme is critical for transmitting the growth-promoting signals necessary for normal mammalian development.