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INS
INS Full Name
insulin
INS Introduction
β-cells of pancreatic islets produce insulin which binds to its specific receptor called the insulin receptor (INSR) to activate metabolic tissues including liver and muscle and adipose tissue. The insulin-INSR binding process leads to receptor autophosphorylation which activates the PI3K–AKT and MAPK signaling pathways. The metabolic homeostasis depends on insulin because it controls glucose uptake and glycogen synthesis and lipid metabolism and protein synthesis. The presence of insulin receptors in brain tissue and blood vessels and immune cells indicates that insulin plays additional roles in neural function and vascular control and immune system regulation.
Figure 1.The in vivo functional characteristics of INS.(Source: Wasserfall C, et al.; 2017)
The insulin signaling pathway enables glucose entry into cells through GLUT4 membrane translocation while it supports anabolic processes and blocks gluconeogenesis and lipolysis. The body maintains precise control of energy balance through insulin signaling which works together with glucagon and IGF-1 and incretins. The body develops insulin resistance because insulin receptor signaling fails through receptor damage or signaling pathway breakdowns or extended metabolic stress. The development of insulin resistance causes glucose homeostasis to fail and lipid profiles to change which results in various metabolic disorders.
The development of type 2 diabetes mellitus and metabolic syndrome and non-alcoholic fatty liver disease and obesity-related complications occurs because of clinical insulin and INSR signaling problems. The insulin receptor develops dysfunction because of mutations which lead to Type A insulin resistance and Rabson–Mendenhall syndrome. The reduction of insulin signaling pathways leads to cardiovascular disease and endothelial dysfunction and cognitive decline which might play a role in neurodegenerative disorders. The unregulated release of insulin results in hypoglycemia and enables tumor growth through its effects on IGF-1 signaling pathways.
Alternate Names for INS
INS; insulin; proinsulin; preproinsulin;
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