Insulin signaling pathway in skeletal muscles
Signalni put insulina u ćelijama skeletnih mišića
Apstrakt
Insulin (INS), the hormone of endocrine pancreas, is one of the most important vertebrate proteins. Increased circulating levels of glucose (Glu) stimulate pancreatic β cells to secrete INS by exocytosis. Insulin receptor (IR) belongs to the group of membrane receptors with tyrosine kinase activity. Skeletal muscles (SM) account for about 85% of total Glu disposal under INS stimulated conditions where it is incorporated and stored as glycogen. Glu entry into cells is a process that requires the involvement of a carrier protein in order to facilitate the movement of Glu across the plasma membrane of a cell and they are identified as glucose transporters (GLUT). In SMs, GLUT1 and GLUT4 are the primary GLUTs expressed. In SMs, INS stimulated Glu disposal is mediated via translocation of GLUT4 from intracellular storage site to the plasma membrane and GLUT1 primary mediates basal, rather than INS mediated Glu uptake. Impairment of the mechanisms responsible for this translocation leads to ...INS resistance. Peripheral INS resistance is a key factor in the pathogenesis of type 2 Diabetes Mellitus (DMT2) and involves defects in Glu transport system in adipocytes and SM. SM is the principal site of Glu uptake under INS stimulated conditions and INS resistance in SM has been identified as the most important site for INS resistance in DMT2 and may result from a defect at the level of Glu transport, Glu phosphorylation or glycogen synthesis. Glu transport is one of the first steps in INS stimulated Glu uptake in SM and it is a rate limiting factor in the whole Glu metabolism.
Insulin (INS) je hormon endokrinog pankreasa i jedan je od najznačajnijih proteina kičmenjaka. Povećana koncentracija glukoze (Glu) u krvi stimuliše β ćelije pankreasa i dovodi do sekrecije INS egzocitozom. Receptor za insulin (IR) pripada grupi membranskih receptora koji poseduju tirozin kinaznu aktivnost. Skeletni mišići (SM) preuzimaju oko 85% ukupne Glu pri insulinskoj stimulaciji i Glu se u njih inkorporira i skladišti u vidu glikogena. Glu u ćelije ulazi uz pomoć proteina nosača koji olakšavaju transport Glu kroz ćelijsku membranu i identifikovani su kao glukozni transporteri (GLUT). U ćelijama SM, lokalizovani su GLUT1 i GLUT4. INS stimulisano preuzimanje Glu u mišićnim ćelijama posredovano je translokacijom GLUT4 na površinu ćelijske membrane, dok GLUT1 posreduje u preuzimanju Glu u mišićne ćelije pri bazalnim uslovima. Poremećaji u mehanizmima koji su odgovorni za ovu translokaciju vode insulinskoj rezistenciji. Periferna insulinska resistencija koja uključuje poremećaje trans...porta Glu u adipocitima i SM, ključni je faktor u patogenezi Diabetesa Mellitusa tipa 2 (DMT2). S obzirom na to da SM preuzimaju najveći deo ukupne Glu, insulinska rezistencija u SM od velikog je značaja za razvoj DMT2 i može se javiti na tri nivoa: na nivou transporta Glu, fosforilacije Glu i na nivou sinteze glikogena. Transport Glu je osnovni korak u preuzimanju Glu u SM pri insulinskoj stimulaciji i ograničavajući je faktor za celokupan metabolizam Glu u organizmu.
Ključne reči:
insulin / skeletal muscles / insulin resistance / Diabetes Mellitus type 2 / insulin / skeletni mišići / insulinska rezistencija / Diabetes Mellitus tipa 2Izvor:
Timočki medicinski glasnik, 2006, 31, 4, 180-185Finansiranje / projekti:
- Molekularni mehanizmi transdukcije hormonskih signala: Biološki markeri modifikacije i integracije signalnih puteva u fiziološkim i patofiziološkim stanjima (RS-MESTD-MPN2006-2010-143030)
Napomena:
- Available at: http://www.tmg.org.rs/v310411.htm
Kolekcije
Institucija/grupa
VinčaTY - JOUR AU - Sudar, Emina AU - Velebit, Jelena AU - Isenović, Esma R. PY - 2006 UR - https://vinar.vin.bg.ac.rs/handle/123456789/10334 AB - Insulin (INS), the hormone of endocrine pancreas, is one of the most important vertebrate proteins. Increased circulating levels of glucose (Glu) stimulate pancreatic β cells to secrete INS by exocytosis. Insulin receptor (IR) belongs to the group of membrane receptors with tyrosine kinase activity. Skeletal muscles (SM) account for about 85% of total Glu disposal under INS stimulated conditions where it is incorporated and stored as glycogen. Glu entry into cells is a process that requires the involvement of a carrier protein in order to facilitate the movement of Glu across the plasma membrane of a cell and they are identified as glucose transporters (GLUT). In SMs, GLUT1 and GLUT4 are the primary GLUTs expressed. In SMs, INS stimulated Glu disposal is mediated via translocation of GLUT4 from intracellular storage site to the plasma membrane and GLUT1 primary mediates basal, rather than INS mediated Glu uptake. Impairment of the mechanisms responsible for this translocation leads to INS resistance. Peripheral INS resistance is a key factor in the pathogenesis of type 2 Diabetes Mellitus (DMT2) and involves defects in Glu transport system in adipocytes and SM. SM is the principal site of Glu uptake under INS stimulated conditions and INS resistance in SM has been identified as the most important site for INS resistance in DMT2 and may result from a defect at the level of Glu transport, Glu phosphorylation or glycogen synthesis. Glu transport is one of the first steps in INS stimulated Glu uptake in SM and it is a rate limiting factor in the whole Glu metabolism. AB - Insulin (INS) je hormon endokrinog pankreasa i jedan je od najznačajnijih proteina kičmenjaka. Povećana koncentracija glukoze (Glu) u krvi stimuliše β ćelije pankreasa i dovodi do sekrecije INS egzocitozom. Receptor za insulin (IR) pripada grupi membranskih receptora koji poseduju tirozin kinaznu aktivnost. Skeletni mišići (SM) preuzimaju oko 85% ukupne Glu pri insulinskoj stimulaciji i Glu se u njih inkorporira i skladišti u vidu glikogena. Glu u ćelije ulazi uz pomoć proteina nosača koji olakšavaju transport Glu kroz ćelijsku membranu i identifikovani su kao glukozni transporteri (GLUT). U ćelijama SM, lokalizovani su GLUT1 i GLUT4. INS stimulisano preuzimanje Glu u mišićnim ćelijama posredovano je translokacijom GLUT4 na površinu ćelijske membrane, dok GLUT1 posreduje u preuzimanju Glu u mišićne ćelije pri bazalnim uslovima. Poremećaji u mehanizmima koji su odgovorni za ovu translokaciju vode insulinskoj rezistenciji. Periferna insulinska resistencija koja uključuje poremećaje transporta Glu u adipocitima i SM, ključni je faktor u patogenezi Diabetesa Mellitusa tipa 2 (DMT2). S obzirom na to da SM preuzimaju najveći deo ukupne Glu, insulinska rezistencija u SM od velikog je značaja za razvoj DMT2 i može se javiti na tri nivoa: na nivou transporta Glu, fosforilacije Glu i na nivou sinteze glikogena. Transport Glu je osnovni korak u preuzimanju Glu u SM pri insulinskoj stimulaciji i ograničavajući je faktor za celokupan metabolizam Glu u organizmu. T2 - Timočki medicinski glasnik T1 - Insulin signaling pathway in skeletal muscles T1 - Signalni put insulina u ćelijama skeletnih mišića VL - 31 IS - 4 SP - 180 EP - 185 UR - https://hdl.handle.net/21.15107/rcub_vinar_10334 ER -
@article{ author = "Sudar, Emina and Velebit, Jelena and Isenović, Esma R.", year = "2006", abstract = "Insulin (INS), the hormone of endocrine pancreas, is one of the most important vertebrate proteins. Increased circulating levels of glucose (Glu) stimulate pancreatic β cells to secrete INS by exocytosis. Insulin receptor (IR) belongs to the group of membrane receptors with tyrosine kinase activity. Skeletal muscles (SM) account for about 85% of total Glu disposal under INS stimulated conditions where it is incorporated and stored as glycogen. Glu entry into cells is a process that requires the involvement of a carrier protein in order to facilitate the movement of Glu across the plasma membrane of a cell and they are identified as glucose transporters (GLUT). In SMs, GLUT1 and GLUT4 are the primary GLUTs expressed. In SMs, INS stimulated Glu disposal is mediated via translocation of GLUT4 from intracellular storage site to the plasma membrane and GLUT1 primary mediates basal, rather than INS mediated Glu uptake. Impairment of the mechanisms responsible for this translocation leads to INS resistance. Peripheral INS resistance is a key factor in the pathogenesis of type 2 Diabetes Mellitus (DMT2) and involves defects in Glu transport system in adipocytes and SM. SM is the principal site of Glu uptake under INS stimulated conditions and INS resistance in SM has been identified as the most important site for INS resistance in DMT2 and may result from a defect at the level of Glu transport, Glu phosphorylation or glycogen synthesis. Glu transport is one of the first steps in INS stimulated Glu uptake in SM and it is a rate limiting factor in the whole Glu metabolism., Insulin (INS) je hormon endokrinog pankreasa i jedan je od najznačajnijih proteina kičmenjaka. Povećana koncentracija glukoze (Glu) u krvi stimuliše β ćelije pankreasa i dovodi do sekrecije INS egzocitozom. Receptor za insulin (IR) pripada grupi membranskih receptora koji poseduju tirozin kinaznu aktivnost. Skeletni mišići (SM) preuzimaju oko 85% ukupne Glu pri insulinskoj stimulaciji i Glu se u njih inkorporira i skladišti u vidu glikogena. Glu u ćelije ulazi uz pomoć proteina nosača koji olakšavaju transport Glu kroz ćelijsku membranu i identifikovani su kao glukozni transporteri (GLUT). U ćelijama SM, lokalizovani su GLUT1 i GLUT4. INS stimulisano preuzimanje Glu u mišićnim ćelijama posredovano je translokacijom GLUT4 na površinu ćelijske membrane, dok GLUT1 posreduje u preuzimanju Glu u mišićne ćelije pri bazalnim uslovima. Poremećaji u mehanizmima koji su odgovorni za ovu translokaciju vode insulinskoj rezistenciji. Periferna insulinska resistencija koja uključuje poremećaje transporta Glu u adipocitima i SM, ključni je faktor u patogenezi Diabetesa Mellitusa tipa 2 (DMT2). S obzirom na to da SM preuzimaju najveći deo ukupne Glu, insulinska rezistencija u SM od velikog je značaja za razvoj DMT2 i može se javiti na tri nivoa: na nivou transporta Glu, fosforilacije Glu i na nivou sinteze glikogena. Transport Glu je osnovni korak u preuzimanju Glu u SM pri insulinskoj stimulaciji i ograničavajući je faktor za celokupan metabolizam Glu u organizmu.", journal = "Timočki medicinski glasnik", title = "Insulin signaling pathway in skeletal muscles, Signalni put insulina u ćelijama skeletnih mišića", volume = "31", number = "4", pages = "180-185", url = "https://hdl.handle.net/21.15107/rcub_vinar_10334" }
Sudar, E., Velebit, J.,& Isenović, E. R.. (2006). Insulin signaling pathway in skeletal muscles. in Timočki medicinski glasnik, 31(4), 180-185. https://hdl.handle.net/21.15107/rcub_vinar_10334
Sudar E, Velebit J, Isenović ER. Insulin signaling pathway in skeletal muscles. in Timočki medicinski glasnik. 2006;31(4):180-185. https://hdl.handle.net/21.15107/rcub_vinar_10334 .
Sudar, Emina, Velebit, Jelena, Isenović, Esma R., "Insulin signaling pathway in skeletal muscles" in Timočki medicinski glasnik, 31, no. 4 (2006):180-185, https://hdl.handle.net/21.15107/rcub_vinar_10334 .