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Učinek sulfasalazina na inzulinsko signalno pot v skeletni mišici = The effect of sulfasalazine on the insulin signalling pathway in skeletal muscleVidović, AnjaUvod: Skeletne mišice so pomembno tarčno tkivo pri zdravljenju sladkorne bolezni tipa 2, saj predstavljajo glavno mesto z inzulinom stimuliranega privzema glukoze v postprandialnem stanju. Pri ... preučevanju delovanja signalnih poti, ki vplivajo na inzulinsko rezistenco, lahko izhajamo iz salicilne kisline. Njeni derivati imajo poleg protivnetnih učinkov, ugodne učinke na delovanje inzulina in presnovo glukoze, tudi zaradi aktivacije z AMP-aktivirane protein kinaze. Namen: Sulfasalazin je predzdravilo iz 5-aminosalicilne kisline in sulfapiridina. Klinični primeri in živalski modeli so nakazali, da bi lahko vplival na koncentracijo glukoze ter zaviral nastanek zapletov sladkorne bolezni. Ker njegov mehanizem na molekularni ravni pri diabetesu ni raziskan, smo želeli ugotoviti, ali učinkuje na inzulinsko signalno pot prek kinaze Akt. Hipoteze: 1) Sulfasalazin poveča bazalno in z inzulinom ali rastnim dejavnikom iz trombocitov (PDGF) spodbujeno fosforilacijo kinaze Akt. 2) Sulfasalazin poveča bazalno in z inzulinom ali s PDGF spodbujeno fosforilacijo AS160. 3) Sulfasalazin ne vpliva na z inzulinom ali s PDGF spodbujeno fosforilacijo kinaze ERK1/2. Metode: Učinke sulfasalazina na znotrajcelično signalizacijo smo preučili na in vitro modelu linije podganjih skeletnomišičnih celic L6. Aktivnost signalnih poti smo ovrednotili z merjenjem fosforilacije proteinov: Akt (Ser473), AS160 (Ser588), ERK1/2 (Thr202/Tyr204), 4E-BP1 (Thr37/Thr46) in acetil-CoA karboksilaze (Ser79). Uporabili smo metodo gelske elektroforeze, metodo prenosa western in zaznali proteine z metodo ojačane kemiluminiscence. Rezultati: Sulfasalazin je zmanjšal z inzulinom spodbujeno fosforilacijo Akt, ni pa vplival na bazalno niti s PDGF spodbujeno fosforilacijo Akt. Sulfasalazin je inhibiral fosforilacijo AS160, tudi ob prisotnosti inzulina ali PDGF. S tem smo zavrgli prvo in drugo hipotezo. Sulfasalazin je zmanjšal s PDGF spodbujeno fosforilacijo ERK1/2, s čimer smo delno podprli tretjo hipotezo. Zaključki: Ugotovili smo, da sulfasalazin zavira z inzulinom in s PDGF spodbujeno fosforilacijo AS160. Kljub temu da naj bi sulfasalazin deloval kot farmakološki aktivator z AMP-aktivirane protein kinaze, predvidevamo, da do translokacije GLUT4 na površino mišičnih celic ne bi prišlo, saj je fosforilacija AS160 pri tem ključen dogodek. Potrebne bi bile dodatne raziskave, s katerimi bi ugotovili, zakaj sulfasalazin zmanjšuje fosforilacijo AS160.Type of material - master's thesis ; adult, seriousPublication and manufacture - Ljubljana : [A. Vidović], 2019Language - slovenianCOBISS.SI-ID - 4778097
Author
Vidović, Anja
Other authors
Pirkmajer, Sergej |
Miš, Katarina
Topics
Sladkorna bolezen tipa 2 |
Insulin |
Zdravljenje |
sulfasalazin |
inzulin |
PDGF |
skeletna mišica |
rastni dejavnik iz trombocitov
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Library/institution |
City | Acronym | For loan | Other holdings |
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Faculty of Pharmacy, Ljubljana | Ljubljana | FFALJ |
reading room 1 cop.
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Year | Impact factor | Edition | Category | Classification | ||||
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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DRS, in which the journal is indexed
Database name | Field | Year |
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Links to authors' personal bibliographies | Links to information on researchers in the SICRIS system |
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Vidović, Anja | 53470 |
Pirkmajer, Sergej | 28351 |
Miš, Katarina | 19318 |
Source: Personal bibliographies
and: SICRIS
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