dc.creatorVidela Cabrera, Luis
dc.creatorVargas, Romina
dc.creatorRiquelme, Barbara
dc.creatorFernández, Javier
dc.creatorFernández Arancibia, Virginia
dc.date.accessioned2018-08-07T20:11:22Z
dc.date.available2018-08-07T20:11:22Z
dc.date.created2018-08-07T20:11:22Z
dc.date.issued2018
dc.identifierExperimental and Clinical Endocrinology & Diabetes, 126 (3): 182-186, marzo 2018
dc.identifier10.1055/s-0043-115533
dc.identifierhttps://repositorio.uchile.cl/handle/2250/150711
dc.description.abstractThyroid hormone (3,3', 5-triiodothyronine, T-3) accelerates energy metabolism in the liver through mechanisms involving upregulation of AMP-activated protein kinase (AMPK). This study aims to assess the influence of T-3 on the expression of the scaffold proteins beta-Klotho, fibroblast growth factor receptor substrate 2 alpha (FRS2 alpha), and Sestrin2 in relation to FGF21-AMPK signaling. Male Sprague-Dawley rats were given 0.1 mg T-3/kg or hormone vehicle (controls) and studies were done 24 h after treatment. These include measurements of the mRNA expression (qPCR) of hepatic beta-Klotho, FGF21, FGF21 receptor-1 (FGFR1), extracellular-signal-regulated kinase 1/2 (ERK1/2), FRS2 alpha, ribosomal S6 kinase-1 (RSK1), liver kinase B1 (LKB1), AMPK, and Sestrin2. Also, protein levels of FGF21, FGFR1 (ELISA), and ERK1/2 (Western blot) were measured. T-3 elicited a calorigenic response with higher hepatic mRNA expression of beta-Klotho, FRS2 alpha, and FGF21, increased serum FGF21, without changes in liver FGFR1 mRNA and its plasma levels. In addition, T-3 enhanced ERK1/2 phosphorylation and the mRNA expression of ERK1/2, RSK1, LKB1, AMPK, and Sestrin2. T-3 administration enhances liver FGF21-AMPK signaling involving upregulation of the scaffold proteins beta-Klotho, FRS2 alpha, and Sestrin2. beta-Klotho and FRS2 induction favours the operation of the FGF21-FGFR1-beta-Klotho complex as evidenced by the enhancement in ERK1/2 phosphorylation, whereas that of Sestrin2 recruits LKB1 to achieved AMPK activation, thus supporting a higher energy expenditure condition that may be desirable in some metabolic disorders
dc.languageen
dc.publisherJohann Ambrosius Barth Verlag Medizinverlage Heidelberg GMBH
dc.sourceExperimental and Clinical Endocrinology & Diabetes
dc.subjectThyroid hormone
dc.subjectLiver
dc.subjectBeta Klotho
dc.subjectSestrin2
dc.subjectFGF21 AMPK signaling
dc.titleThyroid hormone induced expression of the hepatic scaffold proteins sestrin2, beta Klotho, and FRS2 in relation to FGF21 AMPK signaling
dc.typeArtículo de revista


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