Videla LA, Fernández V, Cornejo P, Vargas R, Morales P, Ceballo J, Fischer A, Escudero N, Escobar O. T3-induced liver AMP-activated protein kinase signaling: Redox dependency and upregulation of downstream targets. World J Gastroenterol 2014; 20(46): 17416-17425 [PMID: 25516653 DOI: 10.3748/wjg.v20.i46.17416]
Corresponding Author of This Article
Luis A Videla, Professor, Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Independencia Avenue 1027, Chile. lvidela@med.uchile.cl
Research Domain of This Article
Endocrinology & Metabolism
Article-Type of This Article
Research Report
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Dec 14, 2014; 20(46): 17416-17425 Published online Dec 14, 2014. doi: 10.3748/wjg.v20.i46.17416
T3-induced liver AMP-activated protein kinase signaling: Redox dependency and upregulation of downstream targets
Luis A Videla, Virginia Fernández, Pamela Cornejo, Romina Vargas, Paula Morales, Juan Ceballo, Alvaro Fischer, Nicolás Escudero, Oscar Escobar
Luis A Videla, Virginia Fernández, Pamela Cornejo, Romina Vargas, Paula Morales, Juan Ceballo, Alvaro Fischer, Nicolás Escudero, Oscar Escobar, Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Independencia 1027, Santiago, Chile
Pamela Cornejo, School of Medical Technology, Faculty of Medicine, Diego Portales University, Ejército 141, Santiago, Chile
Author contributions: Videla LA designed the research and wrote the article with the input of Fernández V, Cornejo P and Vargas R; Biochemical and molecular analyses were performed by Vargas R, Morales P, Ceballo J, Fischer A, Escudero N and Escobar O; all authors have approved the final manuscript and declare that there is no conflict in interest that could be perceived as prejudicing the impartiality of the research reported.
Supported by National Commission for Scientific and Technological Research Grant No. 1120034
Correspondence to: Luis A Videla, Professor, Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Independencia Avenue 1027, Chile. lvidela@med.uchile.cl
Telephone: +56-2-29786256 Fax: +56-2-27372783
Received: April 22, 2014 Revised: June 6, 2014 Accepted: July 29, 2014 Published online: December 14, 2014 Processing time: 240 Days and 14 Hours
Core Tip
Core tip: This work investigated the redox dependency and promotion of downstream targets in thyroid hormone (T3)-induced AMP-activated protein kinase (AMPK) signaling. T3 upregulates AMPK with T3-induced reactive oxygen species having a causal role due to its suppression by pretreatment with the antioxidant NAC. Accordingly, AMPK targets acetyl-CoA carboxylase and cyclic AMP response element binding protein are phosphorylated, with the concomitant carnitine palmitoyltransferase-1α activation and higher expression of peroxisome proliferator-activated receptor-γ co-activator-1α and that of the fatty acid oxidation (FAO)-related enzymes. This lead to enhancement in the serum levels of β-hydroxybutyrate, a surrogate marker for hepatic FAO, which represent a key molecular mechanism regulating energy dynamics to limit metabolic stresses.
