title: Quercetin Impacts Expression of Metabolism- and Obesity-Associated Genes in SGBS Adipocytes.
abstract: Obesity is characterized by the rapid expansion of visceral adipose tissue, resulting in a hypoxic environment in adipose tissue which leads to a profound change of gene expression in adipocytes. As a consequence, there is a dysregulation of metabolism and adipokine secretion in adipose tissue leading to the development of systemic inflammation and finally resulting in the onset of metabolic diseases. The flavonoid quercetin as well as other secondary plant metabolites also referred to as phytochemicals have anti-oxidant, anti-inflammatory, and anti-diabetic effects known to be protective in view of obesity-related-diseases. Nevertheless, its underlying molecular mechanism is still obscure and thus the focus of this study was to explore the influence of quercetin on human SGBS (Simpson Golabi Behmel Syndrome) adipocytes' gene expression. We revealed for the first time that quercetin significantly changed expression of adipokine (Angptl4, adipsin, irisin and PAI-1) and glycolysis-involved (ENO2, PFKP and PFKFB4) genes, and that this effect not only antagonized but in part even overcompensated the effect mediated by hypoxia in adipocytes. Thus, these results are explained by the recently proposed hypothesis that the protective effect of quercetin is not solely due to its free radical-scavenging activity but also to a direct effect on mitochondrial processes, and they demonstrate that quercetin might have the potential to counteract the development of obesity-associated complications.
authors.affiliation: Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch A-6800, Austria. andreas.leiherer@vivit.at.|Private University of the Principality of Liechtenstein, Triesen FL-9495, Liechtenstein. andreas.leiherer@vivit.at.|Medical Central Laboratories, Feldkirch A-6800, Austria. andreas.leiherer@vivit.at.
authors.forename: Andreas
authors.initials: A
authors.lastname: Leiherer
authors.affiliation: Private University of the Principality of Liechtenstein, Triesen FL-9495, Liechtenstein. kathrin.stoemmer@gmx.de.
authors.forename: Kathrin
authors.initials: K
authors.lastname: Stoemmer
authors.affiliation: Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch A-6800, Austria. axel.muendlein@vivit.at.|Private University of the Principality of Liechtenstein, Triesen FL-9495, Liechtenstein. axel.muendlein@vivit.at.
authors.forename: Axel
authors.initials: A
authors.lastname: Muendlein
authors.affiliation: Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch A-6800, Austria. christoph.saely@lkhf.at.|Private University of the Principality of Liechtenstein, Triesen FL-9495, Liechtenstein. christoph.saely@lkhf.at.|Department of Medicine and Cardiology, Academic Teaching Hospital Feldkirch, Feldkirch A-6800, Austria. christoph.saely@lkhf.at.
authors.forename: Christoph H
authors.initials: CH
authors.lastname: Saely
authors.affiliation: Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch A-6800, Austria. elena.kinz@vivit.at.|Private University of the Principality of Liechtenstein, Triesen FL-9495, Liechtenstein. elena.kinz@vivit.at.
authors.forename: Elena
authors.initials: E
authors.lastname: Kinz
authors.affiliation: Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch A-6800, Austria. lilli.brandtner@vivit.at.
authors.forename: Eva M
authors.initials: EM
authors.lastname: Brandtner
authors.affiliation: Private University of the Principality of Liechtenstein, Triesen FL-9495, Liechtenstein. pfraunberger@mzl.at.|Medical Central Laboratories, Feldkirch A-6800, Austria. pfraunberger@mzl.at.
authors.forename: Peter
authors.initials: P
authors.lastname: Fraunberger
authors.affiliation: Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch A-6800, Austria. vivit@lkhf.at.|Private University of the Principality of Liechtenstein, Triesen FL-9495, Liechtenstein. vivit@lkhf.at.|Department of Medicine and Cardiology, Academic Teaching Hospital Feldkirch, Feldkirch A-6800, Austria. vivit@lkhf.at.|Drexel University College of Medicine, Philadelphia, PA 19104, USA. vivit@lkhf.at.
authors.forename: Heinz
authors.initials: H
authors.lastname: Drexel
mesh_terms: D017667:Adipocytes / Q000187:drug effects*; D000075803:Angiopoietin-Like Protein 4; D042682:Angiopoietins / Q000235:genetics / Q000378:metabolism; D002460:Cell Line; D005353:Fibronectins / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D006801:Humans; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D009765:Obesity / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism; D025221:Phosphofructokinases / Q000235:genetics / Q000378:metabolism; D010751:Phosphopyruvate Hydratase; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics / Q000378:metabolism; D016133:Polymerase Chain Reaction; D011794:Quercetin / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
chemical_list: C474772:ANGPTL4 protein, human; D000075803:Angiopoietin-Like Protein 4; D042682:Angiopoietins; C577593:FNDC5 protein, human; D005353:Fibronectins; D053583:Interleukin-1beta; D017395:Plasminogen Activator Inhibitor 1; D012333:RNA, Messenger; C051321:SERPINE1 protein, human; D011794:Quercetin; D025221:Phosphofructokinases; D010751:Phosphopyruvate Hydratase; D010100:Oxygen
keywords: 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4; ANGPTL4; CFD; ENO2; FNDC5; IL1B; PAI-1; PFKFB4; PFKP; SERPINE1; adipsin; angiopoietin-like 4; complement factor D; enolase 2; fibronectin type III domain-containing 5; interleukin-1β; irisin; phosopho-fructokinase; phytochemicals; plasminogen activator inhibitor-1; quercetin