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Open AccessArticle

Quercetin Impacts Expression of Metabolism- and Obesity-Associated Genes in SGBS Adipocytes

1
Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch A-6800, Austria
2
Private University of the Principality of Liechtenstein, Triesen FL-9495, Liechtenstein
3
Medical Central Laboratories, Feldkirch A-6800, Austria
4
Department of Medicine and Cardiology, Academic Teaching Hospital Feldkirch, Feldkirch A-6800, Austria
5
Drexel University College of Medicine, Philadelphia, PA 19104, USA
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Nutrients 2016, 8(5), 282; https://doi.org/10.3390/nu8050282
Received: 19 January 2016 / Revised: 4 May 2016 / Accepted: 5 May 2016 / Published: 12 May 2016
(This article belongs to the Special Issue Diet and Metabolic Dysfunction)
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. View Full-Text
Keywords: quercetin; phytochemicals; enolase 2; ENO2; angiopoietin-like 4; ANGPTL4; plasminogen activator inhibitor-1; PAI-1; SERPINE1; phosopho-fructokinase; PFKP; 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4; PFKFB4; complement factor D; adipsin; CFD; fibronectin type III domain-containing 5; irisin; FNDC5; interleukin-1β; IL1B quercetin; phytochemicals; enolase 2; ENO2; angiopoietin-like 4; ANGPTL4; plasminogen activator inhibitor-1; PAI-1; SERPINE1; phosopho-fructokinase; PFKP; 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4; PFKFB4; complement factor D; adipsin; CFD; fibronectin type III domain-containing 5; irisin; FNDC5; interleukin-1β; IL1B
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Leiherer, A.; Stoemmer, K.; Muendlein, A.; Saely, C.H.; Kinz, E.; Brandtner, E.M.; Fraunberger, P.; Drexel, H. Quercetin Impacts Expression of Metabolism- and Obesity-Associated Genes in SGBS Adipocytes. Nutrients 2016, 8, 282.

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