Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery Disease

Increased expression of receptor for advanced glycation end products (RAGE) in adipose tissue has been associated with inflammation, adipocyte hypertrophy, and impaired insulin signal. Epicardial adipose tissue (EAT), a visceral fat surrounding the myocardium, is potentially involved in the onset/pr...

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Main Authors: Elena Dozio, Elena Vianello, Silvia Briganti, John Lamont, Lorenza Tacchini, Gerd Schmitz, Massimiliano Marco Corsi Romanelli
Format: Article
Language:English
Published: Wiley 2016-01-01
Series:Journal of Diabetes Research
Online Access:http://dx.doi.org/10.1155/2016/2327341
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author Elena Dozio
Elena Vianello
Silvia Briganti
John Lamont
Lorenza Tacchini
Gerd Schmitz
Massimiliano Marco Corsi Romanelli
author_facet Elena Dozio
Elena Vianello
Silvia Briganti
John Lamont
Lorenza Tacchini
Gerd Schmitz
Massimiliano Marco Corsi Romanelli
author_sort Elena Dozio
collection DOAJ
description Increased expression of receptor for advanced glycation end products (RAGE) in adipose tissue has been associated with inflammation, adipocyte hypertrophy, and impaired insulin signal. Epicardial adipose tissue (EAT), a visceral fat surrounding the myocardium, is potentially involved in the onset/progression of coronary artery disease (CAD). To date, the role of RAGE in EAT has not been explored much. We examined whether the RAGE expression in EAT was associated with EAT adiposity and metabolic dysfunctions normally found in CAD patients. EAT samples were obtained from 33 patients undergoing open-heart surgery. EAT expression of RAGE, GLUT4, adiponenctin, GLO1, HMGB1, TLR-4, and MyD88 was analyzed by microarray. EAT thickness was quantified by echocardiography. Anthropometric measures and clinical parameters were taken. BMI, HOMA-IR, and LAP indices were calculated. With increasing RAGE expression in EAT we observed increases in EAT thickness, reduced expression of GLUT4, adiponectin, and GLO1, and elevations of HMGB1, TLR-4, and MyD88. There were significant correlations between RAGE and EAT thickness and between RAGE and the genes. LAP was higher in patients with increased RAGE expression. Our data suggest that in CAD patients RAGE may be involved in promoting EAT adiposity and metabolic dysfunction, such as impaired insulin signaling.
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spelling doaj-art-aaaf0403a107426baeca692e61b6c8612025-02-03T01:27:33ZengWileyJournal of Diabetes Research2314-67452314-67532016-01-01201610.1155/2016/23273412327341Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery DiseaseElena Dozio0Elena Vianello1Silvia Briganti2John Lamont3Lorenza Tacchini4Gerd Schmitz5Massimiliano Marco Corsi Romanelli6Department of Biomedical Sciences for Health, University of Milan, Via L. Mangiagalli 31, 20133 Milan, ItalyDepartment of Biomedical Sciences for Health, University of Milan, Via L. Mangiagalli 31, 20133 Milan, ItalyDiabetology and Metabolic Disease Unit, I.R.C.C.S. Policlinico San Donato, Piazza E. Malan 1, 20097 San Donato Milanese, ItalyRandox Laboratories Ltd., R&D, 55 Diamond Road, Crumlin, Antrim, Belfast BT29 4QY, UKDepartment of Biomedical Sciences for Health, University of Milan, Via L. Mangiagalli 31, 20133 Milan, ItalyInstitute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, Universitätsstraße 31, 93053 Regensburg, GermanyDepartment of Biomedical Sciences for Health, University of Milan, Via L. Mangiagalli 31, 20133 Milan, ItalyIncreased expression of receptor for advanced glycation end products (RAGE) in adipose tissue has been associated with inflammation, adipocyte hypertrophy, and impaired insulin signal. Epicardial adipose tissue (EAT), a visceral fat surrounding the myocardium, is potentially involved in the onset/progression of coronary artery disease (CAD). To date, the role of RAGE in EAT has not been explored much. We examined whether the RAGE expression in EAT was associated with EAT adiposity and metabolic dysfunctions normally found in CAD patients. EAT samples were obtained from 33 patients undergoing open-heart surgery. EAT expression of RAGE, GLUT4, adiponenctin, GLO1, HMGB1, TLR-4, and MyD88 was analyzed by microarray. EAT thickness was quantified by echocardiography. Anthropometric measures and clinical parameters were taken. BMI, HOMA-IR, and LAP indices were calculated. With increasing RAGE expression in EAT we observed increases in EAT thickness, reduced expression of GLUT4, adiponectin, and GLO1, and elevations of HMGB1, TLR-4, and MyD88. There were significant correlations between RAGE and EAT thickness and between RAGE and the genes. LAP was higher in patients with increased RAGE expression. Our data suggest that in CAD patients RAGE may be involved in promoting EAT adiposity and metabolic dysfunction, such as impaired insulin signaling.http://dx.doi.org/10.1155/2016/2327341
spellingShingle Elena Dozio
Elena Vianello
Silvia Briganti
John Lamont
Lorenza Tacchini
Gerd Schmitz
Massimiliano Marco Corsi Romanelli
Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery Disease
Journal of Diabetes Research
title Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery Disease
title_full Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery Disease
title_fullStr Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery Disease
title_full_unstemmed Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery Disease
title_short Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery Disease
title_sort expression of the receptor for advanced glycation end products in epicardial fat link with tissue thickness and local insulin resistance in coronary artery disease
url http://dx.doi.org/10.1155/2016/2327341
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