Expression of the receptor for advanced glycation end products in epicardial fat: Link with tissue thickness and local insulin resistance in coronary artery disease

Elena Dozio, Elena Vianello, Silvia Briganti, John Lamont, Lorenza Tacchini, Gerd Schmitz, Massimiliano Marco Corsi Romanelli

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

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.

Original languageEnglish
Article number2327341
JournalJournal of Diabetes Research
Volume2016
DOIs
Publication statusPublished - 2016

Fingerprint

Insulin Resistance
Adipose Tissue
Coronary Artery Disease
Fats
HMGB1 Protein
Adiposity
Advanced Glycosylation End Product-Specific Receptor
Insulin
Intra-Abdominal Fat
Adiponectin
Adipocytes
Hypertrophy
Thoracic Surgery
Echocardiography
Myocardium
Inflammation

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Expression of the receptor for advanced glycation end products in epicardial fat : Link with tissue thickness and local insulin resistance in coronary artery disease. / Dozio, Elena; Vianello, Elena; Briganti, Silvia; Lamont, John; Tacchini, Lorenza; Schmitz, Gerd; Corsi Romanelli, Massimiliano Marco.

In: Journal of Diabetes Research, Vol. 2016, 2327341, 2016.

Research output: Contribution to journalArticle

@article{295b222fb2304832881b1814caf6e517,
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",
abstract = "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.",
author = "Elena Dozio and Elena Vianello and Silvia Briganti and John Lamont and Lorenza Tacchini and Gerd Schmitz and {Corsi Romanelli}, {Massimiliano Marco}",
year = "2016",
doi = "10.1155/2016/2327341",
language = "English",
volume = "2016",
journal = "Journal of Diabetes Research",
issn = "2314-6745",
publisher = "Hindawi Limited",

}

TY - JOUR

T1 - Expression of the receptor for advanced glycation end products in epicardial fat

T2 - Link with tissue thickness and local insulin resistance in coronary artery disease

AU - Dozio, Elena

AU - Vianello, Elena

AU - Briganti, Silvia

AU - Lamont, John

AU - Tacchini, Lorenza

AU - Schmitz, Gerd

AU - Corsi Romanelli, Massimiliano Marco

PY - 2016

Y1 - 2016

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84953923795&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84953923795&partnerID=8YFLogxK

U2 - 10.1155/2016/2327341

DO - 10.1155/2016/2327341

M3 - Article

AN - SCOPUS:84953923795

VL - 2016

JO - Journal of Diabetes Research

JF - Journal of Diabetes Research

SN - 2314-6745

M1 - 2327341

ER -