Reciprocal Effects of Systemic Inflammation and Brain Natriuretic Peptide on Adiponectin Biosynthesis in Adipose Tissue of Patients With Ischemic Heart Disease

 
δείτε την πρωτότυπη σελίδα τεκμηρίου
στον ιστότοπο του αποθετηρίου του φορέα για περισσότερες πληροφορίες και για να δείτε όλα τα ψηφιακά αρχεία του τεκμηρίου*
κοινοποιήστε το τεκμήριο



Reciprocal Effects of Systemic Inflammation and Brain Natriuretic Peptide on Adiponectin Biosynthesis in Adipose Tissue of Patients With Ischemic Heart Disease

Tousoulis, D.
Psarros, C.
Demosthenous, M.
Coutinho, P.
Margaritis, M.
Neubauer, S.
Lee, R.
Ntusi, N.
Karamitsos, Theodoros
Wordsworth, P. B.
Digby, J.
Channon, K. M.
Antonopoulos, A. S.
Sayeed, R.
Antoniades, C.
Patel, R.
De Silva, R.
Bakogiannis, C.
Petrou, M.

OBJECTIVE: To explore the role of systemic inflammation in the regulation of adiponectin levels in patients with ischemic heart disease. APPROACH AND RESULTS: In a cross-sectional study of 575 subjects, serum adiponectin was compared between healthy subjects, patients with coronary artery disease with no/mild/severe heart failure (HF), and patients with nonischemic HF. Adiponectin expression and release from femoral, subcutaneous and thoracic adipose tissue was determined in 258 additional patients with coronary artery bypass grafting. Responsiveness of the various human adipose tissue depots to interleukin-6, tumor necrosis factor-α, and brain natriuretic peptide (BNP) was examined by using ex vivo models of human fat. The effects of inducible low-grade inflammation were tested by using the model of Salmonella typhi vaccine-induced inflammation in healthy individuals. In the cross-sectional study, HF strikingly increased adiponectin levels. Plasma BNP was the strongest predictor of circulating adiponectin and its release from all adipose tissue depots in patients with coronary artery bypass grafting, even in the absence of HF. Femoral AT was the depot with the least macrophages infiltration and the largest adipocyte cell size and the only responsive to systemic and ex vivo proinflammatory stimulation (effect reversible by BNP). Low-grade inflammation reduced circulating adiponectin levels, while circulating BNP remained unchanged. CONCLUSIONS: This study demonstrates the regional variability in the responsiveness of human adipose tissue to systemic inflammation and suggests that BNP (not systemic inflammation) is the main driver of circulating adiponectin in patients with advanced atherosclerosis even in the absence of HF. Any interpretation of circulating adiponectin as a biomarker should take into account the underlying disease state, background inflammation, and BNP levels. © 2014 American Heart Association, Inc.

Article / Άρθρο
info:eu-repo/semantics/article

Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης (EL)
Aristotle University of Thessaloniki (EN)

Αγγλική γλώσσα

2016-10-11T09:10:39Z
2014


Αριστοτέλειο Πανεπιστήμιο Θεσσαλονίκης, Σχολή Επιστημών Υγείας, Τμήμα Ιατρικής

Arteriosclerosis, Thrombosis, and Vascular Biology, vol.34 no.9 [2014] p.2151-2159
urn:ISSN:1079-5642

This record is part of 'IKEE', the Institutional Repository of Aristotle University of Thessaloniki's Library and Information Centre found at http://ikee.lib.auth.gr. Unless otherwise stated above, the record metadata were created by and belong to Aristotle University of Thessaloniki Library, Greece and are made available to the public under Creative Commons Attribution-ShareAlike 4.0 International license (http://creativecommons.org/licenses/by-sa/4.0). Unless otherwise stated in the record, the content and copyright of files and fulltext documents belong to their respective authors. Out-of-copyright content that was digitized, converted, processed, modified, etc by AUTh Library, is made available to the public under Creative Commons Attribution-ShareAlike 4.0 International license (http://creativecommons.org/licenses/by-sa/4.0). You are kindly requested to make a reference to AUTh Library and the URL of the record containing the resource whenever you make use of this material.
info:eu-repo/semantics/openAccess



*Η εύρυθμη και αδιάλειπτη λειτουργία των διαδικτυακών διευθύνσεων των συλλογών (ψηφιακό αρχείο, καρτέλα τεκμηρίου στο αποθετήριο) είναι αποκλειστική ευθύνη των αντίστοιχων Φορέων περιεχομένου.