Tags

Type your tag names separated by a space and hit enter

Human epicardial adipose tissue expresses a pathogenic profile of adipocytokines in patients with cardiovascular disease.
Cardiovasc Diabetol. 2006 Jan 13; 5:1.CD

Abstract

INTRODUCTION

Inflammation contributes to cardiovascular disease and is exacerbated with increased adiposity, particularly omental adiposity; however, the role of epicardial fat is poorly understood.

METHODS

For these studies the expression of inflammatory markers was assessed in epicardial fat biopsies from coronary artery bypass grafting (CABG) patients using quantitative RT-PCR. Further, the effects of chronic medications, including statins, as well as peri-operative glucose, insulin and potassium infusion, on gene expression were also assessed. Circulating resistin, CRP, adiponectin and leptin levels were determined to assess inflammation.

RESULTS

The expression of adiponectin, resistin and other adipocytokine mRNAs were comparable to that in omental fat. Epicardial CD45 expression was significantly higher than control depots (p < 0.01) indicating significant infiltration of macrophages. Statin treated patients showed significantly lower epicardial expression of IL-6 mRNA, in comparison with the control abdominal depots (p < 0.001). The serum profile of CABG patients showed significantly higher levels of both CRP (control: 1.28 +/- 1.57 microg/mL vs CABG: 9.11 +/- 15.7 microg/mL; p < 0.001) and resistin (control: 10.53 +/- 0.81 ng/mL vs CABG: 16.8 +/- 1.69 ng/mL; p < 0.01) and significantly lower levels of adiponectin (control: 29.1 +/- 14.8 microg/mL vs CABG: 11.9 +/- 6.0 microg/mL; p < 0.05) when compared to BMI matched controls.

CONCLUSION

Epicardial and omental fat exhibit a broadly comparable pathogenic mRNA profile, this may arise in part from macrophage infiltration into the epicardial fat. This study highlights that chronic inflammation occurs locally as well as systemically potentially contributing further to the pathogenesis of coronary artery disease.

Authors+Show Affiliations

Unit for Diabetes and Metabolism, Warwick Medical School, University of Warwick, Clinical Sciences Research Institute, UHCW Campus, Coventry, CV2 2DX, UK. a.r.baker@warwick.ac.ukNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16412224

Citation

Baker, Adam R., et al. "Human Epicardial Adipose Tissue Expresses a Pathogenic Profile of Adipocytokines in Patients With Cardiovascular Disease." Cardiovascular Diabetology, vol. 5, 2006, p. 1.
Baker AR, Silva NF, Quinn DW, et al. Human epicardial adipose tissue expresses a pathogenic profile of adipocytokines in patients with cardiovascular disease. Cardiovasc Diabetol. 2006;5:1.
Baker, A. R., Silva, N. F., Quinn, D. W., Harte, A. L., Pagano, D., Bonser, R. S., Kumar, S., & McTernan, P. G. (2006). Human epicardial adipose tissue expresses a pathogenic profile of adipocytokines in patients with cardiovascular disease. Cardiovascular Diabetology, 5, 1.
Baker AR, et al. Human Epicardial Adipose Tissue Expresses a Pathogenic Profile of Adipocytokines in Patients With Cardiovascular Disease. Cardiovasc Diabetol. 2006 Jan 13;5:1. PubMed PMID: 16412224.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Human epicardial adipose tissue expresses a pathogenic profile of adipocytokines in patients with cardiovascular disease. AU - Baker,Adam R, AU - Silva,Nancy F da, AU - Quinn,David W, AU - Harte,Alison L, AU - Pagano,Domenico, AU - Bonser,Robert S, AU - Kumar,Sudhesh, AU - McTernan,Philip G, Y1 - 2006/01/13/ PY - 2005/11/10/received PY - 2006/01/13/accepted PY - 2006/1/18/pubmed PY - 2006/3/25/medline PY - 2006/1/18/entrez SP - 1 EP - 1 JF - Cardiovascular diabetology JO - Cardiovasc Diabetol VL - 5 N2 - INTRODUCTION: Inflammation contributes to cardiovascular disease and is exacerbated with increased adiposity, particularly omental adiposity; however, the role of epicardial fat is poorly understood. METHODS: For these studies the expression of inflammatory markers was assessed in epicardial fat biopsies from coronary artery bypass grafting (CABG) patients using quantitative RT-PCR. Further, the effects of chronic medications, including statins, as well as peri-operative glucose, insulin and potassium infusion, on gene expression were also assessed. Circulating resistin, CRP, adiponectin and leptin levels were determined to assess inflammation. RESULTS: The expression of adiponectin, resistin and other adipocytokine mRNAs were comparable to that in omental fat. Epicardial CD45 expression was significantly higher than control depots (p < 0.01) indicating significant infiltration of macrophages. Statin treated patients showed significantly lower epicardial expression of IL-6 mRNA, in comparison with the control abdominal depots (p < 0.001). The serum profile of CABG patients showed significantly higher levels of both CRP (control: 1.28 +/- 1.57 microg/mL vs CABG: 9.11 +/- 15.7 microg/mL; p < 0.001) and resistin (control: 10.53 +/- 0.81 ng/mL vs CABG: 16.8 +/- 1.69 ng/mL; p < 0.01) and significantly lower levels of adiponectin (control: 29.1 +/- 14.8 microg/mL vs CABG: 11.9 +/- 6.0 microg/mL; p < 0.05) when compared to BMI matched controls. CONCLUSION: Epicardial and omental fat exhibit a broadly comparable pathogenic mRNA profile, this may arise in part from macrophage infiltration into the epicardial fat. This study highlights that chronic inflammation occurs locally as well as systemically potentially contributing further to the pathogenesis of coronary artery disease. SN - 1475-2840 UR - https://www.unboundmedicine.com/medline/citation/16412224/Human_epicardial_adipose_tissue_expresses_a_pathogenic_profile_of_adipocytokines_in_patients_with_cardiovascular_disease_ L2 - https://cardiab.biomedcentral.com/articles/10.1186/1475-2840-5-1 DB - PRIME DP - Unbound Medicine ER -