Cited by 121Cardiovascular Disease and AdiposityAdipokines, Inflammation, and Metabolic DiseasesCardiac Fibrosis and Remodeling

Inflammatory Genes in Epicardial Fat Contiguous With Coronary Atherosclerosis in the Metabolic Syndrome and Type 2 Diabetes

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Sacks, Harold S., Fain, John N., Cheema, Paramjeet, Bahouth, Suleiman W., Garrett, Edward, Wolf, Rodney Y., Wolford, David, Samaha, Joseph·2011·Diabetes Care

Abstract

OBJECTIVE: To determine changes in gene expression in epicardial adipose tissue (EAT) associated with coronary atherosclerosis (CAD) and effects of pioglitazone therapy. RESEARCH DESIGN AND METHODS: Genes were quantified by RT-PCR in EAT and thoracic subcutaneous adipose tissue (SAT) obtained during surgery in CAD patients with metabolic syndrome (MS) or type 2 diabetes and control subjects with minimal or no CAD and no MS or type 2 diabetes. RESULTS: Increased expression of interleukin-1 receptor antagonist (IL-1Ra) and IL-10, a trend for higher IL-1β, and no change in peroxisome proliferator-activated receptor-γ (PPARγ) was found in EAT from MS or type 2 diabetes. Only PPARγ mRNA was reduced in SAT. Pioglitazone therapy in type 2 diabetes was associated with decreased expression of IL-1β, IL-1Ra, and IL-10 in EAT; decreased IL-10 in SAT; and increased PPARγ in SAT. CONCLUSIONS: In MS and type 2 diabetes with CAD, proinflammatory and anti-inflammatory genes were differentially increased in EAT and selectively reduced in association with pioglitazone treatment.

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  • Pioglitazone in CAD patients with T2DM or metabolic syndrome increases PPARγ in SAT and selectively reduces expression of IL-1β, IL-1Ra and IL-10 in EAT, and IL-10 in SAT, irrespective of other clinical variables.

    “The treatment with pioglitazone in CAD patients with T2DM or metabolic syndrome, was shown to increase PPARγ in SAT and to selectively reduce the expression of IL-1β, IL-1Ra and IL-10 in EAT, and of IL-10 in SAT, irrespective of other clinical variables (weight, BMI, waist, fasting blood glucose, A1C, HOMA-IR, ACE inhibitors, angiotensin receptor blockers, statins, aspirin, and metformin) [120].”

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References 16 · Cited by 121

Authors
Sacks, H. S., Fain, J. N., Cheema, P., Bahouth, S. W., Garrett, E., Wolf, R. Y., Wolford, D., & Samaha, J.
Affiliations
  • Baptist Memorial Hospital (US)
  • University of Tennessee Health Science Center (US)
Corresponding author
Sacks, Harold S.
Venue
Diabetes Care
Published
2011-02-17
Volume
34
Issue
3
Pages
730-733
ISSN
  • 0149-5992 (ISSN-L)
  • 1935-5548
OpenAlex
W2098076446
Cited by
121
References
16
Citations by year
2026: 2 · 2025: 6 · 2024: 4 · 2023: 5 · 2022: 12 · 2021: 7 · 2020: 8 · 2019: 8 · 2018: 10 · 2017: 7 · 2016: 6 · 2015: 11 · 2014: 6 · 2013: 17 · 2012: 5
FWCI
7.68
Type
journal article
Language
en
Open access
Locations
  • Diabetes Care (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords
epicardial adipose tissue, coronary artery disease, metabolic syndrome, type 2 diabetes, pioglitazone, interleukin-1 receptor antagonist, IL-1β, IL-10, PPARγ, gene expression, inflammation
MeSH terms
Pioglitazone, Coronary Artery Disease, Diabetes Mellitus, Type 2, Humans, Hypoglycemic Agents, Pericardium, Interleukin-10, Reverse Transcriptase Polymerase Chain Reaction, Metabolic Syndrome, Thiazolidinediones, Interleukin-1beta, Interleukin 1 Receptor Antagonist Protein

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