Inflammatory Genes in Epicardial Fat Contiguous With Coronary Atherosclerosis in the Metabolic Syndrome and Type 2 Diabetes: Changes associated with pioglitazone
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...
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Published in | Diabetes care Vol. 34; no. 3; pp. 730 - 733 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Diabetes Association
01.03.2011
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Subjects | |
Online Access | Get full text |
ISSN | 0149-5992 1935-5548 1935-5548 |
DOI | 10.2337/dc10-2083 |
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Summary: | 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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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0149-5992 1935-5548 1935-5548 |
DOI: | 10.2337/dc10-2083 |