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Association of Adiponectin, Resistin, and Vascular Inflammation Analysis With F-18-Fluorodeoxyglucose Positron Emission Tomography

Authors
Choi, Hae YoonKim, SungeunYang, Sae JeongYoo, Hye JinSeo, Ji A.Kim, Sin GonKim, Nan HeeBaik, Sei HyunChoi, Dong SeopChoi, Kyung Mook
Issue Date
4월-2011
Publisher
LIPPINCOTT WILLIAMS & WILKINS
Keywords
positron emission tomography; adiponectin; inflammation; resistin
Citation
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, v.31, no.4, pp.944 - U471
Indexed
SCIE
SCOPUS
Journal Title
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume
31
Number
4
Start Page
944
End Page
U471
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/112711
DOI
10.1161/ATVBAHA.110.220673
ISSN
1079-5642
Abstract
Objective-Adiponectin and resistin are adipokines that are linked to obesity, inflammation, and atherosclerosis. F-18-Fluorodeoxyglucose (FDG) positron emission tomography is a promising imaging technique that can be used to evaluate vascular inflammation. Methods and Results-We measured adiponectin and resistin levels, as well as traditional cardiovascular risk factors, in 60 obese subjects and 60 nonobese controls. In addition, we compared carotid intima-media thickness and target-to-background ratio (TBR) measured using F-18-fluorodeoxyglucose-positron emission tomography/computed tomography. The mean TBR values were significantly higher in the obese group compared with normal subjects, although their mean carotid intima-media thickness levels were not significantly different. Serum adiponectin levels showed a significant negative correlation with mean TBR values (r = -0.215, P=0.020), whereas resistin levels were positively correlated with mean TBR values (r=0.214, P=0.021). Multiple linear regression analysis showed that mean TBR values were independently associated with body mass index, high-sensitivity C-reactive protein, and resistin levels (R-2=0.308). Conclusion-Adiponectin and resistin may be useful as biomarkers to reflect vascular inflammation. In particular, resistin levels were independently associated with vascular inflammation even after adjusting for other cardiovascular risk factors. (Arterioscler Thromb Vasc Biol. 2011;31:944-949.)
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