Plasma Adiponectin Levels and Sonographic Phenotypes of Subclinical Carotid Artery Atherosclerosis
- 1 December 2005
- journal article
- clinical trial
- Published by Wolters Kluwer Health in Stroke
- Vol. 36 (12) , 2577-2582
- https://doi.org/10.1161/01.str.0000190834.00284.fd
Abstract
Adipose tissue produces and secretes a number of bioactive molecules, conceptualized as adipocytokines. Adiponectin has been identified as one of the adipocytokines, and hypoadiponectinemia was demonstrated in patients with obesity, diabetes mellitus, and coronary artery disease. Whether decreased adiponectin levels are cause or consequence is an important issue in the discussion on the association between adiponectin and atherosclerosis. In the present study, we investigated the association of plasma adiponectin levels with sonographic phenotypes of subclinical atherosclerosis, which may represent different stages of disease as well as common and distinct determinants. A total of 1515 middle-aged healthy white subjects (940 males and 575 females) were included. Common carotid artery intima-media thickness (CIMT) and presence of atherosclerotic plaques were assessed by B-mode ultrasound. After adjustment for established risk factors, per 1 microg/mL decrease in adiponectin CIMT increased on the average by 3.48 microm in males (95% CI, 1.23 to 5.73 microm) and by 2.39 microm in females (95% CI, 0.50 to 4.27 microm). After dichotomizing adiponectin levels at the median and adjustment for established risk factors, the mean difference of CIMT between subjects with low and high adiponectin levels was 20.42 microm in men (95% CI, 6.80 to 34.04; P=0.003) and 20.75 microm in women (95% CI, 1.08 to 40.42; P=0.039). No significant relationship was found between adiponectin levels and presence of atherosclerotic plaques. Our results demonstrate an independent negative association of adiponectin levels and CIMT, whereas no relationship with presence of atherosclerotic plaques was found, thus suggesting hypoadiponectinemia as a risk factor in the development of early atherosclerosis.Keywords
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