Levels of the adipocyte-derived plasma protein, adiponectin, have a close relationship with atheroma.
BACKGROUND
Inflammation is a key process in atherosclerotic formation. Structural changes in the carotid arterial wall including detection of focal plaques are measured as the intima-media thickness (IMT) providing an index of atheroma. Coronary arterial plaques may be considered as vascular structural changes. Distensibility of the arteries can be assessed by functional changes in pulse wave velocity (PWV) providing an index of sclerosis. Adiponectin has potential antiatherosclerotic properties. We hypothesized that adiponectin was associated with atherosclerotic vascular changes involved in inflammation.


METHODS
We enrolled 142 patients with coronary artery disease (CAD) and 108 control patients, matched for age, sex, and body mass index (BMI) with CAD patients. We investigated the relationship between adiponectin, C-reactive protein (CRP), and atherosclerotic vascular changes.


RESULTS
CRP (p=0.0009), high-density lipoprotein cholesterol (HDL-C; p=0.02), and IMTmax (p=0.02) were determinants of adiponectin independent of glucose intolerance (p=0.0001), BMI (p=0.002), and CAD (p=0.03), all of which have been significantly associated with adiponectin (r=0.38). Adiponectin was not correlated with PWV. CRP, glucose intolerance, and HDL-C that correlated with adiponectin were inversely correlated with IMTmax and CAD. CRP was negatively correlated with HDL-C (r=-0.24, p=0.0002) and positively correlated with glucose intolerance (r=0.15, p=0.01).


CONCLUSIONS
Adiponectin has a close relationship with CRP, IMTmax, CAD, HDL-C, and other established risk factors. CRP, glucose intolerance, and HDL-C are common mediators between adiponectin and atheromatous vascular changes, which are contrary to each other. The exacerbation of atherogenesis may be involved in a decrease of adiponectin through abnormal glyco- and lipid-metabolism by promoting inflammation.
Kojima
Sunao
S
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto City 860-8556, Japan. kojimas@kumamoto-u.ac.jp
Funahashi
Tohru
T
Maruyoshi
Hidetomo
H
Honda
Osamu
O
Sugiyama
Seigo
S
Kawano
Hiroaki
H
Soejima
Hirofumi
H
Miyamoto
Shinzo
S
Hokamaki
Jun
J
Sakamoto
Tomohiro
T
Yoshimura
Michihiro
M
Kitagawa
Akira
A
Matsuzawa
Yuji
Y
Ogawa
Hisao
H
D052242:Adiponectin; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001161:Arteriosclerosis / Q000097:blood* / Q000000981:diagnostic imaging; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D003331:Coronary Vessels / Q000378:metabolism; D016894:Endarterectomy, Carotid / Q000379:methods; D005260:Female; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D012307:Risk Factors; D014463:Ultrasonography / Q000379:methods
D052242:Adiponectin; D036341:Intercellular Signaling Peptides and Proteins; D002097:C-Reactive Protein