title: Levels of the adipocyte-derived plasma protein, adiponectin, have a close relationship with atheroma.
abstract: 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.
authors.affiliation: 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
authors.forename: Sunao
authors.initials: S
authors.lastname: Kojima
authors.forename: Tohru
authors.initials: T
authors.lastname: Funahashi
authors.forename: Hidetomo
authors.initials: H
authors.lastname: Maruyoshi
authors.forename: Osamu
authors.initials: O
authors.lastname: Honda
authors.forename: Seigo
authors.initials: S
authors.lastname: Sugiyama
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Kawano
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Soejima
authors.forename: Shinzo
authors.initials: S
authors.lastname: Miyamoto
authors.forename: Jun
authors.initials: J
authors.lastname: Hokamaki
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Michihiro
authors.initials: M
authors.lastname: Yoshimura
authors.forename: Akira
authors.initials: A
authors.lastname: Kitagawa
authors.forename: Yuji
authors.initials: Y
authors.lastname: Matsuzawa
authors.forename: Hisao
authors.initials: H
authors.lastname: Ogawa
mesh_terms: 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
chemical_list: D052242:Adiponectin; D036341:Intercellular Signaling Peptides and Proteins; D002097:C-Reactive Protein