Is pentraxin 3 involved in obesity-induced decrease in arterial distensibility?
OBJECTIVE
Obesity is a strong risk factor for cardiovascular morbidity and mortality. In addition, decreased central arterial distensibility is recognized as an independent risk factor for cardiovascular disease (CVD). Obese subjects exhibit low arterial distensibillity; however, the mechanism responsible for the decrease in arterial distensibility in obese subjects has not yet been elucidated. Pentraxin 3 (PTX3), a recently identified member of the pentraxin family of proteins, is produced in areas of atherosclerosis. A recent study has revealed that the PTX3 level may indicate the vascular inflammatory status. The aim of this study was to investigate plasma PTX3 concentrations and arterial distensibility in obese subjects.


METHODS
Eleven obese men (age: 44+/-2 years, body mass index [BMI]: 32+/-1 kg/m(2)) and 14 nonobese men (age: 42+/-2 years, BMI: 26+/-1 kg/m(2)) participated in this study. We measured arterial compliance (using simultaneous B-mode ultrasound and arterial applanation tonometry of the common carotid artery); beta-stiffness index, an index of arterial compliance adjusted for distending pressure; and plasma PTX3 concentrations.


RESULTS
Arterial compliance was significantly lower and the beta-stiffness index was significantly higher in obese men than in non-obese men. Plasma PTX3 concentration was markedly higher in obese than non-obese men.


CONCLUSIONS
Obese men have lower arterial distensibility and higher circulating PTX3 levels than non-obese men; therefore, higher PTX3 levels and decreased arterial distensibility coexist in obese men. The high PTX3 concentrations in obese men may be involved in the mechanism underlying the obesity-induced decrease in arterial distensibility.
Division of Sports Medicine, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Asako
A
Miyaki
Seiji
S
Maeda
Mutsuko
M
Yoshizawa
Maiko
M
Misono
Hiroyuki
H
Sasai
Nobutake
N
Shimojo
Kiyoji
K
Tanaka
Ryuichi
R
Ajisaka
D000328:Adult; D001158:Arteries / Q000473:pathology; D050197:Atherosclerosis / Q000175:diagnosis / Q000378:metabolism; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000096:biosynthesis* / Q000502:physiology*; D002339:Carotid Arteries / Q000473:pathology; D006801:Humans; D007249:Inflammation; D008297:Male; D008365:Manometry / Q000379:methods; D008875:Middle Aged; D008954:Models, Biological; D009765:Obesity / Q000097:blood* / Q000175:diagnosis; D012307:Risk Factors; D000683:Serum Amyloid P-Component / Q000096:biosynthesis* / Q000502:physiology*; D014463:Ultrasonography / Q000379:methods; D000099153:Pentraxins
D002097:C-Reactive Protein; D000683:Serum Amyloid P-Component; D000099153:Pentraxins