Smoking induces lipoprotein-associated phospholipase A(2) in cardiovascular disease free adults: The ATTICA Study

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Μικρογραφία εικόνας

Ημερομηνία

Συγγραφείς

Tselepis, A. D.
Panagiotakos, D. B.
Pitsavos, C.
Tellis, C. C.
Chrysohoou, C.
Stefanadis, C.

Τίτλος Εφημερίδας

Περιοδικό ISSN

Τίτλος τόμου

Εκδότης

Elsevier Ireland

Περίληψη

Τύπος

Είδος δημοσίευσης σε συνέδριο

Είδος περιοδικού

peer reviewed

Είδος εκπαιδευτικού υλικού

Όνομα συνεδρίου

Όνομα περιοδικού

Atherosclerosis

Όνομα βιβλίου

Σειρά βιβλίου

Έκδοση βιβλίου

Συμπληρωματικός/δευτερεύων τίτλος

Περιγραφή

Objectives: We studied the association of lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) mass and activity with various lifestyle, clinical and biochemical characteristics in cardiovascular disease (CVD) free adults. Background: Lipoprotein-associated phospholipase A(2) is a novel biomarker of inflammation and risk for CVD. The Lp-PLA(2) mass and activity are primarily influenced by the plasma levels of low-density lipoprotein (LDL), however, the influence of various lifestyle characteristics on Lp-PLA(2) have not been adequately studied. Methods and results: In a random sub-sample of 186 subjects, 64 men (52 +/- 13 years) and 122 women (48 +/- 13 years) from the ATTICA Study (Greece), LP-PLA(2) activity and mass in total plasma as well as the enzyme activity and mass associated with high-density lipoprotein (HDL-Lp-PLA(2)) were determined using established methods. Several socio-demographic, lifestyle, clinical and biochemical parameters were assessed in all participants. Multiple linear regression analysis revealed that among the lifestyle characteristics, total plasma Lp-PLA(2) activity and mass were positively and independently associated with current smoking (p = 0.02 and p = 0.05, respectively), as well as with exposure to second-hand smoke (p = 0.02 and p = 0.01, respectively). Furthermore, HDL-Lp-PLA(2) activity and mass were inversely and independently associated with current smoking (p = 0.04 and p = 0.09, respectively). Conclusions: Smoking is associated with and might even induce an increase in proatherogenic total plasma Lp-PLA(2), but attenuates antiatherogenic HDL-Lp-PLA(2). These results further support the role of smoking as an important avoidable cause of CVD. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

Περιγραφή

Λέξεις-κλειδιά

atherosclerosis, cardiovascular disease, inflammation, lp-pla(2), smoking, platelet-activating-factor, factor-acetylhydrolase activity, cigarette-smoking, human plasma, secondhand smoke, blood-plasma, risk-factors, dense ldl, paf-ah, inflammation

Θεματική κατηγορία

Παραπομπή

Σύνδεσμος

<Go to ISI>://000270002000049
http://ac.els-cdn.com/S0021915009001439/1-s2.0-S0021915009001439-main.pdf?_tid=3bf49dc78a0db9dfb8b07ae5006969d4&acdnat=1333112226_2b43b2a8e83fd64b217007232e3daec5

Γλώσσα

en

Εκδίδον τμήμα/τομέας

Όνομα επιβλέποντος

Εξεταστική επιτροπή

Γενική Περιγραφή / Σχόλια

Ίδρυμα και Σχολή/Τμήμα του υποβάλλοντος

Πανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείας

Πίνακας περιεχομένων

Χορηγός

Βιβλιογραφική αναφορά

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