Adiponectin circulating levels and 10-year (2002–2012) cardiovascular disease incidence:the ATTICA Study

Purpose: Adiponectin is an adipokine with anti-inflammatory and cardiovascular-protective properties. Existing epidemiological evidence is conflicting on the exact relationship between adiponectin and long-term cardiovascular disease (CVD) risk. Our aim was to prospectively assess whether circulating adiponectin is associated with long-term incident CVD. Methods: A population-based, prospective study in adults (>18 years) without previous CVD history (ATTICA study). Circulating total adiponectin levels were measured at baseline (2001–2002) in a sub-sample (n = 531; women/men: 222/309; age: 40 ± 11 years) of the ATTICA cohort and complete 10-year follow-up data were available in 366 of these participants (women/men: 154/212; age: 40 ± 12 years). Results: After adjusting for multiple factors, including age, sex, body mass index, waist circumference, smoking, physical activity, Mediterranean diet adherence, hypertension, diabetes, and hypercholesterolemia, our logistic regression analysis indicates that an increase in circulating total adiponectin levels by 1 unit was associated with 36% lower CVD risk (relative risk [RR]: 0.64, 95% confidence interval [CI] 0.42–0.96; p = 0.03). Further adjusting for interleukin-6 plasma levels had no significant impact (RR: 0.60, 95% CI 0.38–0.94; p = 0.03), while additional adjustment for circulating C-reactive protein (CRP) modestly attenuated this association (RR: 0.63, 95% CI 0.40–0.99; p = 0.046). Conclusions: In our study, elevated circulating total adiponectin levels were associated with lower 10-year CVD risk in adults without previous CVD, independently of other established CVD risk factors. This association appeared to be modestly attenuated by CRP, yet was not mediated by interleukin-6 which is the main endocrine/circulating pro-inflammatory cytokine

Effects of smoking cessation on markers of inflammation

Background: Evidence on the association of leptin and adiponectin and smoking is limited and discordant. Leptin and adiponectin represent the most abundant adipokines in human plasma that play crucial roles in the pathophysiology of metabolic syndrome, atherosclerosis and insulin resistance. Leptin up-regulates the expression of several pro-inflammatory cytokines and is increased upon weight gain. Adiponectin has been shown to possess insulin sensitizing, anti -inflammatory and anti-atherogenic properties and is increased upon weight reduction. Our aim was to assess the effects of smoking cessation on serum leptin and adiponectin levels.Methods: We compared subjects who successfully quit smoking with 26 healthy non-smokers. Serum leptin and adiponectin levels, serum CRP and BMI were evaluated at the beginning of the study and at 3, 6 months after smoking cessation. Successful cessation was confirmed by an exhaled carbon monoxide measurement.Results: Among the sample group, 32 subjects had quitted smoking at 3 months and 29 subjects at 6 months. Samples’ leptin increased significantly from baseline to three months (mean change 3.76 ng/ml [95% CI 0.89, 6.64], p =0.012) and then decreased significantly from three to six months of smoking cessation (mean change -4,29ng/ml [95% CI -7.34, -6.64], p=0.078). Samples’ adiponectin increased significantly from baseline to three months of abstinence from smoking (mean change 2.34 [95% CI -0.05, 4.73], p=0.05).BMI was significantly increased (mean change 2.03kg/m² [95% CI 1.60, 2.46], p <0.05), while CRP decreased significantly from baseline to 6 months of smoking cessation (mean change -0.68 mg/dl [95% CI -1.06, - 0.30], p=0.001).Conclusions: Smoking quitters’ leptin levels appear to increase 3 months after smoking cessation and then decrease from 3 to 6 months of abstinence from smoking. Adiponectin levels increase during the first trimester of smoking cessation. The decrease in CRP levels indicates that the low grade inflammation observed in smokers is gradually restored. The alterations of serum leptin and adiponectin after 6 months of smoking cessation suggest the same but do not reach statistically significant levels. Weight gain and changes in fat distribution may attenuate the beneficial effects of smoking cessation.Σκοπός: Τα δεδομένα που αφορούν την συσχέτιση της λεπτίνης και της αδιπονεκτίνης με το κάπνισμα είναι περιορισμένα και συγκρουόμενα. Η λεπτίνη και η αδιπονεκτίνη είναι οι αδιποκίνες που υπάρχουν σε μεγαλύτερη συγκέντρωση στο πλάσμα και κατέχουν σημαντικό ρόλο στην παθοφυσιολογία του μεταβολικού συνδρόμου, της αθηρωμάτωσης και της αντίστασης στην ινσουλίνη. Η λεπτίνη ενισχύει την έκφραση αρκετών κυτταροκινών φλεγμονής και αυξάνεται με την αύξηση του σωματικού βάρους. Η αδιπονεκτίνη έχει αντιφλεγμονώδη δράση και ενισχύει την ευαισθησία στην ινσουλίνη ενώ προστατεύει από την αθηρωματική νόσο. Η συγκέντρωση της αυξάνεται όταν παρατηρηθεί μείωση του σωματικού βάρους. Σκοπός της εργασίας ήταν η μελέτη της επίδρασης της διακοπής καπνίσματος στα επίπεδα λεπτίνης και αδιπονεκτίνης πλάσματος.Μεθοδολογία: Συγκρίναμε ασθενείς που διέκοψαν επιτυχώς το κάπνισμα με 26 υγιείς μη καπνιστές. Τα επίπεδα λεπτίνης και αδιπονεκτίνης καθώς και τα επίπεδα CRP και το BMI μετρήθηκαν κατά την ένταξη στην μελέτη καθώς και 3 και 6 μήνες μετά την διακοπή καπνίσματος. Η επιτυχής διακοπή καπνίσματος επιβεβαιωνόταν με την μέτρηση του εκπνεομένου μονοξειδίου του αζώτου.Αποτελέσματα: Στην ομάδα του δείγματος, 32 άτομα διέκοψαν το κάπνισμα για 3 μήνες και 29 άτομα για 6 μήνες. Η λεπτίνη παρουσίασε σημαντική αύξηση στην ομάδα του δείγματος από την ένταξη μέχρι το τρίμηνο της διακοπής καπνίσματος (mean change 3.76 ng/ml [95% CI 0.89, 6.64], p =0.012) και έπειτα παρουσίασε στατιστικώς σημαντική μείωση από το τρίμηνο μέχρι το εξάμηνο της αποχής από το κάπνισμα (mean change -4,29ng/ml [95% CI -7.34, -6.64], p=0.078). Η αδιπονεκτίνη αυξήθηκε σημαντικά στην ομάδα του δείγματος από την ένταξη μέχρι το τρίμηνο της διακοπής καπνίσματος (mean change 2.34 [95% CI -0.05, 4.73], p=0.05). Το BMI αυξήθηκε σημαντικά (mean change 2.03kg/m² [95% CI 1.60, 2.46], p <0.05), ενώ η CRP παρουσίασε στατιστικώς σημαντική μείωση (mean change -0.68 mg/dl [95% CI -1.06, - 0.30], p=0.001) από την ένταξη μέχρι το εξάμηνο της αποχής από το κάπνισμαΣυμπεράσματα: Τα επίπεδα λεπτίνης πλάσματος αυξάνονται 3 μήνες μετά την διακοπή καπνίσματος και στη συνέχεια μειώνονται από το τρίμηνο μέχρι το εξάμηνο της αποχής από το κάπνισμα. Τα επίπεδα της αδιπονεκτίνης αυξάνονται τρείς μήνες μετά την διακοπή καπνίσματος. Η μείωση των επιπέδων της CRP υποδεικνύει ότι η φλεγμονώδης αντίδραση που παρατηρείται στους καπνιστές αρχίζει σταδιακά να αναστρέφεται. Το ίδιο εισηγούνται και οι μεταβολές της λεπτίνης και της αδιπονεκτίνης στο εξάμηνο της διακοπής καπνίσματος χωρίς όμως να φτάνουν σε στατιστικώς σημαντικά επίπεδα. Η πρόσληψη βάρους και οι μεταβολές στην κατανομή του λιπώδους ιστού ίσως μειώνουν τα οφέλη της διακοπής καπνίσματος

Elevated Tnf-&#945; and Interleukin-6 levels In breath condensate and serum of patients with Non-Cf bronchiectasis comparison to COPD

Intoduction: Exhaled breath condensate (EBC) allows non invasive studies in airway diseases. In bronchiectasis (Br-ect), chronic airway inflammation is an important feature. Methods: To evaluate the levels of TNF- and IL-6 in EBC and serum of patients (pts) with Br-ect and to compare to COPD, we studied 19 bronchiectatic, nonsmoker pts (mean age\ub1sd 59 \ub115y, 12F), 18 COPD pts, ex-smokers (68\ub16.2 y, 3F), and 18 non smoker controls (63\ub16y, 5F). Spirometry was performed and the concentration of the inflammatory markers was determined by enzyme immunoassay (Chayman Chem, USA). Results: Results on the table are expressed as mean (\ub1SD) TNF \u2013 (EBC,pg/ml) TNF- (serum,pg/ml) IL-6 (EBC,pg/ml) IL-6 (serum,pg/ml) FEV1 (%pred) FVC (%pred) FEV1/FVC Bronchiectasis 7.1 (\ub10.1) 14.7(\ub13.1) 5.7(\ub10.3) 18.5(\ub19.0) 65,1\ub127 81.5\ub122 63\ub111 COPD 7.7 (\ub10.3) 15.2 (\ub12.8) 8.1(\ub10.3) 26.4(\ub112.9) 56.3\ub115 75.5\ub118,2 58.7\ub18,6 Controls 6.4 (\ub10.6) 7.2 (\ub11.1) 4.9(\ub10.6) 10.6(\ub13.1) 94\ub15 98\ub16 95 Conclusions :In Br-ect the concentration of TNF- and IL-6 in both EBC and serum was significantly higher than in controls and lower than in COPD (p<0.0001). In Br-ect group, no correlation was found between TNF-, IL-6 levels and the lung function parameters. In COPD group a negative correlation was found between IL-6 in EBC and FEV1/FVC (p=0.02, r=-0.5). In bronchiectasis TNF- and IL-6 may reflect airway inflammation as they are elevated in EBC and serum, compared to healthy controls, but they are lower than in COPD. In COPD, IL-6 in EBC may be related to the disease severity

Effects of smoking cessation on serum leptin and adiponectin levels

Background: Evidence on the association of leptin and adiponectin and smoking is limited and discordant. Leptin and adiponectin represent the most abundant adipokines in human plasma that play crucial roles in the pathophysiology of metabolic syndrome, atherosclerosis and insulin resistance. Leptin up-regulates the expression of several pro-inflammatory cytokines and is increased upon weight gain. Adiponectin has been shown to possess insulin sensitizing, anti -inflammatory and anti-atherogenic properties and is increased upon weight reduction. Our aim was to assess the effects of smoking cessation on serum leptin and adiponectin levels. Methods: We assessed the changes in serum leptin and adiponectin levels, serum CRP levels and BMI in apparently healthy smokers after 3 and 6 months of abstinence from smoking. Successful cessation was confirmed by an exhaled carbon monoxide measurement. 26 healthy non-smokers were recruited as controls. Results: Among the sample group, 32 subjects had quitted smoking at 3 months and 29 subjects at 6 months. Samples' leptin increased significantly from baseline to three months (mean change 3.76 ng/ml [95 % CI 0.89, 6.64], p = 0.012) and then decreased significantly from three to six months of smoking cessation (mean change -4,29 ng/ml [95 % CI -7.34, -6.64], p = 0.008). Samples' adiponectin increased significantly from baseline to three months of abstinence from smoking (mean change 2.34 [95 % CI -0.05, 4.73], p -0.05). BMI was significantly increased (mean change 2.03 kg/m(2) [95 % CI 1.60, 2.46], p < 0.05), while CRP decreased significantly from baseline to 6 months of smoking cessation (mean change -0.68 mg/dl [95 % CI -1.06, -0.30], p = 0.001). Conclusions: Smoking quitters' leptin levels appear to increase 3 months after smoking cessation and then decrease from 3 to 6 months of abstinence from smoking. Adiponectin levels increase during the first trimester of smoking cessation. The decrease in CRP levels indicates that the low grade inflammation observed in smokers is gradually restored. The alterations of serum leptin and adiponectin after 6 months of smoking cessation suggest the same but do not reach statistically significant levels. Weight gain and changes in fat distribution may attenuate the beneficial effects of smoking cessation