Plasma visfatin concentrations after a lifestyle intervention were directly associated with inflammatory markers.
OBJECTIVE
The biological activity and regulation of the novel adipokine visfatin are still largely unknown. Our aim was to evaluate if visfatin plasma concentrations may be influenced by a lifestyle intervention.


RESULTS
Out of 335 dysmetabolic patients from a population-based cohort, randomized to receive a lifestyle intervention program (intervention group) or family physician usual care (controls), 20 patients per group were randomly selected for plasma visfatin determination. The before-after variation (Delta) in visfatin concentration at 1-year from randomization, and the correlations between (Delta)visfatin and intervention-induced changes in waist circumference, fasting glucose, markers of inflammation, and oxidative stress were evaluated. The intervention group showed a significant improvement in waist circumference, and many metabolic/inflammatory variables, while the controls worsened. Visfatin concentrations slightly decreased in the former and significantly increased in the controls ((Delta)visfatin=-2.4 vs 66.0 ng/ml, p<0.001). In robust regression models, the following variables resulted associated with (Delta)visfatin: (Delta)waist circumference, (Delta)fasting glucose, (Delta)hs-CRP (high-sensitivity C-reactive protein) and (Delta)TNFalpha (tumor necrosis factor-alpha). Significant effects on (Delta)visfatin of (Delta)TNFalpha (beta=16.8; 6.1-25.6; p=0.003) and, modified by group, of (Delta)hs-CRP (beta=29.8; 95% CI 15.4-44.2; p<0.001 and beta=4.2; 2.9-5.5; p<0.001 in the control and intervention group, respectively) were detected. By controlling for (Delta)waist, the effects of (Delta)TNFalpha and of (Delta)hs-CRP on (Delta)visfatin by group did not change, while (Delta)waist was no longer associated. The association between (Delta)visfatin and (Delta)glucose was no longer significant, after adjusting for (Delta)hs-CRP.


CONCLUSIONS
Visfatin values increased with waist circumference and were associated with variations of inflammatory markers, suggesting participation in inflammatory mechanisms.
Bo
S
S
Department of Internal Medicine, University of Turin, Corso Dogliotti 14, Turin 10126, Italy. sbo@molinette.piemonte.it
Ciccone
G
G
Baldi
I
I
Gambino
R
R
Mandrile
C
C
Durazzo
M
M
Gentile
L
L
Cassader
M
M
Cavallo-Perin
P
P
Pagano
G
G
D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D016207:Cytokines / Q000097:blood*; D004032:Diet; D015444:Exercise; D005215:Fasting / Q000097:blood; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000503:physiopathology / Q000628:therapy*; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*; D018384:Oxidative Stress; D040242:Risk Reduction Behavior; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D055105:Waist Circumference
D015415:Biomarkers; D001786:Blood Glucose; D016207:Cytokines; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human