Association of circulating visfatin concentrations with insulin resistance and low-grade inflammation after dietary energy restriction in Spanish obese non-diabetic women: role of body composition changes.
OBJECTIVE
To assess the influence of body composition changes on circulating serum visfatin after following 12 weeks of energy restricted diet intervention. We also examined the possible role of visfatin in glucose metabolism and in obesity-associated low-grade inflammation.


RESULTS
A total of 78 obese (BMI 34.0 ± 2.8 kg/m²) women aged 36.7±7 y volunteered to participate in the study. We measured by DXA body fat mass (FM) and lean mass (LM). Fasting serum visfatin, glucose, insulin, adiponectin, leptin, IL-1β, IL-6, IL-8, TNF-α and CRP concentrations were analyzed before and after the intervention and HOMA and QUIKI indexes were calculated. Mean weight loss 7.7 ± 3.0 kg and HOMA decreased in 24 ± 35%. Serum visfatin concentration change was negatively associated with LM difference (P < 0.05), whereas no significant relationship was observed with FM changes after energy restricted diet intervention. Changes in circulating serum visfatin levels were significantly and inversely associated with HOMA-IR (P < 0.01) and positively with QUICKI index (P < 0.02) after energy restricted diet intervention, regardless of achieved body weight loss. We did not find any significant association between changes in visfatin levels and IL-1β, IL-6, IL-8, TNF-α and CRP levels after dietary intervention (all P > 0.2).


CONCLUSIONS
Circulating visfatin concentration is associated with sensitivity improvement achieved after energy restricted diet intervention induced weight loss. Furthermore, LM changes could be an influencing factor on visfatin concentrations and consequently, on the improvement of insulin sensitivity after weight loss in obese non-diabetic women. Our findings did not provide any evidence for a role of visfatin increase on low-grade inflammation after weight loss.
Agueda
M
M
Department of Nutrition and Food Science, University of the Basque Country, Vitoria, Spain.
Lasa
A
A
Simon
E
E
Ares
R
R
Larrarte
E
E
Labayen
I
I
D015502:Absorptiometry, Photon; D050154:Adiposity; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition; D015992:Body Mass Index; D031204:Caloric Restriction; D016207:Cytokines / Q000097:blood*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000276:immunology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D016014:Linear Models; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*; D009765:Obesity / Q000097:blood / Q000178:diet therapy* / Q000453:epidemiology / Q000276:immunology; D013030:Spain / Q000453:epidemiology; D013997:Time Factors; D016896:Treatment Outcome; D015431:Weight Loss
D001786:Blood Glucose; D016207:Cytokines; D018836:Inflammation Mediators; D007328:Insulin; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human