Visfatin in juvenile obesity - the effect of obesity intervention and sex

• Published in: European journal of clinical investigation 2011-12, Vol.41 (12), p.1284-1291
• Main Authors: Krzystek-Korpacka, Malgorzata, Patryn, Eliza, Bednarz-Misa, Iwona, Hotowy, Katarzyna, Noczynska, Anna
• Format: Article
• Language: English
• Subjects: Adipocytokine; Adipokines - metabolism; Adolescent; Age Factors; Biological and medical sciences; Body Mass Index; Case-Control Studies; Cohort Studies; Cytokines - blood; Female; General aspects; Humans; insulin resistance; Insulin Resistance - physiology; Leptin - blood; Male; Medical sciences; Metabolic diseases; metabolic syndrome; Metabolic Syndrome - blood; Metabolic Syndrome - complications; Miscellaneous; Nicotinamide Phosphoribosyltransferase - blood; Obesity; Obesity - blood; Obesity - complications; Other metabolic disorders; Sex Factors; Statistics as Topic; visfatin; Weight Loss
• ISSN: 0014-2972; 1365-2362
• DOI: 10.1111/j.1365-2362.2011.02538.x

Eur J Clin Invest 2011; 41 (12): 1284–1291 Background  The association of visfatin, an adipocytokine relevant to the development of inflammation and metabolic disorders, with juvenile obesity needs to be re‐established as previously used tests occurred to be nonspecific. Objective  To evaluate visfatin association with a metabolic profile of 88 overweight/obese and 26 lean children/adolescents as well as changes in its levels following weight reduction programme (diet + enhanced physical activity ± metformin). Design  A case–control and cohort study. Results  Visfatin was higher in obese than lean and overweight individuals (2·07 vs. 1·53 and 1·47 ng mL−1, P = 0·034). Of metabolic syndrome components, central obesity combined with either insulin resistance (IR) or hyperinsulinemia (HI) was associated with increases in circulating visfatin. In girls, visfatin correlated with leptin (r = 0·40, P = 0·009) and thiols (r = −0·36, P = 0·009), which explained 24% in visfatin variability. In boys, visfatin correlated with waist circumference (r = 0·36, P = 0·036), BMI% (r = 0·38, P = 0·025), whole body insulin sensitivity index (r = −0·36, P = 0·036), IL‐6 (r = 0·38, P = 0·024) and thiobarbituric acid reactive substances (TBARS) (r = 0·52, P = 0·001), of which IL‐6 and TBARS were independent predictors of visfatin elevation, explaining 42% in data variability. Visfatin was significantly lower following weight reduction programme than at baseline (1·43 vs. 1·83 ng mL−1, P = 0·033). Visfatin reduction correlated neither with changes in metabolic parameters nor was it affected by metformin. ΔVisfatin correlated exclusively with baseline visfatin (r = 0·612, P