title: Visfatin in juvenile obesity - the effect of obesity intervention and sex.
abstract: 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).
  
  
  METHODS
  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 < 0·0001), which explained 38% in data variability.
  
  
  CONCLUSIONS
  Central obesity combined with HI/IR contributes to visfatin elevation. Visfatin association with metabolic/biochemical variables is gender dependent. Diet + enhanced physical activity are effective in visfatin reduction, the degree of which depends on baseline visfatin.
authors.affiliation: Department of Medical Biochemistry Department of Endocrinology and Diabetology of Children and Adolescents, Wroclaw Medical University, Wroclaw, Poland. krzystek@bioch.am.wroc.pl
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Krzystek-Korpacka
authors.forename: Eliza
authors.initials: E
authors.lastname: Patryn
authors.forename: Iwona
authors.initials: I
authors.lastname: Bednarz-Misa
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Hotowy
authors.forename: Anna
authors.initials: A
authors.lastname: Noczynska
mesh_terms: D054392:Adipokines / Q000378:metabolism*; D000293:Adolescent; D000367:Age Factors; D015992:Body Mass Index; D016022:Case-Control Studies; D015331:Cohort Studies; D016207:Cytokines / Q000097:blood*; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D020738:Leptin / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood* / Q000150:complications; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*; D009765:Obesity / Q000097:blood* / Q000150:complications; D012737:Sex Factors; D013223:Statistics as Topic; D015431:Weight Loss
chemical_list: D054392:Adipokines; D016207:Cytokines; D020738:Leptin; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human