title: Visfatin in human pregnancy: maternal gestational diabetes vis-à-vis neonatal birthweight.
abstract: OBJECTIVE
  Adipose tissue dysfunction, characterized by dysregulation of adipokines production and/or secretion, has been implicated in the pathophysiology of type-2 diabetes mellitus, a metabolic complication closely related to gestational diabetes mellitus (GDM). Recently, an association between circulating maternal visfatin, a novel adipokine with metabolic and immunoregulatory properties, and impaired glucose metabolism as well as with altered fetal growth, has been proposed. The aims of this study were to determine whether there is an association between maternal plasma visfatin concentration, GDM, and a large-for-gestational-age (LGA) newborn.
  
  
  METHODS
  This cross-sectional study, included pregnant women at term in the following groups: 1) normal pregnancy and an appropriate-for-gestational-age (AGA) neonate (n=54); 2) normal pregnancy and an LGA newborn (n=47); 3) GDM and an AGA newborn (n=56); 4) GDM and an LGA newborn (n=45). The study population was further stratified by first trimester BMI (<25 vs. > or =25 kg/m(2)). Maternal plasma visfatin concentration was determined by ELISA. Parametric and non-parametric statistics were used for analysis.
  
  
  RESULTS
  1) Among women who delivered an AGA neonate, the median maternal plasma concentration of visfatin was higher in patients with GDM than in those with a normal pregnancy; 2) Among women with a normal pregnancy, those who delivered an LGA neonate had a higher median maternal plasma visfatin concentration than those who delivered an AGA neonate; 3) among patients with normal BMI, there were no significant differences in the median maternal plasma visfatin concentration between the four study groups; and 4) maternal GDM, as well as delivery of an LGA neonate were independently associated with a higher maternal plasma visfatin concentrations.
  
  
  CONCLUSIONS
  The linkage between increased maternal circulating visfatin and the presence of GDM or delivery of an LGA neonate supports the hypothesis that perturbation of adipokines homeostasis may play a role in the pathophysiology of GDM or excess fetal growth.
authors.affiliation: Perinatology Research Branch, Intramural Division, NICHD/NIH/DHHS, Bethesda, MD, USA.
authors.forename: Shali
authors.initials: S
authors.lastname: Mazaki-Tovi
authors.forename: Roberto
authors.initials: R
authors.lastname: Romero
authors.forename: Juan Pedro
authors.initials: JP
authors.lastname: Kusanovic
authors.forename: Edi
authors.initials: E
authors.lastname: Vaisbuch
authors.forename: Offer
authors.initials: O
authors.lastname: Erez
authors.forename: Nandor Gabor
authors.initials: NG
authors.lastname: Than
authors.forename: Tinnakorn
authors.initials: T
authors.lastname: Chaiworapongsa
authors.forename: Chia-Ling
authors.initials: CL
authors.lastname: Nhan-Chang
authors.forename: Percy
authors.initials: P
authors.lastname: Pacora
authors.forename: Francesca
authors.initials: F
authors.lastname: Gotsch
authors.forename: Lami
authors.initials: L
authors.lastname: Yeo
authors.forename: Sun Kwon
authors.initials: SK
authors.lastname: Kim
authors.forename: Samuel S
authors.initials: SS
authors.lastname: Edwin
authors.forename: Sonia S
authors.initials: SS
authors.lastname: Hassan
authors.forename: Pooja
authors.initials: P
authors.lastname: Mittal
mesh_terms: D000328:Adult; D003430:Cross-Sectional Studies; D016640:Diabetes, Gestational / Q000097:blood*; D005260:Female; D005320:Fetal Macrosomia; D006801:Humans; D007231:Infant, Newborn; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*; D011247:Pregnancy; D055815:Young Adult
chemical_list: D054409:Nicotinamide Phosphoribosyltransferase