title: Omentin-1 is decreased in maternal plasma, placenta and adipose tissue of women with pre-existing obesity.
abstract: OBJECTIVE
  The aim of this study was to determine (i) the effect of maternal obesity and gestational diabetes mellitus (GDM) on (i) the circulating levels of omentin-1 in cord and maternal plasma, and (ii) gene expression and release of omentin-1 from human placenta and adipose tissue. The effect of pregnancy on circulating omentin-1 levels was also determined.
  
  
  METHODS
  Omentin-1 levels were measured in maternal and cord plasma from obese and non-obese normal glucose tolerant women (NGT; n = 44) and women with GDM (n = 39) at the time of term elective Caesarean section. Placenta and adipose tissue expression and release of omentin-1 was measured from 22 NGT and 22 GDM women collected at the time of term elective Caesarean section. Omentin-1 levels were also measured in maternal plasma from 13 NGT women at 11 and 28 weeks gestation and 7 weeks postpartum.
  
  
  RESULTS
  Maternal obesity was associated with significantly lower omentin-1 levels in maternal plasma; however, there was no effect of maternal obesity on cord omentin levels. Omentin-1 gene expression was lower in placenta and adipose tissue obtained from women with pre-existing obesity. In addition to this, adipose tissue release of omentin-1 was significantly lower from obese pregnant women. Omentin-1 levels were significantly lower in non-obese GDM compared to non-obese NGT women. However, there was no difference in omentin-1 levels between obese NGT and obese GDM women. There was no effect of GDM on cord omentin levels, and placental and adipose tissue omentin-1 expression. Maternal omentin-1 levels were negatively correlated with fetal birthweight and fetal ponderal index.
  
  
  CONCLUSIONS
  The data presented in this study demonstrate that pre-existing maternal obesity is associated with lower omentin-1 expression in placenta, adipose tissue and maternal plasma. Alteration in omentin-1 in pregnancy may influence the development of metabolic disorders in offspring later in life.
authors.affiliation: Department of Obstetrics and Gynaecology, University of Melbourne, Victoria, Australia.
authors.forename: Gillian
authors.initials: G
authors.lastname: Barker
authors.forename: Ratana
authors.initials: R
authors.lastname: Lim
authors.forename: Harry M
authors.initials: HM
authors.lastname: Georgiou
authors.forename: Martha
authors.initials: M
authors.lastname: Lappas
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis* / Q000097:blood*; D016640:Diabetes, Gestational / Q000097:blood*; D005260:Female; D058851:GPI-Linked Proteins / Q000096:biosynthesis / Q000097:blood; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007333:Insulin Resistance; D037102:Lectins / Q000096:biosynthesis* / Q000097:blood*; D009765:Obesity / Q000150:complications / Q000378:metabolism*; D010920:Placenta / Q000378:metabolism*; D010949:Plasma / Q000378:metabolism*; D011247:Pregnancy; D011248:Pregnancy Complications; D011262:Pregnancy Trimester, Second; D014018:Tissue Distribution
chemical_list: D001786:Blood Glucose; D016207:Cytokines; D058851:GPI-Linked Proteins; C432397:ITLN1 protein, human; D037102:Lectins