title: Leptin and bone turnover in monochorionic twins complicated by twin-twin transfusion syndrome.
abstract: BACKGROUND
  To test the hypothesis that the bone metabolism of a growth-restricted foetus is regulated by genetic, placental and/or foetal factors through leptin, we investigated the foetal bone turnover in monochorionic pregnancies complicated with or without twin-twin transfusion syndrome (TTTS).
  
  
  METHODS
  Maternal and cord bloods were collected from gestational-age-matched monochorionic twins with (n=15) and without (n=15) TTTS. The samples were assayed for leptin, cross-linked carboxyl terminal telo-peptide (ICTP, a marker of bone resorption) and pro-peptide (PICP, a marker of bone formation) of type I collagen by radioimmunoassay (RIA).
  
  
  RESULTS
  In the growth-restricted donor twin, the plasma concentration of leptin (P < 0.001), PICP (P < 0.001) was lower, while that of ICTP (P < 0.001) was higher than the recipient twin of the TTTS group. In contrast, leptin, PICP and ICTP were comparable in non-TTTS twins. In the recipient twin of TTTS and non-TTTS twins, leptin was positively associated with PICP (r=0.73; n=45, P < 0.001) and negatively with ICTP (r=-0.68; n=45; P < 0.001). No such association was found between leptin and bone marker in the growth-restricted donor twin of the TTTS group.
  
  
  CONCLUSIONS
  Our data suggest that, in AGA twins, leptin maintains bone metabolism by inhibiting resorption and enhancing bone formation. In contrast, growth-restricted donor twins have high bone turnover and this does not seem to be due to leptin deficiency.
authors.affiliation: Academic Unit of Obstetrics and Gynaecology, St. Mary's Hospital, Manchester, UK. rbajoria@doctors.net.uk
authors.forename: R
authors.initials: R
authors.lastname: Bajoria
authors.forename: S R
authors.initials: SR
authors.lastname: Sooranna
authors.forename: R
authors.initials: R
authors.lastname: Chatterjee
mesh_terms: D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000097:blood; D001724:Birth Weight / Q000502:physiology; D001862:Bone Resorption / Q000503:physiopathology; D024042:Collagen Type I; D005260:Female; D005312:Fetal Blood / Q000737:chemistry; D005317:Fetal Growth Retardation / Q000503:physiopathology; D005330:Fetofetal Transfusion / Q000503:physiopathology*; D005865:Gestational Age; D006801:Humans; D007231:Infant, Newborn; D020738:Leptin / Q000097:blood / Q000502:physiology*; D010012:Osteogenesis / Q000502:physiology*; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides; D011247:Pregnancy; D011347:Procollagen / Q000097:blood; D014430:Twins, Monozygotic / Q000502:physiology*
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D020738:Leptin; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C042813:procollagen type I carboxy terminal peptide