title: Release of inositol phosphoglycan P-type by the human placenta following insulin stimulus: a multiple comparison between preeclampsia, intrauterine growth restriction, and gestational hypertension.
abstract: OBJECTIVE
  Abnormal metabolism of inositol phosphoglycan P-type (P-IPG) has been described in insulin-resistant states. Recently, a definite link between P-IPG and preeclampsia has been reported. P-IPG release after insulin stimulus has been described in the placental tissue of healthy women and a complete absence of P-IPG release has been found in preeclamptic samples, associated with disturbed insulin signaling. This study was undertaken to assess the release of this mediator in intrauterine growth restriction (IUGR) and hypertensive disorders other than preeclampsia.
  
  
  METHODS
  Seven women with IUGR, seven with gestational hypertension, 11 with preeclampsia, and 12 controls were recruited for this study. Fresh placental membranes were prepared and incubated with human recombinant insulin. Bioactivity of P-IPG released after insulin stimulus was assessed using a specific bioassay. A multiple comparison between groups was carried out. The study population provided a statistical power of 0.94.
  
  
  RESULTS
  P-IPG release was highest and lowest from healthy and preeclamptic samples, respectively (p < 0.01). Specimens from patients with IUGR and gestational hypertension released less P-IPG than did controls (p < 0.05).
  
  
  CONCLUSIONS
  Abnormal release of P-IPG from placentas of IUGR and gestational hypertensive mothers seems to confirm an association between these disorders of human pregnancy and insulin resistance.
authors.affiliation: Department of Immunology and Molecular Pathology, Molecular Medicine Unit, Royal Free and University College London Medical School, London, UK. marcoscioscia@gmail.com
authors.forename: Marco
authors.initials: M
authors.lastname: Scioscia
authors.forename: Malcolm A
authors.initials: MA
authors.lastname: Paine
authors.forename: Khalid
authors.initials: K
authors.lastname: Gumaa
authors.forename: Charles H
authors.initials: CH
authors.lastname: Rodeck
authors.forename: Thomas W
authors.initials: TW
authors.lastname: Rademacher
mesh_terms: D000328:Adult; D001724:Birth Weight / Q000502:physiology; D016022:Case-Control Studies; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D046110:Hypertension, Pregnancy-Induced / Q000378:metabolism* / Q000473:pathology; D007231:Infant, Newborn; D007295:Inositol Phosphates / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology*; D009924:Organ Culture Techniques; D010920:Placenta / Q000187:drug effects* / Q000378:metabolism* / Q000473:pathology; D011134:Polysaccharides / Q000378:metabolism*; D011225:Pre-Eclampsia / Q000378:metabolism* / Q000473:pathology; D011247:Pregnancy
chemical_list: D007295:Inositol Phosphates; D007328:Insulin; D011134:Polysaccharides; C028039:inositol phosphate glycan