Inositol phosphoglycan P-type in healthy and preeclamptic pregnancies

• Published in: Journal of reproductive immunology Vol. 76; no. 1; pp. 85 - 90
• Main Authors: Scioscia, Marco, Gumaa, Khalid, Whitten, Melissa, Selvaggi, Luigi E, Rodeck, Charles H, Rademacher, Thomas W
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Shannon Elsevier Ireland Ltd 01.12.2007; Elsevier Science
• Subjects: Amniotic fluid; Amniotic Fluid - metabolism; Biological and medical sciences; Danger theory; Embryology: invertebrates and vertebrates. Teratology; Female; Fetal Blood - metabolism; Fetal urine; Fetus - metabolism; Fundamental and applied biological sciences. Psychology; Humans; Inositol Phosphates - blood; Inositol Phosphates - metabolism; Inositol Phosphates - urine; Inositol phosphoglycan; Insulin - metabolism; Insulin Resistance; Obstetrics and Gynecology; Placenta - metabolism; Polysaccharides - blood; Polysaccharides - metabolism; Polysaccharides - urine; Pre-Eclampsia - blood; Pre-Eclampsia - metabolism; Pre-Eclampsia - urine; Preeclampsia; Pregnancy; Insulin resistance; Inositol phosphoglycan; Fetal urine; Danger theory; Preeclampsia; Amniotic fluid; Endocrinopathy; Urine; Biological fluid; Inositol; Pregnancy disorders; Hepatoprotector; Theory; B-Vitamins; Pregnancy toxemia; Pregnancy; Target tissue resistance; Vertebrata; Mammalia; Fetus
• ISSN: 0165-0378; 1872-7603
• DOI: 10.1016/j.jri.2007.03.016

Abstract An association between inositol phosphoglycan P-type (P-IPG) and preeclampsia has been demonstrated over recent years. This molecule can mediate many of the metabolic and growth promoting effects of insulin. Dysregulation of the mediator family is associated with insulin resistance. An increased concentration of P-IPG has been reported in preeclamptic placenta, although its precursor (GPI) was undetectable in those placental samples. Insulin administration, that induces P-IPG release in normal human placenta, was shown not to cause production/release of the mediator from preeclamptic placental tissue as a consequence of a disturbed insulin signalling. Amniotic fluid is enriched of this mediator, with further increase during preeclampsia. We have found that the fetus released increasing amounts of P-IPG in the urine between 13 and 18 weeks of gestation, reaching a plateau beyond 20 weeks. Cord blood of infants of preeclamptic mothers showed an increased content of soluble P-IPG compared to controls and to the mother.