title: Gastrointestinal hormones (anorexigenic peptide YY and orexigenic ghrelin) influence neural tube development.
abstract: Gastrointestinal (GI) hormones play an important role in GI secretion, motility, and eating behaviors. It was recently suggested that GI hormones may have a trophic role in GI tract. Here we demonstrate that two principal GI hormones, anorexigenic peptide YY (PYY) and orexigenic ghrelin, affect neural tube development. Chronic administration into the pregnant mice or transgenic overexpression of PYY led to a neural tube defect (NTD) in the embryos that was blocked by ghrelin. PYY Y1 receptor antagonist prevented the occurrence of NTD induced not only by PYY but also by vitamin A, a well-known teratogen in humans and animals. Y1 receptor deficiency also engendered NTDs, indicating the need to maintain normal Y1 receptor signaling. The present study is the first linking GI hormones to the leading cause of infant mortality and provides a novel insight for neurogenesis in which materno-fetal communication through GI hormones appears to be important.
authors.affiliation: Division of Diabetes, Digestive and Kidney Diseases, Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Hideki
authors.initials: H
authors.lastname: Yuzuriha
authors.forename: Akio
authors.initials: A
authors.lastname: Inui
authors.forename: Akihiro
authors.initials: A
authors.lastname: Asakawa
authors.forename: Naohiko
authors.initials: N
authors.lastname: Ueno
authors.forename: Masato
authors.initials: M
authors.lastname: Kasuga
authors.forename: Michael M
authors.initials: MM
authors.lastname: Meguid
authors.forename: Jun-ichi
authors.initials: J
authors.lastname: Miyazaki
authors.forename: Maiko
authors.initials: M
authors.lastname: Ninomiya
authors.forename: Herbert
authors.initials: H
authors.lastname: Herzog
authors.forename: Mineko
authors.initials: M
authors.lastname: Fujimiya
mesh_terms: D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000627:therapeutic use; D001921:Brain / Q000002:abnormalities / Q000196:embryology; D001923:Brain Chemistry; D003510:Cyclohexanes / Q000627:therapeutic use; D004435:Eating / Q000187:drug effects; D005260:Female; D005492:Folic Acid / Q000627:therapeutic use; D005804:Genes, Lethal; D005813:Genes, Synthetic; D054439:Ghrelin; D008431:Maternal-Fetal Exchange; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009436:Neural Tube Defects / Q000139:chemically induced* / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D009478:Neuropeptide Y / Q000494:pharmacology; D010191:Pancreatic Polypeptide / Q000633:toxicity; D010446:Peptide Fragments / Q000494:pharmacology; D036361:Peptide Hormones / Q000097:blood / Q000502:physiology* / Q000627:therapeutic use; D019894:Peptide YY / Q000097:blood / Q000235:genetics / Q000502:physiology / Q000633:toxicity*; D011247:Pregnancy; D017476:Receptors, Neuropeptide Y / Q000037:antagonists & inhibitors / Q000235:genetics / Q000502:physiology*; D011993:Recombinant Fusion Proteins / Q000009:adverse effects; D013723:Teratogens / Q000633:toxicity; D014801:Vitamin A / Q000633:toxicity; D014966:Xanthenes / Q000627:therapeutic use
chemical_list: D003510:Cyclohexanes; D054439:Ghrelin; C410588:L 152804; D009478:Neuropeptide Y; D010446:Peptide Fragments; D036361:Peptide Hormones; D017476:Receptors, Neuropeptide Y; D011993:Recombinant Fusion Proteins; D013723:Teratogens; D014966:Xanthenes; C062924:neuropeptide Y (13-36); C097212:neuropeptide Y-Y1 receptor; D019894:Peptide YY; D014801:Vitamin A; D010191:Pancreatic Polypeptide; D005492:Folic Acid; D001120:Arginine; C117416:BIBO 3304; C514549:peptide YY (1-36)