title: Prepartum maternal plasma glucose concentrations and placental glucose transporter mRNA expression in cows carrying somatic cell clone fetuses.
abstract: In this study, the plasma glucose concentrations of cows carrying a somatic cell clone fetus during late pregnancy and placental glucose transporter (GLUT) mRNA levels at parturition were examined. Parturition was induced using dexamethasone, prostaglandin F(2α) and estriol in cows bearing a clone (Clone) or a fetus fertilized in vivo as a control (DEX). Plasma glucose concentrations were measured in the cows (days 257 and 271 of pregnancy and at parturition) and newborn calves. Cotyledon and caruncle tissues removed just after parturition were used for mRNA extraction. Expression of mRNA was also analyzed in control cows that were induced to undergo parturition without dexamethasone (PG) or that spontaneously delivered (SP). The glucose concentrations of the Clone group were significantly low at all points examined, but those of the calves were normal. The increase in the maternal glucose concentration from day 257 to parturition was significantly lower in the Clone group. Glucose concentrations were negatively correlated with birth weight for clones (day 257; r=-0.584, day 271; r=-0.286, parturition; r=-0.549). There was no difference in mRNA levels in the cotyledons among the animals examined. In the caruncles, the Clone and PG groups showed significantly higher GLUT1 and GLUT3 mRNA levels than the SP group, and the GLUT3 mRNA level was significantly higher in the Clone group than in the DEX group. The glucocorticoid receptor α mRNA level was significantly lower in the SP group than in the DEX group. Although spontaneous parturition and administration of dexamethasone suppressed the placental GLUT mRNA levels, the action was not observed in clone pregnancy. These results raise the possibility of facilitation of glucose transportation through the placenta to meet increased nutritional requirements of overgrown clone fetuses.
authors.affiliation: Animal Research Center, Hokkaido Research Organization, Hokkaido, Japan. hirayama-hiroki@hro.or.jp
authors.forename: Hiroki
authors.initials: H
authors.lastname: Hirayama
authors.forename: Ken
authors.initials: K
authors.lastname: Sawai
authors.forename: Muneyuki
authors.initials: M
authors.lastname: Hirayama
authors.forename: Tomokazu
authors.initials: T
authors.lastname: Hirai
authors.forename: Soichi
authors.initials: S
authors.lastname: Kageyama
authors.forename: Sadao
authors.initials: S
authors.lastname: Onoe
authors.forename: Akira
authors.initials: A
authors.lastname: Minamihashi
authors.forename: Satoru
authors.initials: S
authors.lastname: Moriyasu
mesh_terms: D000818:Animals; D001724:Birth Weight; D001786:Blood Glucose / Q000032:analysis*; D002417:Cattle; D019976:Cloning, Organism / Q000662:veterinary*; D003907:Dexamethasone / Q000494:pharmacology; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D051246:Glucose Transport Proteins, Facilitative / Q000235:genetics / Q000378:metabolism*; D051272:Glucose Transporter Type 1 / Q000235:genetics / Q000378:metabolism; D051274:Glucose Transporter Type 3 / Q000235:genetics / Q000378:metabolism; D007003:Hypoglycemia; D007751:Labor, Induced / Q000662:veterinary; D053652:Nuclear Transfer Techniques / Q000662:veterinary*; D010120:Oxytocics / Q000494:pharmacology; D010920:Placenta / Q000187:drug effects / Q000378:metabolism*; D011247:Pregnancy; D011257:Pregnancy Proteins / Q000235:genetics / Q000378:metabolism; D011270:Pregnancy, Animal / Q000097:blood* / Q000235:genetics / Q000378:metabolism*; D011965:Receptors, Glucocorticoid / Q000235:genetics / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D051246:Glucose Transport Proteins, Facilitative; D051272:Glucose Transporter Type 1; D051274:Glucose Transporter Type 3; D010120:Oxytocics; D011257:Pregnancy Proteins; D011965:Receptors, Glucocorticoid; C411470:glucocorticoid receptor alpha; D003907:Dexamethasone