title: Effect of maternal nutrition on brown adipose tissue and its prolactin receptor status in the fetal lamb.
abstract: We investigated the influence of maternal nutritional enhancement during the second half of gestation on prolactin receptor (PRLR) abundance in fetal brown adipose tissue (BAT) and liver close to term (i.e. 141-144 d gestation). Ewes were provided with 100% (i.e. control; n = 8) or 150% (i.e. well-fed; n = 7) of their metabolic requirements from 80 to 144 d gestation. Crude plasma membranes were prepared from fetal BAT and hepatic tissue, and individual molecular weight isoforms for the long and short forms of the PRLR were detected by immunoblotting. Mitochondrial preparations were prepared from BAT to measure the amount of the BAT-specific mitochondrial uncoupling protein-1 and its thermogenic activity (i.e. guanosine 5'-diphosphate binding). Fetuses sampled from well-fed ewes were heavier (controls, 3927 +/- 196 g; well-fed, 4783 +/- 219 g; p = 0.01) but possessed less BAT per kilogram body weight (controls, 5.92 +/- 0.43 g/kg; well-fed, 3.85 +/- 0.19 g/kg; p = 0.001), which had a greater uncoupling protein-1 abundance (controls, 56 +/- 5% of reference; well-fed, 78 +/- 9% of reference; p < 0.01) and higher thermogenic activity (controls, 157 +/- 41 pmol guanosine 5'-diphosphate per milligram mitochondrial protein; well-fed, 352 +/- 36 pmol guanosine 5'-diphosphate per milligram mitochondrial protein; p < 0.01) than controls. Multiple isoforms of the long and short forms of the P1LR were detected in all tissues. BAT from well-fed fetuses had a higher abundance of the 15-kD isoform of the long form of the PRLR (controls, 1.6 +/- 0.4 densitometric units; well-fed, 16.3 +/- 2.0 densitometric units; p < 0.001). This isoform was not detected in hepatic tissue. Maternal nutrient intake had no effect on any other isoforms of the PRLR in BAT or liver. In conclusion, increasing the quantity of feed provided in late gestation acts to promote fetal weight and BAT maturation, the combination of which will enhance neonatal viability.
authors.affiliation: Academic Division of Child Health, School of Human Development, University Hospital, Queen's Medical Centre, Nottingham, United Kingdom.
authors.forename: H
authors.initials: H
authors.lastname: Budge
authors.forename: J
authors.initials: J
authors.lastname: Bispham
authors.forename: J
authors.initials: J
authors.lastname: Dandrea
authors.forename: E
authors.initials: E
authors.lastname: Evans
authors.forename: L
authors.initials: L
authors.lastname: Heasman
authors.forename: P M
authors.initials: PM
authors.lastname: Ingleton
authors.forename: C
authors.initials: C
authors.lastname: Sullivan
authors.forename: V
authors.initials: V
authors.lastname: Wilson
authors.forename: T
authors.initials: T
authors.lastname: Stephenson
authors.forename: M E
authors.initials: ME
authors.lastname: Symonds
mesh_terms: D002001:Adipose Tissue, Brown / Q000378:metabolism*; D000818:Animals; D005260:Female; D008099:Liver / Q000196:embryology / Q000378:metabolism; D009747:Nutritional Physiological Phenomena; D011247:Pregnancy; D020033:Protein Isoforms / Q000378:metabolism*; D011981:Receptors, Prolactin / Q000378:metabolism*; D012756:Sheep / Q000378:metabolism*
chemical_list: D020033:Protein Isoforms; D011981:Receptors, Prolactin