Prolactin receptor gene expression and foetal adipose tissue.
We have investigated the effects of increasing gestational age, maternal undernutrition or restricted placental growth on prolactin receptor (PRLR) gene expression in perirenal adipose tissue collected from foetal sheep during late gestation (term = 147 d +/- 3 d of gestation). Foetal nutrient supply was reduced by either restriction of placental growth following removal of endometrial caruncles before mating or by reducing maternal feed intake by 50% from 115 d of gestation. Total RNA was extracted from adipose tissue taken from foetal sheep between 90 and 145 d of gestation, and only at 141-145 d in placentally restricted, nutrient restricted and control foetuses. Messenger RNAs encoding the long (PRLR1) and short (PRLR2) forms of the PRLR and glyceraldehyde-phosphate-dehydrogenase (GAPDH) were detected and quantified in a ribonuclease protection assay using an antisense RNA probe complementary to ovine PRLR2 and GAPDH. There was a 7.5-fold increase in the amount of perirenal adipose tissue between 90 and 125 d of gestation, compared with a 1.3-fold increase between 125 and 145 d of gestation. The abundance of mRNA encoding PRLR1 and PRLR2 in perirenal adipose tissue increased 10- and sixfold, respectively, between 90 and 125 d of gestation, and then declined by 145 d of gestation. Both placental restriction and maternal undernutrition significantly reduced foetal adipose tissue deposition. The abundance of PRLR1 but not PRLR2 mRNA was reduced in adipose tissue from the placentally restricted group, where as GAPDH mRNA was three times higher than in controls. In contrast, maternal undernutrition from 115 d of gestation did not affect PRLR1, PRLR2 or GAPDH mRNA expression in foetal adipose tissue. It is concluded that during the period of rapid deposition of perirenal adipose tissue, there is a concomitant increase in PRLR gene expression. This indicates that prolactin may play an important role in the growth and maturation of foetal adipose tissue which occurs before birth.
Symonds
M E
ME
Division of Child Health, School of Human Development, University Hospital, Queen's Medical Centre, Nottingham, UK. Michael.Symonds@nottingham.ac.uk
Phillips
I D
ID
Anthony
R V
RV
Owens
J A
JA
McMillen
I C
IC
D000273:Adipose Tissue / Q000196:embryology* / Q000378:metabolism; D000818:Animals; D005260:Female; D005333:Fetus / Q000378:metabolism*; D015870:Gene Expression / Q000502:physiology*; D005865:Gestational Age; D007668:Kidney; D008431:Maternal-Fetal Exchange / Q000502:physiology; D009748:Nutrition Disorders / Q000503:physiopathology; D010920:Placenta / Q000502:physiology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology; D011981:Receptors, Prolactin / Q000235:genetics*; D012756:Sheep / Q000196:embryology
D011981:Receptors, Prolactin