) (IGFBP-1–6) ( Clemmons 1997 ). In general, IGFBPs inhibit the actions of IGFs, by competing with the IGF receptors for the peptide. Slowing of fetal growth, as in intrauterine growth restriction (IUGR), probably involves decreased expression of IGFs and
A M Carter, M J Kingston, K K Han, D M Mazzuca, K Nygard and V K M Han
Rupasri Ain, Lindsey N Canham and Michael J Soares
pregnancy. Disruptions in trophoblast development can lead to early pregnancy loss or intrauterine growth restriction (IUGR). These represent serious health problems whose etiologies are not sufficiently understood. Differentiation of trophoblast cells can
Shiao Y Chan, Laura A Hancox, Azucena Martín-Santos, Laurence S Loubière, Merlin N M Walter, Ana-Maria González, Phillip M Cox, Ann Logan, Christopher J McCabe, Jayne A Franklyn and Mark D Kilby
Introduction Intrauterine growth restriction (IUGR) describes the failure of a fetus to attain its genetically determined growth potential, with the most common underlying etiology being uteroplacental failure associated with abnormal placental
S-Y Chan, J A Franklyn, H N Pemberton, J N Bulmer, T J Visser, C J McCabe and M D Kilby
thyroxine (T4) and 3,3′,5-tri-iodothyronine (T3) in neonates with congenital hypothyroidism and absent endogenous thyroid function ( Vulsma et al. 1989 ). Babies born with intrauterine growth restriction (IUGR) are major contributors to perinatal
Cun Li, Thomas J McDonald, Guoyao Wu, Mark J Nijland and Peter W Nathanielsz
appetitive drive postnatally ( Kirk et al . 2009 , Steculorum & Bouret 2011 b , Sarr et al . 2012 ). We have developed a nonhuman primate, baboon model of intrauterine growth restriction (IUGR) to determine the effects of this common pathophysiological
Meredith A Kelleher, Hannah K Palliser, David W Walker and Jonathan J Hirst
Introduction Foetuses that are born small for gestational age due to intrauterine growth restriction (IUGR) are at higher risk for perinatal morbidity, mortality and long-term disability ( Larroque et al . 2001 ). Abnormal foetal growth is
Karine Bibeau, Mélissa Otis, Jean St-Louis, Nicole Gallo-Payet and Michèle Brochu
normal pregnant rats ( Bedard et al . 2005 ). We recently showed that AT 1 R and P450aldo mRNA expression was enhanced in intrauterine growth restriction (IUGR) foetal adrenal glands and was associated with an increase in serum aldosterone levels
EC Houdijk, MJ Engelbregt, C Popp-Snijders and HA Delemarre-Vd Waal
Bilateral uterine artery ligation in late gestation was performed in pregnant dams in order to determine the effects of intrauterine growth retardation (IUGR) on long-term postnatal somatic growth and the GH neuroendocrine axis in the adult female and male rat. Body weight (BW), nose-anus length (NAL) and tail length (TL) were recorded at regular intervals in both the IUGR and control (CON) offspring until the age of 93 days. Spontaneous 6-h GH secretory profiles and serum IGF-I were determined around the age of 100 days in both the IUGR and the CON group. No catch-up growth in BW, NAL or TL was observed in young adult male IUGR rats. Female IUGR rats did catch up in NAL beyond the age of 57 days and in TL before weaning, but did not catch up at any time in BW. Spontaneous 6-h GH secretory profiles in female and male IUGR rats at a mean age of 100+/-4 days were similar to their controls at a mean age of 101+/-4 days. Overall median 6-h rat GH plasma concentrations, rat GH peak amplitude, number of rat GH peaks and sum of peak area were not significantly different. Median serum IGF-I levels in young adult female and male IUGR rats showed no difference when compared with their respective controls. These results demonstrate that IUGR, after bilateral uterine artery ligation in late gestation, leads to incomplete BW catch-up growth in young adult rats of both sexes with physiological GH/IGF-I secretion, suggesting intrauterine modulation of tissue responsiveness to GH and IGF-I. Female IUGR rats do catch up in NAL and TL, developing disturbed body proportions.
D. F. SWAAB, M. VISSER and F. J. H. TILDERS
We have studied whether endogenous α-MSH has a function in stimulating intra-uterine growth in the rat. The approach used was to determine whether or not this hormone is present during the intra-uterine growth spurt, and if binding of endogenous foetal α-MSH by antibodies would inhibit this growth.
Antibodies against α-MSH or ACTH 1-24, either purified or non-purified, induced immunofluorescence in the intermediate lobe of adult male control rats. Using purified anti-α-MSH, fluorescence appeared in the foetal intermediate lobe on day 18 of pregnancy, the day that biologically active MSH was first seen. A negative correlation was observed between the pituitary MSH content and foetal body weight only on day 19 of pregnancy. Injection of purified anti-α-MSH induced a drop in foetal body weight, but no effect on placental weight was observed. Purified anti-ACTH 1-24 had no effect upon body weight but caused an increase in placental weight.
These results support our previous findings and indicate that endogenous MSH has a function in the stimulation of foetal growth.
CT Huizinga, CB Oudejans and HA Delemarre-van de Waal
A reduction in the availability of oxygen and nutrients across the placenta in the last trimester of pregnancy may lead to intrauterine growth retardation (IUGR) which, in turn, may cause a persistent postnatal growth failure. However, it is unknown whether this persistent growth retardation is centrally mediated through alterations in the components of the growth hormone (GH)-axis. We tested the hypothesis that alterations in the development of the central components of the GH-axis contribute to the persistent growth failure observed after experimentally induced IUGR or early postnatal food restriction (FR) in the rat. Using semi-quantitative in situ hybridization, we compared somatostatin (SS), GH-releasing hormone (GHRH) and neuropeptide Y (NPY) mRNA levels in adult rats experimentally subjected to IUGR or FR. We report that IUGR increased the expression of SS mRNA in the periventricular nucleus (PeN) of adult male and female rats by 128% and 153% respectively, did not alter the expression of GHRH mRNA in the arcuate nucleus (ARC) and decreased the NPY mRNA expression in the ARC by 73% in males and 61% in females, whereas in the FR group no changes in the expression of these mRNAs were observed. These data show that the timing of malnutrition or the presence of the placenta is important for the long-term alterations since the effects only occurred in the prenatally induced growth retardation and not in the early postnatally induced growth retardation group.