Department of Obstetrics and Gynecology, Kurume University School of Medicine, 67 Asahi-machi, Kurume-city, Fukuoka 830-0011, Japan.
Placenta. 2010 May;31(5):358-64. doi: 10.1016/j.placenta.2010.02.013. Epub 2010 Mar 25.
Ghrelin, a peptide hormone produced mainly in the stomach, is an endogenous ligand for the growth hormone secretagogue receptor (GHS-R). The existence of placental ghrelin and its receptor has been confirmed in normal pregnancy. However, few reports have so far referred to placental ghrelin and its receptor in intrauterine growth restriction (IUGR).
The dynamics of ghrelin production and its receptor expression was investigated to clarify the role of placental ghrelin in an IUGR pregnancy using pregnant Dahl salt-sensitive (Dahl S) rats as a model for IUGR.
Pregnant Dahl S rats were fed a high-salt diet to develop hypertensive pregnancy with IUGR (IUGR-preg). The levels of ghrelin peptide in the placenta, stomach and plasma of the dams, together with the expression levels of mRNAs for ghrelin and its functional receptor (GHS-R1a) in the placenta, were measured in the IUGR-preg rats at 2 and 3 weeks of gestation, and compared to those in the control pregnant Dahl S rats fed standard chow (Normal-preg).
The levels of placental ghrelin peptide at 2 weeks of gestation and placental ghrelin mRNA at each gestational week in IUGR-preg were significantly higher than those in Normal-preg. The level of GHS-R1a mRNA in the placenta of IUGR-preg, which was lower at 2 weeks of gestation in comparison to Normal-preg, significantly increased from 2 to 3 weeks of gestation. No significant difference was observed in the level of ghrelin peptide in the plasma or stomach of the dams between the two groups.
The profile of placental ghrelin production and the expression of its receptor using Dhal S rats in the IUGR-preg was different from that in the control. The placental ghrelin-ghrelin receptor system thus continues to work until the term of pregnancy in the IUGR-preg in contrast to Normal-preg, which might act as a compensational mechanism for fetal growth.
胃饥饿素是一种主要在胃中产生的肽激素，是生长激素促分泌素受体（GHS-R）的内源性配体。正常妊娠中已证实胎盘存在胃饥饿素及其受体。然而，迄今为止，关于宫内生长受限（IUGR）中胎盘胃饥饿素及其受体的报道很少。
以宫内生长受限模型（Dahl S 盐敏感大鼠），研究胃饥饿素产生及其受体表达的动态变化，以阐明胎盘胃饥饿素在 IUGR 妊娠中的作用。
用高盐饮食喂养怀孕的 Dahl S 大鼠，使其发生高血压妊娠合并 IUGR（IUGR-preg）。在妊娠 2 和 3 周时，测量 IUGR-preg 大鼠胎盘中胃饥饿素肽的水平、母体血浆中的胃饥饿素水平以及胎盘组织中胃饥饿素和其功能受体（GHS-R1a）的 mRNA 表达水平，并与正常怀孕的 Dahl S 大鼠（Normal-preg）进行比较。
IUGR-preg 大鼠 2 周龄时胎盘中胃饥饿素肽的水平以及每个妊娠周的胎盘胃饥饿素 mRNA 水平均显著高于 Normal-preg。与 Normal-preg 相比，IUGR-preg 大鼠胎盘中 GHS-R1a mRNA 的水平在 2 周时较低，但从 2 周到 3 周时显著增加。两组母体血浆或胃中胃饥饿素肽的水平无显著差异。
与正常妊娠相比，IUGR-preg 中 Dahl S 大鼠胎盘胃饥饿素的产生和受体表达的模式不同。因此，与正常妊娠相反，IUGR-preg 中的胎盘胃饥饿素-胃饥饿素受体系统在妊娠足月时仍继续运作，可能作为胎儿生长的代偿机制。
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