Persistent changes in somatostatin and neuropeptide Y mRNA levels but not in growth hormone-releasing hormone mRNA levels in adult rats after intrauterine growth retardation

Citation
Ct. Huizinga et al., Persistent changes in somatostatin and neuropeptide Y mRNA levels but not in growth hormone-releasing hormone mRNA levels in adult rats after intrauterine growth retardation, J ENDOCR, 168(2), 2001, pp. 273-281
Citations number
36
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF ENDOCRINOLOGY
ISSN journal
00220795 → ACNP
Volume
168
Issue
2
Year of publication
2001
Pages
273 - 281
Database
ISI
SICI code
0022-0795(200102)168:2<273:PCISAN>2.0.ZU;2-4
Abstract
A reduction in the availability of oxygen and nutrients across the placenta in the last trimester of pregnancy may lead to intrauterine growth retarda tion (IUGR) which, in turn, may cause a persistent postnatal growth failure . However, it is unknown whether this persistent growth retardation is cent rally 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 f ailure observed after experimentally induced IUGR or early postnatal food r estriction (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 periventricu lar nucleus (PeN) of adult male and female rats by 128% and 153% respective ly, 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 mRN As were observed. These data show that the timing of malnutrition or the pr esence 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.