scholarly journals 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

2001 ◽  
Vol 168 (2) ◽  
pp. 273-281 ◽  
Author(s):  
CT Huizinga ◽  
CB Oudejans ◽  
HA Delemarre-van de Waal
Keyword(s):  
Growth Hormone ◽  
Neuropeptide Y ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Growth Failure ◽  
Female Rats ◽  
Mrna Levels ◽  
Adult Rats ◽  
Releasing Hormone ◽  
Intrauterine Growth

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.

scholarly journals Decreased galanin mRNA levels in growth hormone-releasing hormone neurons after perinatally induced growth retardation

2001 ◽  
Vol 170 (3) ◽  
pp. 521-528 ◽  
Author(s):  
CT Huizinga ◽  
CB Oudejans ◽  
HA Delemarre-Van de Waal
Keyword(s):  
Growth Hormone ◽  
Growth Retardation ◽  
Adult Stage ◽  
Postnatal Growth ◽  
Hybridization Technique ◽  
Mrna Levels ◽  
Adult Rats ◽  
Double Labeling ◽  
Releasing Hormone ◽  
Gh Secretion

Intrauterine growth retardation (IUGR) is associated with persistent postnatal growth retardation accompanied by dysfunction of the hypothalamic components of the growth hormone (GH) axis. At the adult stage, this is reflected by increased somatostatin (SS) and decreased neuropeptide Y (NPY) mRNA levels, whereas the GH-releasing hormone (GHRH) mRNA levels are normal and the output of GH remains unchanged. To extend our insight into the hypothalamic control of GH secretion in growth retarded rats, we determined galanin (GAL) mRNA levels at the adult stage of perinatally malnourished (i.e. IUGR and early postnatally food restricted) rats. Analyses included comparison of GAL mRNA levels in GHRH neurons in perinatally malnourished adult rats using a semi-quantitative double labeling in situ hybridization technique. We report that IUGR is accompanied by a 60% decrease in GAL mRNA levels in all GHRH neurons in the male IUGR group whereas a tendency towards a decrease was observed in the male early postnatally food restricted (FR) group. These effects became more pronounced when the analysis was restricted to GHRH neurons coexpressing GAL mRNA i.e. decreased GAL mRNA levels were seen in both male and female IUGR rats and in FR males. These data show that GAL mRNA levels in GHRH neurons are persistently decreased after perinatal malnutrition. Taking these results together with our previous data on SS, NPY and GHRH mRNA levels, we can conclude that IUGR leads to a reprogramming of the hypothalamic regulation of GH secretion.

Clinical response to growth hormone in children with intrauterine growth retardation without catch-up growth in Castilla y León (Spain)

2018 ◽  
Vol 65 (10) ◽  
pp. 584-591
Author(s):  
Eduardo Gutiérrez-Abejón ◽  
Eva P. Campo-Ortega ◽  
Pablo Prieto-Matos ◽  
María P. Bahíllo-Curieses ◽  
María T. Breñas-Villalón ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Clinical Response ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Intrauterine Growth ◽  
Castilla Y Leon ◽  
Catch Up

Increased human placental growth hormone at midtrimester pregnancies may be an index of intrauterine growth retardation related to preeclampsia

2006 ◽  
Vol 16 (5-6) ◽  
pp. 290-296 ◽  
Author(s):  
E. Papadopoulou ◽  
S. Sifakis ◽  
E. Giahnakis ◽  
Y. Fragouli ◽  
N. Karkavitsas ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Intrauterine Growth ◽  
Placental Growth Hormone

GROWTH RESPONSES TO HUMAN GROWTH HORMONE IN PATIENTS WITH INTRAUTERINE GROWTH RETARDATION

1975 ◽  
Vol 30 (2) ◽  
pp. 113-114
Author(s):  
THOMAS P. FOLEY ◽  
ROBERT G. THOMPSON ◽  
MAURICE SHAW ◽  
ALICE BAGHDASSARIAN ◽  
S. PETER NISSLEY ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Human Growth Hormone ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Human Growth ◽  
Growth Responses ◽  
Intrauterine Growth

Induction of growth hormone (GH) mRNA by pulsatile GH-releasing hormone in rats is pattern specific

2000 ◽  
Vol 278 (5) ◽  
pp. E885-E891 ◽  
Author(s):  
Russell J. Borski ◽  
Wellington Tsai ◽  
Roberta Demott-Friberg ◽  
Ariel L. Barkan
Keyword(s):  
Growth Hormone ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Somatic Growth ◽  
Pulse Amplitude ◽  
Female Rats ◽  
Mrna Levels ◽  
Female Rat ◽  
Constant Frequency ◽  
Releasing Hormone

Growth hormone-releasing hormone (GHRH) is a main inducer of growth hormone (GH) pulses in most species studied to date. There is no information regarding the pattern of GHRH secretion as a regulator of GH gene expression. We investigated the roles of the parameters of exogenous GHRH administration (frequency, amplitude, and total amount) upon induction of pituitary GH mRNA, GH content, and somatic growth in the female rat. Continuous GHRH infusions were ineffective in altering GH mRNA levels, GH stores, or weight gain. Changing GHRH pulse amplitude between 4, 8, and 16 μg/kg at a constant frequency (Q3.0 h) was only moderately effective in augmenting GH mRNA levels, whereas the 8 μg/kg and 16 μg/kg dosages stimulated weight gain by as much as 60%. When given at a 1.5-h frequency, GHRH doubled the amount of GH mRNA, elevated pituitary GH stores, and stimulated body weight gain. In the rat model, pulsatile but not continuous GHRH administration is effective in inducing pituitary GH mRNA and GH content as well as somatic growth. These studies suggest that the greater growth rate, pituitary mRNA levels, and GH stores seen in male compared with female rats are likely mediated, in part, by the endogenous episodic GHRH secretory pattern present in males.

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