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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been suggested that children with constitutional growth delay might have a transient immaturity of the neurotransmitter pathways necessary for the control of growth hormone releasing hormone (GHRH) secretion. In this study we evaluated the effects of two consecutive GHRH boluses (1 microgram/kg, i.v.) in nine prepubertal boys with constitutional growth delay. Growth hormone (GH) responses to GHRH administration were similar to that observed in normal children (first GHRH bolus, GH net incremental area under the curve (nAUC) +/- SE: 788 +/- 244 vs 984 +/- 242 ng/ml per hour; second bolus, GHnAUC: 657 +/- 122 vs 541 +/- 129 ng/ml per hour, respectively). These data suggest that no relevant abnormalities in the mechanisms determining the somatotroph sensitivity to GHRH are present in children with constitutional growth delay.
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PMID:Effect of two consecutive administrations of GHRH in children with constitutional growth delay. 197 18

Studies of the maturation of hypothalamic control of adenohypophyseal hormone secretion are reviewed with particular reference to the somato-tropic axis in the ovine fetus. In the ovine fetus, circulating growth hormone concentrations are 20-fold higher than postnatal concentrations falling in the 72 h prior to delivery. These high fetal growth hormone concentrations are postulated to reflect an immaturity of hypothalamic control mechanisms. Synthetic human growth hormone releasing factor (10 micrograms/kg) markedly stimulates fetal circulating growth hormone release between 77 and 135 days of gestation. The response decreases with advancing maturation. Thus fetal growth hormone release is not under maximal stimulation. Fetal growth hormone, thyrotropin and gonadotropin release is pulsatile in nature and the growth hormone and thyrotropin pulses have exaggerated amplitudes compared to the postnatal pattern. It is suggested that in each case, this enhanced pulsatility is a consequence of immature feedback loops. Stereotaxic lesioning of the fetal median eminence at 110 days of gestation abolishes the pulsatility of fetal growth hormone release. However the basal secretion of growth release remains elevated in some fetuses compared to postnatal growth hormone concentrations. The basis for this high basal rate of secretion is speculative but it is postulated to reflect immaturity of inhibitory control mechanisms, in particular of the negative feedback loop. Neuropharmacological studies of circulating growth hormone release in the perinatal period are reviewed. These demonstrate that the potential for many neurotransmitters to influence fetal circulating growth hormone release has differentiated by midgestation. However antagonist studies have not demonstrated a tonic role for any stimulatory neurotransmitters, only for the inhibitory neurotransmitter, GABA. Growth hormone does not exert a major influence upon fetal growth. Studies of the ontogeny of growth hormone receptors in the ovine liver show that somatotropic receptors are first detected in the newborn lamb suggesting receptor immaturity as the basis for this lack of an effect of growth hormone in utero. The two insulin-like growth factors, IGF-I and IGF-II show different patterns of secretion in the perinatal period. IGF-I levels are low in utero, rise gradually through gestation with a marked postnatal rise perhaps related to the development of hepatic growth hormone receptors. IGF-II levels are high in the fetus and fall over the 3 days prior to delivery but are not affected by fetal decapitation. The role of placental lactogen as a stimulus of fetal IGF-II secretion is suggested.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Functional maturation of the neuroendocrine system in the perinatal period: studies of the somatotropic axis in the ovine fetus. 674 30

Changes of growth hormone receptivity in the ovary during the reproductive cycle were studied in rainbow trout (Oncorhynchus mykiss). A method for characterizing growth hormone receptors in crude ovary homogenate was required for this. Binding of radiolabelled recombinant rainbow trout growth hormone (125I-labelled rtGH) to crude ovary preparation was dependent on ovarian tissue concentration. The sites were specific to growth hormone, with no affinity for prolactins and gonadotrophins. Similar high affinities for 125I-labelled rtGH were obtained with crude ovary (4.2 x 10(9) +/- 0.3 mol l-1) and crude liver preparations (4.9 x 10(9) +/- 0.1 mol l-1) at all stages of ovogenesis, and with ovarian membrane preparations (8.2 x 10(9) mol l-1) tested at the beginning of vitellogenesis. Ovarian growth hormone receptor concentration was highest during the early phases of follicular development (endogenous vitellogenesis: 315-310 fmol g-1 ovary) and decreased regularly during oocyte and follicular growth (exogenous vitellogenesis) to reach a minimal value at oocyte maturation (42 fmol g-1 ovary). In postovulated fish, binding was at a similar level (297 fmol g-1 ovary) to that found in endogenous vitellogenesis. Conversely, the absolute binding capacity of the whole ovary was low from immaturity to early exogenous vitellogenesis (0.1-0.6 pmol per pair of gonads), increased slowly during vitellogenesis and more markedly during rapid oocyte growth and at the time of final maturation (10.8 pmol per pair of gonads). In postovulated fish, the absolute binding capacity decreased partially (4.4 pmol per pair of gonads). Mean hepatic growth hormone receptor concentration did not vary with the reproductive stage for most of the cycle (3.0-4.5 pmol g-1 liver) except in endogenous vitellogenesis where significantly higher concentrations were observed (6.7 pmol g-1 liver). Individual ovarian growth hormone receptor concentrations were correlated with hepatic growth hormone receptor concentrations, indicating that they are regulated in a similar way. We conclude that growth hormone receptors are present in the ovary during the entire ovarian cycle in rainbow trout, probably mainly in somatic cells as indicated by the same concentration of binding sites in immature and in postovulated fish. Growth hormone is potentially important during oocyte recruitment in vitellogenesis and initiation of growth and during final follicular maturation.
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PMID:Growth hormone receptors in ovary and liver during gametogenesis in female rainbow trout (Oncorhynchus mykiss). 1043 33