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

In the mature rat, subcutaneous administration of insulin (0.02 IU/g body wt.) produced hypoglycemia and a profound activation of the sympatho-adrenal pathway, as indicated by a marked depletion of adrenal catecholamines. Cellular glucopenia caused by administration of 2-deoxyglucose also produced a sympatho-adrenal response. In contrast, in 2-day-old rats, the systemic injection of insulin evoked only a small depletion of catecholamines even though severe hypoglycemia was present, and 2-deoxyglucose also produced a diminished response. The central administration of insulin at an equivalent dose (0.02 IU/g brain) stimulated brain ornithine decarboxylase activity in both neonates and adults, but was ineffective in evoking hypoglycemia or adrenal catecholamine release. These results suggest that: (a) direct interaction of insulin with its receptors in the central nervous system is not required for activation of the sympatho-adrenal pathway, and (b) the lack of sensitivity of neonatal adrenal catecholamine release to subcutaneous administration of insulin is likely associated with immaturity of splanchnic neurotransmission rather than with absence of central insulin receptors or impaired peripheral responsiveness to insulin.
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PMID:Central and sympatho-adrenal responses to insulin in adult and neonatal rats. 331 47

To study the mechanism of imparied insulin secretion from rat fetal islets, the insulin responsiveness of islets from fetuses (day 21.5 of gestation) to a variety of secretagogues was compared with that of adult rat islets. Forskolin (30 microM)-induced insulin release from fetal and adult islets was 2.7-and 2.5-fold higher, respectively, than that from islets treated with 5.6 mM glucose alone. The effects of 12-O-tetradecanoyl phorbol-13-acetate (TPA) (200 nM) were also similar in fetal and adult islets. Thus, the responsiveness to forskolin and TPA showed no significant difference in adult and fetal islets. A synergistic effect of combinations of various insulin secretagogues was observed in adult islets; however, a weak synergistic effect was present with gliclazide plus TPA only in fetal islets. After islets were cultured in RPMI 1640 (containing 11.1 mM glucose), gliclazide-, forskolin-, and TPA-induced insulin release reached the levels obtained in adult islets. However, the synergistic effect of gliclazide and TPA disappeared after culture of the islets. These results suggest that the poor insulin secretion from fetal islets is not due to a defect in the activating system of either cAMP or C-kinase, but to the immaturity of the interaction of those messenger systems.
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PMID:Rat fetal islets as a useful model for the study of insulin release failure. 332 83

The birth and fate of 818 lambs born to 571 ewes on a low-ground farm in the Scottish Borders with a history of substantial perinatal mortality were monitored with a range of physiological, biochemical and pathological measurements. In lambs which survived, the rectal temperature, birthweight and plasma concentrations of fructose, insulin, thyroxine and the third component of complement at birth, and the weight at four months of age, decreased with litter size. One hundred and thirty-seven lambs were stillborn or died within four days and seven others died later. The mothers of 77 per cent of these lambs had low condition scores, but the lamb deaths did not correlate significantly with the condition scores. From data relating to birthweight, temperature, packed cell volume and plasma composition it was deduced that placental insufficiency was involved in 24 per cent of these deaths; acute hypoxaemia at birth accounted for 35 per cent, inadequate thermogenesis for 12 per cent and starvation for 13 per cent. The remaining 16 per cent of dead lambs could not be assigned to any of these categories. Using only clinicopathological criteria, 37 per cent of the lamb deaths were attributed to antenatal influences which included immaturity, developmental anomalies, and degenerative or inflammatory changes. Thirty-three per cent of the deaths were due to post natal factors which included, in declining order of frequency, starvation, enteritis, misadventure, pneumonia, navel infections and septicaemia. No conclusions could be drawn from the pathological examinations alone in the remaining 30 per cent, although almost half of these had low rectal temperatures after birth, death being attributed to hypothermia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical, biochemical and pathological study of perinatal lambs in a commercial flock. 359 May 87

Twenty-one placentae from type I (insulin-dependent) pregnant diabetic patients, treated with continuous subcutaneous insulin infusion (CSII), were studied morphologically. Despite a near-optimal blood glucose control the placental changes were identical to those previously reported in diabetic pregnancy. The most frequently observed lesion was that of relative placental immaturity; this, when extensive, was related to antenatal fetal asphyxia. These data indicate that near normoglycaemia, achieved with CSII, does not modify the morphological expression of the disease in the placenta. Furthermore, it highlights the importance of placental development in the context of diabetic pregnancy.
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PMID:Morphological findings in placentae of insulin-dependent diabetic patients treated with continuous subcutaneous insulin infusion (CSII). 361 74

The effect of equivalent doses of insulin on the adrenal of both adult and neonatal rats was compared. Glycemia in treated adults dropped to one third of the control, in contrast to the neonatal rat values, which decreased to about one half. After insulin, a large percentage of adult chromaffin cells showed cytoplasmic degranulation and vacuolization. In contrast, a smaller percentage of cytoplasmic changes was seen in the adrenal cells of 4- and 7-day-old rats. In rats of 10 days of age, the percentage of modified cells was similar to the adults. The morphological changes in neonatal medullae were characterized by widening of the perigranular space and enlargement of the endoplasmic reticulum cisternae. No cytoplasmic vacuolization was seen. This response of neonatal rats to insulin may indicate immaturity of the adrenal chromaffin tissue and/or of the centers involved in the mechanism of hypoglycemia-catecholamine release.
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PMID:Effect of insulin on neonatal and adult adrenal medulla in the rat. 389 3

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

Glucose, insulin and C-peptide were determined in amniotic fluid from 28 normal and 46 insulin-treated diabetic pregnant women. Glucose, insulin and C-peptide concentrations in amniotic fluid were higher in the diabetics than in the normal subjects. In diabetic women insulin levels did not correlate with birth weight or birth weight adjusted for gestational age, but C-peptide did. C-peptide correlated poorly with insulin (p < 0.05) in diabetics but closely (p < 0.002) in normal subjects. These results suggest that amniotic fluid investigations in insulin-treated diabetic women should use C-peptide assays as these seem to reflect more closely the insulin production of the fetus than do insulin assays. There were no differences in amniotic fluid glucose, insulin and C-peptide concentrations where the amniotic fluid lecithin-sphingomyelin ratio indicated fetal pulmonary maturity or immaturity.
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PMID:Amniotic fluid C-peptide in normal and insulin-dependent diabetic pregnancies. 699 99

Twenty-one Thai patients with beta-thalassemia/haemoglobin E and haemoglobin H diseases, 8-20-years-old, were studied. These patients had receive none or minimal blood transfusion. The important clinical endocrine abnormalities were growth retardation and sexual immaturity. GH secretion was found to be impaired in the majority of patients. Oral GTT showed chemical diabetes in one out of sixteen tests, a much lower incidence than in thalassaemic patients treated by hypertransfusion in the West. The mean insulin levels basally and after glucose loading were lower than those of the normal controls. Thyroid function was normal in all of the patients. Serum cortisol and 24-h urinary oxogenic steroids 917 OGS) levels were normal, as was adrenal cortical reserve in all the patients. The literature on endocrine function in in thalassaemia is reviewed.
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PMID:Endocrine function in thalassaemia. 726 14

The inability of the human fetal beta cell to secrete insulin in response to glucose has been exhaustively studied. In comparison, little attempt has been made to understand if the kinetics of insulin synthesis are as mature as those of an adult beta cell. Using a purified cell population in which 41% of the cells are beta cells, we generated a dose-response curve to glucose with half-maximal synthesis at 4.6 mM glucose, identical to that seen in adult islets. Unlike adult islets, however, in the absence of glucose, agents that raise cyclicAMP (cAMP) (theophylline and forskolin) generated dose-response curves similar to those obtained for glucose. cAMP levels in these cells were enhanced twofold in response to glucose and fourfold to theophylline. Inhibition of cAMP metabolism with 1 mM MDL 12,330A (RMI) reduced insulin synthesis stimulated by glucose and completely inhibited insulin synthesis stimulated by theophylline. Substances that block glucose transport (100 microM cytochalasin B) and protein synthesis (1 mM cycloheximide) also markedly reduced insulin biosynthesis. These results indicate that the regulation of insulin biosynthesis in the human fetal beta cell is cAMP dependent, although glucose transport is a limiting factor when glucose is used as the stimulus. Thus, the human fetal beta cell is relatively mature in its synthesis of insulin, unlike its immaturity in insulin release.
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PMID:Control of insulin biosynthesis in the human fetal beta cell. 766 44

A 17-year-old girl presented with amenorrhea, sexual immaturity and a remote history of head trauma. Provocative testing of the pituitary with thyrotropin releasing hormone, gonadotropin releasing hormone and insulin-induced hypoglycemia revealed intact pituitary function, with hypothalamic insufficiency. Furthermore, magnetic resonance imaging of the brain demonstrated loss of the hypothalamic infundibulum. To our knowledge, these structural defects have not been found with magnetic resonance imaging in cases of hypothalamic atrophy. This case suggests that the infundibulum or pituitary stalk may be vulnerable to traumatic damage, leading to hypothalamic insufficiency persisting into adulthood.
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PMID:Hypothalamic atrophy presenting as amenorrhea and sexual infantilism in a female adolescent. A case report. 780 90


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