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Query: UMLS:C0029713 (
immaturity
)
4,335
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The survival and prognosis of the prematurely born human infant are dependent on a successful transition from the intrauterine to the extrauterine environment. This is largely a consequence of the maturation of sufficient gastrointestinal function to provide adequate nutrition. However, the gastrointestinal tract of the premature infant, and to some extent, of the full-term infant, may be unprepared to provide the requisite absorptive function. Data presented in this symposium emphasize the dissociations in the development of human gastrointestinal function. Morphological maturation is completed early in gestation while
glucose
absorption increases with gestational age. Sucrase and maltase activities appear early; lactase activity begins to increase at 30 weeks and increases steadily to term. The latter pattern is accompanied by increased production of cortisol and thyroid in the fetus. The intraluminal phase of fat digestion is immature even in the full-term neonate. Both pancreatic secretory function and bile salt metabolism mature postnatally. Despite this relative
immaturity
, breast milk fat is absorbed with great efficiency by the term infant, and breast milk provides other important influences on intestinal development: mitogenic factor, immunological support, control of intestinal flora. The goals of nutrition support of the premature infant have been to maintain intrauterine growth standards; yet premature infants receiving pooled breast milk from mothers at 40 weeks or more may be given too little protein for their needs. Human milk from mothers of premature infants may be a more appropriate nutrient source. Supplements with higher contents of amino acids may lead to amino acid imbalance or hyperammonaemia. Additional stresses and requirements are imposed by illness or congenital anomalies. While we must apply current research findings to clinical care, we must also extend our knowledge of extrauterine human development. The ultimate measure of success in this field will be the physical and neurological capacities of infants followed prospectively.
...
PMID:The immature intestine: implications for nutrition of the neonate. 9 85
Plasma concentrations of
glucose
, alanine, and glucagon were measured after 24 hour fasting in newborn and infant sheep and in response to infusion of alanine alone and concurrently with theophylline. The plasma glucagon response to alanine was minimal in newborn sheep; in contrast, alanine produced a brisk response in plasma glucagon concentration in infant sheep.
Glucose
concentrations were unchanged in both groups. Theophylline enhanced blood glucagon and
glucose
responses to alanine in newborn animals but had minimal effects on the response of the infant sheep. These data, considered with earlier data in fetal sheep, suggest a progressive maturation of pancreatic islet alpha-cell glucagon secretion in the sheep during the postnatal period and suggest that the blunted glucagon response observed in the neonate is related to
immaturity
of the glucagon secretion mechanisms rather than deficient synthesis of the hormone. This
immaturity
may be related to impaired synthesis and/or enhanced degradation of cyclic adenosine monophosphate (cAMP) or to diminished responsiveness to cAMP.
...
PMID:Effects of fasting and theophylline on alanine-stimulated glucagon secretion in neonatal and infant sheep. 17 57
No marked gluconeogenetic performance was recordable from nursed piglets aged, between one and five days, in response to ACTH nor glucocorticosteroid application. Store pigs, aged twelve weeks, however, exhibited
glucose
rises of 34 per cent one hour after injection or 55 per cent three hours from ACTH application. The point was made, in an attempt to elucidate the above findings, that in newborn piglets, few days after birth, the gluconeogenetic capacity is insufficient because of functional
immaturity
of the liver. The behaviours of several metabolites in the liver and muscles of store pigs were examined under differentiated model conditions to check up and verify that view.
...
PMID:[Gluconeogenetic capacity of suckling piglets and young pigs]. 18 37
Tiny babies have the potential problem of hypoglycemia due to diminished hepatic glycogen stores, which can be potentiated by conditions frequently present in this birth weight group: asphyxia, cold stress, hypoxia, polycythemia. Despite the early administration of fluid and feeding, tiny babies are still at risk for developing hypoglycemia. Their
immaturity
, expressed by their limited ability to tolerate parenteral
glucose
infusions, puts them at risk for becoming hyperglycemic as well. Hence careful
glucose
administration and frequent monitoring of blood
glucose
are essential during the first several days after birth, in anticipation of hypoglycemia as well as hyperglycemia.
...
PMID:Perinatal glucose homeostasis: the unique character of hyperglycemia and hypoglycemia in infants of very low birth weight. 33 33
Some hematological and cardiovascular parameters of the underweight neonatal piglets have been compared with normal-weight 1 and 7-day-old swine (Sus scrofa domestica). The underweight swine had a significantly lower leukocyte count, plasma protein level and blood
glucose
level, but a significantly higher plasma LDH level. Heart rate and arterial blood pressure were significantly lower in the underweight group. Based on the observed results it was postulated that the piglets born with a low body weight could also be physiologically immature since the cardiovascular parameters measured approximated those reported for normal fetuses of the same weight. Further studies are required to ascertain if a functional
immaturity
persists in the neonatal animals.
...
PMID:Basic cardiovascular parameters in the underweight neonatal swine. 73 36
1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on
glucose
tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous
glucose
loads. 3. The rate of disappearance of
glucose
from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood
glucose
concentration between normal and malnourished rats 5 and 10 min after an oral
glucose
load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood
glucose
concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous
glucose
, intravenous tolbutamide and intravenous
glucose
plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous
glucose
and intravenous tolbutamide. However, their insulin response to stimulation with intravenous
glucose
plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a 'functional
immaturity
' of the pancreas.
...
PMID:Glucose tolerance and insulin release in malnourished rats. 81 69
Insulin release was studied in vitro using pieces of pancreas from rabbits of between 24 days gestational age and 6 weeks postnatal age. When allowance was made for the fraction of pancreas which was endocrine, 16-5mM-
glucose
caused increasing stimulation of insulin release as development advanced and 3-3 mM-
glucose
caused a similar rate of secretion at all ages. Secretion was not significantly influenced by insulin destruction in the incubation medium. Glucagon (5 mug/ml) did not stimulate insulin secretion from 24-day foetal pancreas but did so postnatally. Theophylline (1 mmol/1) stimulated insulin release at all ages and was equipotent on 24-day foetal pancreas in 3-3 or 16-5 mM-
glucose
. The stimulation of insulin release from 24-day foetal pancreas by 1 mM-theophylline occurred in the absence of extracellular
glucose
, pyruvate, fumarate and glutamate and in the presence of mannoheptulose and 2-deoxyglucose (each 3 mg/ml). Adrenaline (1 mumol/1) and diazoxide (250 mug/ml) abolished or attenuated the stimulation of insulin release by
glucose
, leucine plus arginine or theophylline from 24-day foetal, 1 day and 6 weeks postnatal pancreas. The stimulation of insulin release from 6-week-old pancreas by 1mM-barium was blocked by adrenaline and diazoxide but the effect became less with increasing
immaturity
. The experimental results illustrate some of the ways in which insulin secretion by the rabbit beta cell changes as a function of development and draw attention to the importance of
glucose
and cyclic adenosine monophosphate in this process.
...
PMID:Development of pathways of insulin secretion in the rabbit. 109 Jun 94
Experiments were conducted on 162 female rats which had sustained alloxan diabetes during the period of sexual
immaturity
and had latent insular insufficiency (prediabetes and latent diabetes). Possibilities of chlorpropamide under conditions promoting decompensation development were studied. The animals were given propamide in daily doses of 100 mg per 1 kg of weight for one month, including the period of sexual maturation. Observation period--up to 5 months. A favourable effect of chlorpropamide was noted by the end of puberty and persisted in the course of further observation; the difference from control animals by the frequency of latent and manifest diabetes was intensified under the effect of
glucose
overfeeding during the perinatal period. Chlorpropamide improved the course of latent insular insufficiency in the rats and was capable of preventing its change into manifest diabetes.
...
PMID:[The effect of chlorpropamide on the course of latent insular insufficiency in rats under conditions favorable for its transition to patent diabetes]. 125 24
In the neonatal rat, the response of the hypothalamo-pituitary-adrenal axis to stressful stimuli is markedly decreased during the first 2 weeks of life. This peculiar period was named "stress hyporesponsive period." In this report, we studied the effect of insulin-induced hypoglycemia, known as a strong stimulator of the corticotroph function in the adult rat. Rats (8- or 20-day-old) were injected ip with 3 IU/kg synthetic insulin and were killed at various times. In 20-day-old rats, hypoglycemia induced a rapid drop in blood
glucose
concentrations accompanied by a stimulation of ACTH and corticosterone secretion which reached maximal values within 30 min. On the opposite, in 8-day-old rats, despite a rapid decrease in blood
glucose
levels, insulin injection induced a gradual rise of plasma ACTH and corticosterone concentrations which peaked at 90 min. This delayed response of the hypothalamo-pituitary-adrenal axis to hypoglycemia in the youngest rats does not seem to be due to a difference of sensitivity to insulin-induced hypoglycemia since injection of increasing doses of insulin (0.3, 0.75, or 3 IU/kg body wt) induced a dose-related decrease of blood
glucose
concentrations and a rise in plasma ACTH and corticosterone levels, comparable in the two age group studied. Basal or hypoglycemia-stimulated absolute corticosterone values were much lower in 8-day-old rats than in 20-day-old animals, suggesting an
immaturity
of the adrenal glands in the youngest animals. Daily ACTH injection, starting 3 days before the experiment, had a trophic effect on the adrenal glands leading to a more important increase of corticosterone levels after hypoglycemia in 8-day-old rats. Our results confirm that there is an
immaturity
of the adrenal glands in young rats, probably due to the low plasma ACTH levels during the neonatal period. To determine the respective role of the two major hypothalamic ACTH secretagogues, we studied the effect of passive immunization against CRF or arginine vasopressin (AVP) on plasma ACTH response after hypoglycemia. Passive immunization against AVP decreased significantly hypoglycemia-stimulated ACTH secretion in both 8- and 20-day-old rats, while no change of plasma ACTH response to insulin injection was observed after passive immunization against CRF. This results suggest that CRF does not seem to be involved in the regulation of ACTH secretion after hypoglycemia in the young rat while AVP seems to be the main hypothalamic stimulatory factor for anterior pituitary corticotrophs response to hypoglycemia during the postnatal period.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Stimulation of adrenocorticotropin secretion by insulin-induced hypoglycemia in the developing rat involves arginine vasopressin but not corticotropin-releasing factor. 131 56
Prolonged infusion of the beta 2-adrenergic agonist, ritodrine, into sheep during late pregnancy decreased maternal plasma K+ from 3.6 to 2.5 mmol l-1 during the first 6-8 h of infusion, as it does during tocolysis in women. This decrease was not accompanied by significant change in fetal plasma K+ concentration. Ritodrine infusion (1-3.5 micrograms kg-1 min-1) directly into the fetus also did not decrease fetal plasma K+ significantly. In contrast, insulin (2.5 mU kg-1 min-1), infused together with
glucose
(3.6 mg kg-1 min-1) directly into the fetus decreased fetal plasma K+ concentration by 0.8 mmol l-1 within 1 h. The results suggest
immaturity
in beta 2-adrenergic receptor regulation of electrogenic K+ uptake by muscle in fetal lambs.
...
PMID:Effects of the beta-adrenergic agonist, ritodrine, and insulin on plasma potassium concentrations in fetal lambs. 135 75
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