Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric acid secretion was measured in 20 infants aged 6-438 days. The values for the basal acid output and that after stimulation with 6 mug/kg pentagastrin subcutaneously were found to be related to age, body weight and body surface area. But these correlations were not comparable to those in adults. Standard values for different age groups in childhood must therefore be established. Furthermore, the results indicate parietal-cell immaturity during the first six months of life. Measurement of fasting serum-gastrin concentration by radioimmunoassay in 74 infants, aged 1-438 days, and 154 adults as controls revealed a high serum-gastrin level in infants, with an exponential decrease during the first year of life. Despite comparable pH values in gastric juice at one year of life, the gastrin concentrations were higher than those in adults (at a statistically significant level). On the other hand, normal serum-gastrin concentrations were found in ten pregnant women just before delivery. The results suggest a negative feed-back mechanism between gastric-acid secretion and fasting serum-gastrin levels, but such mechanism probably being limited by extragastric gastrin secretion.
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PMID:[Serum-gastrin levels and gastric-acid secretion in infants (author's transl)]. 1 82

In the term human and ovine fetus, plasma gastrin is elevated, but gastric acid secretion is below adult levels, suggesting a developmentally related immaturity in gastrin and gastric acid regulation. This study investigated a number of elements of the gastric acid regulatory system: gastrin and its glycine-extended precursor, somatostatin, and the H+/K(+)-ATPase. Measurements were made in blood, antrum, and fundus of the ovine fetus during the last half of gestation, of 15-day-old lambs, and of adult sheep at the level of mRNA synthesis, tissue storage, and secretion. Plasma amidated gastrin (gastrin-amide) was elevated at or above adult values from 125 days (term is 145 days) and steadily increased with development, peaking in the lamb. Similar changes occurred with plasma glycine-extended gastrin (gastrin-gly). The peak concentration of antral gastrin-amide was present in the lamb, while the maximum antral gastrin-gly level occurred 1 week before birth. Gastrin mRNA paralleled the changes in antral gastrin-gly. The proportion of higher mol wt species of gastrin decreased during gestation in both plasma and antrum. Low amounts of mRNA for the H+/K(+)-ATPase was present from at least 120 days of gestation and antedated gastric acid secretion. However, there was a 3-fold increase in H+/K(+)-ATPase mRNA from the 140-day-old fetus to the lamb, the period when the greatest reduction in gastric pH occurred (pH 5 to 2). Antral and fundic somatostatin increased rapidly in the fetus at 120 days gestation and were above adult values at term and in the lamb. Somatostatin mRNA changed in parallel to somatostatin peptide. Somatostatin-14 was the major species in antrum and fundus throughout development. The increase in circulating and antral gastrin-amide after birth may be the result of increased amidation of gastrin-gly as well as increased expression of gastrin mRNA. Amidation of gastrin may be a regulatory step in the production of biologically active gastrin during development. The major increase in gastrin and the H+/K(+)-ATPase that occurs in the week before and after gestation correlated with the onset of increased gastric acidity.
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PMID:Ontogeny of gastrin, somatostatin, and the H+/K(+)-ATPase in the ovine fetus. 134 9

In the sheep fetus, plasma levels of gastrin are raised above adult levels from 2 weeks before birth. This observation initiated the present study on the maternal and fetal secretion rate, metabolism and placental transfer of gastrin. The experiments were performed on conscious pregnant ewes with chronically cannulated fetuses and on newborn lambs. Metabolic clearance rate (MCR), production rate (PR) and placental transfer of gastrin were measured by alternate steady-state infusion of gastrin into the mother and fetus. Plasma levels of gastrin were measured by radioimmunoassay. Metabolic clearance rate was similar in the pregnant and non-pregnant ewe (8.4 +/- 1.1 (S.E.M.) and 9.0 +/- 1.4 ml/min per kg) respectively. However, fetal MCR was significantly increased. Term was 145 days. Metabolic clearance rate was 15.5 +/- 1.7 at 110-125 days of gestation, 25.6 +/- 2.9 at 126-135 days, 29.7 +/- 4.9 at 136-145 days and remained raised in the first 2 weeks post partum. Gastrin did not cross the placenta in either direction. Placental destruction of gastrin was not responsible for the increased fetal MCR as umbilical artery and umbilical vein levels were not significantly different during fetal gastrin infusion. Furthermore, MCR remained raised in the newborn lambs. Gastrin PR was significantly increased at all ages. The results showed that the previously reported fetal hypergastrinaemia is from fetal sources and is not a result of immaturity of clearance mechanisms. In fact, fetal MCR was significantly increased. The increased fetal plasma gastrin levels are due to an increased rate of production from the fetus.
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PMID:Fetal and maternal production and metabolism of gastrin in sheep. 710 9

Six extragonadal teratomas that contained pancreatic tissue were retrieved from archival material at the University of Minnesota Hospital, Minneapolis. The neuroendocrine cells were studied immunohistochemically for insulin, glucagon, somatostatin, pancreatic polypeptide, vasoactive intestinal polypeptide, gastrin, chromogranin, and synaptophysin. Pancreatic tissue from autopsies of 10 stillbirths (20 to 40 weeks' gestational age) was evaluated similarly. The features of the teratomatous pancreatic tissue were compared with those of the fetal pancreata and with data from previous studies of normal pancreatic development and adult pancreata. The pancreatic tissue in all six teratomas contained abundant mature islets that contained beta, alpha, delta, and pancreatic polypeptide cells; however, they also showed widespread nesidioblastosis with the same cell types, resembling third-trimester fetal and neonatal pancreata. Increased proportions of alpha and delta cells were observed in three and five cases (relative to those of adult tissue), respectively, providing further evidence of immaturity. Two cases showed a lack of alpha cells. None of the teratomas contained pancreatic cells that were positive for vasoactive intestinal polypeptide or gastrin. Mechanisms that regulate neuroendocrine cell differentiation in the normal pancreas also seem to operate in the teratomatous pancreas; they may eventuate in features similar to those of the late fetal and neonatal pancreas. Abnormal differentiation in teratomas may result in deficient hormone production.
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PMID:Immunohistochemical characterization of teratomatous and fetal neuroendocrine pancreas. 831 55

1. Plasma gastrin releasing peptide (GRP) is elevated in the foetal and maternal circulations of pregnant sheep. To determine the mechanisms for this increase the synthesis, secretion rate, metabolism and placental transfer of GRP were measured. 2. Foetal metabolic clearance rate of GRP was significantly increased (P < 0.05) compared to the non-pregnant ewe (19.9 +/- 2.6 (s.e.m.) and 11.8 +/- 2.0 mL/min per kg, respectively). Production rate of GRP in the foetus was four-fold higher than in the non-pregnant ewe reflecting the combination of the increased basal concentration and metabolic clearance rate in the foetus. 3. Infused GRP did not cross the placenta. However, endogenous GRP was higher in the umbilical vein than in the umbilical artery, suggesting a uteroplacental origin for some of the GRP in the foetal circulation. 4. Gastrin releasing peptide mRNA was synthesized in the pregnant endometrium with lower amounts found in the pregnant myometrium. No GRP mRNA was detected in the amnion or chorioallantois. 5. The results show that the previously reported increase in foetal concentration of GRP is from foetal and uteroplacental sources and is not a result of immaturity of clearance mechanisms but rather from an increased production of GRP. With the demonstration that the uteroplacental unit synthesizes and stores GRP, additional studies on the regulation of GRP production from these sources were warranted.
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PMID:Foetal metabolism, placental transfer and origin of gastrin releasing peptide in the sheep. 891 26