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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most frequently, placental glycogen has been studied as an index of fetal nutrition. There are no published studies of placental glycogen as an index of fetal stress. In this study of 1573 samples from 71 placentae, glycogen levels in the placental disk, fetal membranes and umbilical cord of normal uncomplicated pregnancies were compared with those in complicated pregnancies. The complicated pregnancies included preterm delivery, hypertensive disorders, inadequate prenatal care, substance abuse, maternal fever or infection, obesity, diabetes mellitus, premature rupture of membranes, intrauterine growth retardation, sickle cell trait, and acute meconium staining of amniotic fluid at delivery. The data showed that the only significant differences were in the subgroup complicated by meconium-stained amniotic fluid in which the placental disks and umbilical cords had significantly lower (P=0.0006) glycogen levels. This finding suggests a relatively specific association. It is interesting to speculate that the passage of meconium with its vasoconstrictive effect increases utilization of local glycogen stores, decreases local glycogen reserves needed for the work of further vasoconstriction, and, in the event of subsequent acute stress, impairs vascular perfusion of tissues. In this way, meconium could predispose the infant to asphyxia.
Placenta 1998 May
PMID:Decreased placental and umbilical cord glycogen levels associated with meconium-stained amniotic fluid. 963 25

Human placentae from well-controlled diabetic women were collected after 37 weeks of gestation and divided into three groups according to the duration and severity of diabetes mellitus established by White classification criteria. A fourth group of subjects served as matched controls. Various morphometric variables not estimated hitherto (including the star volumes of villous 'domains' and intervillous 'pores' and trophoblast surface denudation) were assessed stereologically. The aims were to test whether or not (1) control values of these structural quantities are preserved in well-controlled diabetes mellitus, and (2) differences occurred between alternative diabetic groups. Placental specimens were obtained by systematic random sampling procedures and paraffin sections were cut at random positions and orientations. Volume densities of peripheral (terminal+intermediate) villi and intervillous spaces were estimated by test point counting and multiplied by placental volumes in order to convert them into absolute volumes. Volume estimates were also obtained for trophoblast, syncytiotrophoblast nuclei and intervillous fibrin-type fibrinoid. Villous surface areas were estimated by intersection counting and the star volumes of villi and intervillous pores were obtained by measuring the lengths of point-sampled intercepts. Calculations were also made of the theoretical numbers of villous domains and intervillous pores and of the numbers of syncytiotrophoblast nuclei. No significant differences were detected between control and diabetic placentae, or between White classes, for any of the estimated quantities. It is concluded that normal values are preserved by good glycaemic control regardless of diabetic grouping.
Placenta
PMID:Quantitative studies on the villi, trophoblast and intervillous pores of placentae from women with well-controlled diabetes mellitus. 969 57

Nitrotyrosine residues (NT), an index of oxidative stress arising from peroxynitrite formation and action, are found in placental vasculature of pregnancies complicated by pre-eclampsia (PE) or pregestational insulin-dependent diabetes mellitus (IDDM). This study correlates conventional placental pathology with NT immunostaining in 20 cases of perinatal mortality (13 stillbirths and seven cases of neonatal mortality) associated with PE, IDDM, amniotic fluid infection syndrome (AFIS), or from fetal/neonatal demise not related to these conditions (congenital anomalies) (n = five/group). Patients with PE have more decidual arteriolopathy and Tenney-Parker change, while patients with IDDM and ascending infection have more villous cytotrophoblastic hyperplasia. Archival paraffin-embedded placental sections were immunostained for NT for correlation with clinical features and H&E histological findings. The intensity of immunostaining for NT varied from absent (n = 7) to 1+ (n = 5) or 2+ (n = 8). All eight placentae with 2+ staining showed increased villous extracellular matrix (ECM), compared to none of five with 1+ staining and two of seven with no staining (chi2 = 14.3, P = 0.001). There was no statistically significant difference in the percentage of stem villi with luminal vascular abnormalities (5.7 vs 10 vs 35.7 per cent, F = 2.3, P = 0.1). Our data show that increased production of reactive oxygen species by placental tissue may be associated with increased extracellular matrix, itself produced by fibroblasts under the influence of oxygen. NT immunostaining may therefore help differentiate those cases of perinatal morbidity/mortality associated with post-placental hypoxia provided that the secondary impact of intrauterine fetal death can be excluded by future studies.
Placenta 2001 Apr
PMID:Nitrotyrosine immunostaining correlates with increased extracellular matrix: evidence of postplacental hypoxia. 1131 30

With the goal to establish a model that relates birth weight to placenta weight, adjusted for the most documented predictors of birth weight, 300 live newborns were studied, all were products of single gestation. Inclusion criteria were newborns with gestational age of 37 weeks or older according to the date of last menstruation, whose mothers did not have diabetes mellitus, high blood pressure, pre-eclampsia, or eclampsia. The weight of the newborn was identified from the anthropometry data collected by previously trained nursing personnel in each of the participating hospitals. Immediately after delivery, the placenta was weighed. Multiple linear regression was used to see the effect of placenta weight and each variable on birth weight. The mean of birth weight was 3,369 g with a standard deviation (SD) of 445 g. Placenta weight had a mean of 537 g (SD: 96 g). The relation between the weight of the placenta and the birth weight was significant, and we found that for each gram increase in placenta weight, birth weight is increased by 1.98 g (SE = 0.25, p < 0.01) and this relation is not linear, since the quadratic term is significant. Placenta weight has a nonlinear relation to the birth weight and is an important predictor of birth weight. Together with the gestational age and the maternal age and size, it explains 32% of the variability of birth weight. Placenta weight can be a 'sentinel' indicator of nutritional and/or environmental problems.
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PMID:Relation between birth weight and placenta weight. 1150 10

The examinations were carried out on 3 placentas from normal pregnancies and 12 placentas from pathological pregnancies (gestosis, cholestasis, type A diabetes pregnancies and premature outflow of amniotic fluids). Placenta sections were fixed in glutaraldehyde and subsequently embedded in Epon 812. Semithin sections 1 mu thick were stained with methylene blue and azure. Moreover, changes in terminal villi were assessed. In comparison with the control placentas changes in blood vessels, stroma and syncytiotrophoblast were found.
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PMID:Histological changes in placenta villi in some types of pathological pregnancy. 1197 99

Intrauterine growth restriction (IUGR) is a significant cause of infant mortality and morbidity. It is now clear that IUGR infants exhibit higher rates of coronary heart disease, type 2-diabetes, hypertension and stroke as adults. Therefore, fetal growth not only impacts the outcome of the perinatal period, but also impacts adult well-being. The etiologies of IUGR are numerous, but are often associated with abnormalities in placental structure and function. The process of implantation and placentation requires the production of a plethora of growth factors, cell-adhesion molecules, extracellular matrix proteins, hormones and transcription factors. Many of these exhibit altered expression within the placenta of IUGR pregnancies. However, it has been difficult to fully assess their role during the development of placental insufficiency (PI) in the human, underscoring the need for animal models. Using an ovine model of PI-IUGR we have observed changes in the expression of vascular endothelial growth factor, placental growth factor, their common receptors, as well as angiopoietin 2 and its receptor, Tie 2. We found that changes in these growth factors can be associated with both acute and chronic changes in placental vascular structure and function. These studies and others are providing needed insight into the developmental chronology of placental insufficiency.
Placenta 2002 Apr
PMID:Placental development in normal and compromised pregnancies-- a review. 1197 69

Many of the transport processes across the syncytiotrophoblast (ST), such as amino acid transport, are Na(+)-coupled. The maintenance of a low intracellular Na(+) concentration by Na(+)/K(+)-ATPase is therefore crucial for placental transport of nutrients and consequently, foetal growth. In pregnancies complicated by diabetes foetal growth is often accelerated despite rigorous glycemic control of the mother, however the underlying mechanisms are not fully understood. We tested the hypothesis that Na(+)/K(+)-ATPase in ST plasma membranes is up-regulated in diabetic pregnancies associated with accelerated growth. ST microvillous (MVM) and basal (BM) plasma membranes were purified from term placentas of normal pregnancies (control, n=13) and pregnancies complicated by insulin-dependent diabetes mellitus (n=7) or gestational diabetes (n=6). All mothers with diabetes gave birth to large for gestational age babies. The Na(+)/K(+)-ATPase alpha(1)-subunit protein expression (Western blot) in MVM and BM was unaltered by diabetes. Na(+)/K(+)-ATPase activity (K(+)-stimulated, ouabain-sensitive phosphatase activity) in ST plasma membranes was not affected by diabetes. This is the first study of Na(+)/K(+)-ATPase in ST membranes of the human placenta in diabetes. Our data show that accelerated foetal growth in diabetic pregnancies is not associated with elevated ST Na(+)/K(+)-ATPase protein expression or activity.
Placenta 2002 May
PMID:Na(+)/K(+)-ATPase activity and expression in syncytiotrophoblast plasma membranes in pregnancies complicated by diabetes. 1206 54

Glucose transporters in the placental, epithelial syncytiotrophoblast barrier are asymmetrically arranged (microvillous>basal), leading to the hypothesis of a rate-limiting role for the basal membrane in transepithelial transport. This is significant since the changes which have been observed in basal membrane glucose transporter expression over gestation and in conditions such as diabetes would generate changes in maternal-to-foetal glucose transport. This study was designed to test whether the basal membrane of the syncytiotrophoblast is the rate-limiting step in transepithelial transport and to investigate the effects of metabolism on transpithelial transport. In the absence of a transporting syncytiotrophoblast monolayer, the BeWo choriocarcinoma cell line, derived from trophoblast and plated on a permeable support, was used as a model since it has an asymmetric distribution of glucose transporter activity, similar to the syncytiotrophoblast. Inhibition of basal membrane glucose transport with p -chloromercuribenzene-sulfonate (p CMBS) produced a proportional change in transepithelial transport, whereas this latter parameter was relatively insensitive to inhibition of microvillous membrane glucose transporters. These data demonstrate that the basal membrane is the rate-limiting step in transepithelial glucose transport. Experiments involving stimulation and inhibition of cellular glucose consumption demonstrated that there is a single intracellular glucose pool in BeWo cells, supplying both metabolism and transcellular transport.
Placenta
PMID:Transepithelial glucose transport and metabolism in BeWo choriocarcinoma cells. 1236 84

Alternate mRNA splicing of human leptin receptor generates four membrane isoforms with different C-terminal sequences. They differ by the length of their intracellular domain which include specific motifs crucial for the specificity of leptin signalling. As a step towards functional studies, we have characterized leptin receptors in human placenta from normal pregnancies and pregnancies associated with diabetes and pre-eclampsia. Leptin and leptin receptors were visualized by immunohistochemistry of placentas obtained from first and third trimester pregnancies. Antibodies against N and C-terminal epitopes showed signals in the apical membrane of the syncytiotrophoblast in early and term placental villi as well as in JAr and BeWo derived trophoblast cells. In addition, a distinct isoform recognized by its extracellular juxtamembrane epitope was exclusively localized in cytotrophoblast cells and likely stains the soluble receptor. At contrast with the transmembrane receptors, the expression of this isoform is increased in placentas of pre-eclamptic and diabetic women which synthesize more leptin than placenta from uncomplicated pregnancy. These data demonstrate that short and long transmembrane leptin receptors are expressed in the trophoblast and indicate that leptin synthetized within the placenta can act locally through both receptor isoforms. Being also accessible to leptin from maternal origin, these transmembrane receptors may signal differently in pregnancy with normal and increased leptin production. The co-localization of leptin and the soluble receptor isoform suggests that this isoform serves for modulating maternal free leptin levels through modification of leptin binding capacities.
Placenta 2003 Jan
PMID:Placental leptin receptor isoforms in normal and pathological pregnancies. 1249 64

Neonates born after pregnancies complicated by diabetes or intrauterine growth restriction (IUGR) have increased incidence of hypocalcaemia. Furthermore, IUGR is associated with reduced bone mineralization in infancy and osteoporosis in adult life. We tested the hypothesis that placental calcium transport is altered in these pregnancy complications. Transport of calcium into syncytiotrophoblast basal plasma membrane (BM) vesicles was studied by rapid filtration and protein expression of Ca(2+) ATPase by Western blot. In IUGR Ca(2+) ATPase activity was increased by 48 per cent (n=13; P< 0.05) whereas protein expression was 15 per cent lower (n=13; P< 0.05) than in controls (n=16). Basal membrane ATP dependent calcium transport was unaltered in gestational diabetes (GDM) but increased by 54 per cent in insulin dependent diabetes (IDDM) compared to controls (P< 0.05; n =14). Diabetes did not affect Ca(2+) ATPase expression in BM. We have previously shown that the mid-molecular fragment of parathyroid hormone related peptide (PTHrP midmolecule) stimulates BM Ca(2+) ATPase in vitro. PTHrP midmolecule concentrations in umbilical cord plasma were measured using radioimmunoassay. The concentrations in umbilical cord plasma were increased in IUGR, but unaltered in diabetes. In conclusion, placental calcium pump is activated in IUGR and IDDM, which may be secondary to increased foetal calcium demand. We speculate that PTHrP midmolecule may be one mechanism for activating BM Ca(2+) ATPase in IUGR.
Placenta 2003 May
PMID:ATP dependent Ca2+ transport across basal membrane of human syncytiotrophoblast in pregnancies complicated by intrauterine growth restriction or diabetes. 1274 20


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