Fetus

About: Fetus is a research topic. Over the lifetime, 21567 publications have been published within this topic receiving 646380 citations. The topic is also known as: foetus & fœtus.

Insulin and the IGF system in the human placenta of normal and diabetic pregnancies.

Abstract: The insulin/insulin-like growth factor (IGF) system regulates fetal and placental growth and development. In maternal diabetes, components of this system including insulin, IGF1, IGF2 and various IGF-binding proteins are deregulated in the maternal or fetal circulation, or in the placenta. The placenta expresses considerable amounts of insulin and IGF1 receptors at distinct locations on both placental surfaces. This makes the insulin and the IGF1 receptor accessible to fetal and/or maternal insulin, IGF1 and IGF2. Unlike the receptor for IGF1, the insulin receptor undergoes a gestational change in expression site from the trophoblast at the beginning of pregnancy to the endothelium at term. Insulin and IGFs are implicated in the receptor-mediated regulation of placental growth and transport, trophoblast invasion and placental angiogenesis. The dysregulation of the growth factors and their receptors may be involved in placental and fetal changes observed in diabetes, i.e. enhanced placental and fetal growth, placental hypervascularization and higher levels of fetal plasma amino acids.

Maternal ethanol exposure induces transient impairment of umbilical circulation and fetal hypoxia in monkeys.

Abstract: When ethanol was administered intravenously to pregnant monkeys, a transient but marked collapse of umbilical vasculature was observed uniformly within about 15 minutes. The ethanol-induced impairment of umbilical circulation produced severe hypoxia and acidosis in the fetus; recovery occurred during the succeeding hour. This striking interruption of feto-placental circulation may explain one of the mechanisms of mental retardation, a frequent manifestation in children afflicted with fetal alcohol syndrome.

Abnormal Umbilical Cord Coiling Is Associated with Adverse Perinatal Outcomes

Abstract: The normal umbilical cord coil index is one coil/5 cm, i.e., 0.2 ± 0.1 coils completed per cm. We report the frequency and clinical correlations of abnormally coiled cords among 1329 cases referred to our placental pathology services. Twenty-one percent of cords were overcoiled and 13% were undercoiled. Abnormal cord coiling was seen at all gestational ages. Principal clinical correlations found in overcoiled cords were fetal demise (37%), fetal intolerance to labor (14%), intrauterine growth retardation (10%), and chorioamnionitis (10%). For undercoiled cords, the frequencies of these adverse outcomes were 29%, 21%, 15%, and 29%, respectively. Abnormal cord coiling was associated with thrombosis of chorionic plate vessels, umbilical venous thrombosis, and cord stenosis. Thus, abnormal cord coiling is a chronic state, established in early gestation, that may have chronic (growth retardation) and acute (fetal intolerance to labor and fetal demise) effects on fetal well-being. The cause of abnormal cord coiling is not known. Its effects on neurological status of survivors are also unknown. Antenatal detection of abnormal cord coil index by ultrasound could lead to elective delivery of fetuses at risk, thereby reducing the fetal death rate by about one-half. We recommend that the cord coil index become part of the routine placental pathology examination.

Placental 11 beta-hydroxysteroid dehydrogenase-2 and fetal cortisol/cortisone shuttle in small preterm infants.

Abstract: Glucocorticoids rate among the most controversial topics in today's perinatology and neonatology. Many sick preterm infants exhibit signs of adrenal insufficiency, the etiology, diagnostic criteria, and optimal treatment of which are under debate. Moreover, most of these infants are exposed to pharmacological glucocorticoid doses both in utero and after birth. In face of this, surprisingly little is known about the physiological glucocorticoid exposure before early preterm birth. This exposure is highly variable and mainly regulated by the placental enzyme 11 beta-hydroxysteroid dehydrogenase-2 (11 beta-HSD2), which converts excess cortisol (F) to inactive cortisone (E). Impaired activity of this enzyme is common in intrauterine growth restriction and preeclampsia, conditions frequently associated with early preterm birth. To identify clinical determinants associated with decreased placental 11 beta-HSD2 function, we studied 107 small preterm infants [mean birth weight, 1067 g (range, 395-2453 g); gestational age, 28.2 wk (range, 22.4-32.0 wk)] by determining their placental 11 beta-HSD2 activity rate (per milligram protein) and total activity (per placenta) as well as cord vein F and E concentrations. An E/(E+ F) ratio expresses the overall balance of the F/E shuttle. There were positive correlations between relative birth weight and placental 11 beta-HSD2 activity rate (r = 0.30; P = 0.002) and total activity (r = 0.56; P < 0.0001) as well as E/(E+ F) ratio (r = 0.27; P = 0.01) and E concentration (r = 0.32; P = 0.003). Infants with increased umbilical artery resistance had lower total placental 11 beta-HSD2 activity (P = 0.02), E/(E+ F) ratio (P = 0.04), and E concentration (P = 0.0002). Gestational age was inversely associated with placental 11 beta-HSD2 activity rate (r = -0.25; P = 0.009). We conclude that, in small preterm infants, reduced placental 11 beta-HSD2 function is associated with low relative birth weight and severe fetal distress. Whether these conditions are associated with early postnatal adrenal insufficiency or long-term cardiovascular risk remains an important issue for further study.