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At least 19 recordsLinked to original sources
PubMed1992

Glucose, insulin, HGH and IGF-I levels in maternal serum, amniotic fluid and umbilical venous serum: a comparison between late normal pregnancy and pregnancies complicated with diabetes and fetal growth retardation.

Fetal growth and development is dependent upon various growth factors such as glucose, insulin, HGH and IGF-I. These growth factors were measured in maternal serum (MS), amniotic fluid (AF) and umbilical venous serum (UV) in late gestation in normal, insulin dependent diabetic pregnancies (IDDM) and in pregnancies complicated with intrauterine growth retardation (IUGR). The UV glucose values of 1.9 +/- 0.9 mmol/L and UV insulin values of 8.0 +/- 1.8 mU/L were the lowest in IUGR pregnancies, and the highest were in UV serum from IDDM pregnancies, and the difference was statistically significant for this two groups. IGF-I values in UV indicated that there was significant difference in IGF-I concentrations when both, IUGR and IDDM groups were compared to the controls. There was a parallel shift in AF and MS glucose and insulin concentration as birthweight increased. The highest IGF-I values of 7.2 +/- 9.6 mumol/L in AF and MS were found in pregnancies with infants whose birthweight was 3500 grams and greater. Infants from pregnancies complicated with IUGR and IGF-I low values of 0.6 +/- 1.2 mumol/L in AF. HGH concentrations of 15.6 +/- 9.4 micrograms/L in UV were observed in IDDM pregnancies and significantly lower than the values in IUGR and normal pregnancies. HGH umbilical venous values decreased with duration of pregnancy and with increase in fetal size. The high HGH concentrations in the fetus and its dramatic fall after parturition, and the obtained negative correlation between HGH and IGF-I in umbilical vein may exhibit the maturation of the hypothalamic-growth hormone-IGF-I axis. It seems likely that changes in maternal serum, umbilical venous and amniotic fluid insulin-like growth factor I influence birthweight in normal and IUGR infants and in those of diabetic mothers.

Amniotic Fluid↗
PubMed1987

Interactions between chronic murine Trypanosoma cruzi infection and pregnancy: fetal growth retardation.

Fetal growth, reproductive capacity, and parasitemia were studied in three groups of BALB/c mice: pregnant and chronically infected with Trypanosoma cruzi, non-pregnant but similarly infected, and pregnant but noninfected. The pregnant mice were killed on day 17 of pregnancy. Comparisons of the two pregnant groups showed significant differences in fetal weights and x18 magnified ossification lengths of radius and cubitus, whereas placental weights were not modified. The results indicate that intrauterine growth retardation occurs during chronic murine T. cruzi infection. No difference was noted between the reproductive capacities of the two pregnant groups. Parasitemias were similar in infected pregnant and control groups. Mice of all groups survived infection until killing. Pregnancy, therefore, does not influence chronic murine T. cruzi infection. Parasites were never found in fetal blood, indicating a very low, if any, frequency of transplacental transmission of parasite during the chronic phase of infection.

Animals↗
PubMedDate not supplied

[Measuring subcutaneous fatty tissue as a sonographic parameter for detection of fetal growth retardation and fetal hypertrophy in pregnancy].

This investigation contains a statistical evaluation of sonographic results concerning fetal subcutaneous adipose tissue aiming to examine and assess the relevance of this new sonographic parameter for the detection of fetal growth retardation, resp. fetal hypertrophy during pregnancy. The diagrammatic presentation of the growth of the subcutaneous adipose tissue of eutrophic fetuses shows low validity for the differentiation of hyper- and hypotrophic fetuses. To enable the differentiation between "asymmetric" and "symmetric" types of retardation, the different degrees of growth of the subcutaneous adipose tissue of hypertrophic fetuses have to be taken into consideration. The relation between birthweight and growth of the subcutaneous adipose tissue shows no distinct differentiation of the birthweight, however, presents overlapping categories of the birthweight for diagnostic orientation.

Adipose Tissue↗
PubMedDate not supplied

Monitoring of murine feto-placental growth by pregnancy-specific serum proteins in an experimentally induced fetal growth retardation model.

Fetal growth retardation was induced in 14 day pregnant female mice by ligation of the uterine arteries. Maternal serum levels of pregnancy-associated murine protein-2 (PAM-2) and murine alpha-fetoprotein (m-AFP) were recorded. The ligation resulted in a reduction in fetal growth and a corresponding decrease in maternal circulatory m-AFP, whereas placental growth and maternal circulating PAM-2 were not significantly affected.

Animals↗
PubMed1991

Brain growth among fetuses exposed to cocaine in utero: asymmetrical growth retardation.

Fetal growth retardation may be associated with maternal cocaine use during pregnancy. The pattern of fetal growth retardation was analyzed in infants born to 80 women who used cocaine, but not alcohol, during pregnancy, and in two comparison groups: 100 infants born to mothers who used neither alcohol nor cocaine during pregnancy and 67 infants whose mothers used alcohol but not cocaine during pregnancy. There were statistically significant differences in head size between the unexposed and cocaine-exposed infants (P less than .001). Notably, head circumference was reduced proportionately more than birth weight in cocaine-exposed infants, a pattern similar to that observed in alcohol-exposed infants. Alcohol- and cocaine-exposed infants were not statistically different in head circumference. We conclude that brain growth of cocaine-exposed infants is similar to that reported for alcohol-exposed infants, and that cocaine-exposed infants may be characterized as having asymmetrical growth retardation.

Alcohol Drinking↗
PubMed1983

Intrauterine growth retardation.

Fetal growth retardation ranks third after prematurity and malformations as a cause of perinatal deaths. Antenatal fetal monitoring (biochemical testing of fetoplacental function plus cardiotocography) has emerged as the most important means of reduction in the number of stillbirths and improvement in the quality of survival of infants who are born alive. Clinical acumen combined with biochemical and/or ultrasonographic testing will identify no more than 70% of growth retarded fetuses. However, not all small for dates fetuses are at risk, and many doomed to die in utero are not by definition, growth retarded. It should be the obstetrician's aim to identify the fetus at risk of death from hypoxia whether growth retarded or not. Biochemical and ultrasonographic methods of testing are not truly comparable, since some aim to identify the growth retarded fetus, irrespective of his state of health, whereas others aim to detect fetoplacental dysfunction, irrespective of whether or not the fetus is growth retarded. With present methods of antenatal diagnosis and treatment and timing of delivery determined by nonstressed cardiotocography, the physical and intellectual prognosis of growth retarded infants is most satisfactory; follow-up studies have shown that only about 2% of these infants are severely handicapped.

Delivery, Obstetric↗
PubMed1992

Intrauterine growth retardation: fetal glucose transport is diminished in lung but spared in brain.

"Uteroplacental insufficiency" often causes asymmetric fetal growth retardation. Glucose transporters control cell glucose utilization and thus may be critical in the control of fetal growth. We hypothesized that uteroplacental insufficiency might alter glucose transporter activity, protein, and gene expression and thereby affect discordant organ growth in small-for-gestational-age (SGA) fetuses. We performed bilateral uterine artery ligation in pregnant rats on d 19 of gestation (term-21.5 d) to cause uteroplacental insufficiency and obtained fetal brain and lung tissue on d 20. The brain mass of SGA fetuses did not differ from that of sham and normal fetuses, but lung mass was significantly diminished. Glucose transport, measured with [3H]2-deoxyglucose, was similar in glial cells and brain tissue of SGA, sham, and normal fetuses. In contrast, type II pneumocytes, lung fibroblasts, and lung tissue of SGA fetuses had significantly decreased glucose transport. The intrinsic activity of the glucose transporter (Km) was not altered in the brain or lung of SGA fetuses. Total glucose transporter protein measured by cytochalasin-B binding and glucose transporter 1 mRNA was diminished in SGA lung tissue and type II pneumocytes, but not in SGA brain tissue or glial cells. We could not detect glucose transporter 3 mRNA in significant quantity in any tissue. With uteroplacental insufficiency, glucose transport is differentially altered in lung and brain. Glucose transporter protein and gene expression are diminished in the lung and normal in the brain of SGA fetuses. These changes may contribute to fetal growth retardation and the phenomenon of "brain sparing."

Animals↗
PubMed1990

Epidermal development in the growth retarded fetal rat.

Intrauterine growth retardation (IUGR) due to vascular insufficiency in humans results in newborn infants with marked loss of subcutaneous fat and a poorly characterized "dysmature" appearance of the epidermis. In this study, we examined selected indices of epidermal development in 20 and 21 day old growth retarded fetal rats. IUGR was produced by unilateral ligation of the uterine artery and vein on gestational day 17. Littermate rats from the opposite uterine horn were utilized as pair matched experimental controls. A total of 49 consecutive fetal pairs were examined. Mean body weight (+/- SEM) for controls was 4.2 +/- 0.1 g versus 2.6 +/- 0.2 g for the treatment group on gestational day 20 (n = 74, P less than 0.01) and 6.0 +/- 0.1 versus 4.0 +/- 0.2 g, respectively, on the day 21 (n = 24, P less than 0.01). Examination by light and electron microscopy showed marked diminution in overall epidermal thickness in the growth retarded animals, particularly of the stratum granulosum and stratum corneum. Epidermal DNA content was decreased in IUGR pups on day 20 (0.99 +/- 0.05 versus 1.26 +/- 0.07 micrograms DNA/mg wet weight, P less than 0.05). Soluble epidermal proteins showed a similar reduction in IUGR animals (30.2 + 0.8 versus 34.7 +/- 1.6 micrograms protein/mg wet weight, P less than 0.05). IUGR also decreased the total amount of epidermal protein extractable in 8 M urea. Differentiation-specific epidermal proteins (keratins, filaggrin) were markedly reduced in the growth retarded animals following normalization to epidermal surface area and analysis by polyacrylamide gel electrophoresis. Overall, these changes in the growth retarded fetal rat lead to formation of a thin, hypoplastic, and poorly keratinized epidermal covering.

Animals↗
PubMed1991

Retarded fetal growth patterns and early neonatal mortality in a Mexico City population.

The study reported here classified 9,660 newborn infants delivered at a maternal and child health center in Mexico City by length of gestation, presence or absence of growth retardation, and (in the case of growth-retarded infants) proportionate or disproportionate growth retardation in terms of the infants' weight and length. It was found that preterm infants (delivered before 38 weeks of gestation) had nine times the early neonatal mortality of term infants, irrespective of growth retardation patterns. Also, the type of fetal growth retardation involved (proportionate or disproportionate) in those cases where such retardation was present was found to have an impact on early neonatal mortality. That is, preterm and term infants classified as having proportionate growth retardation respectively exhibited 1.5 and 9.5 times the early neonatal mortality of preterm and term infants with disproportionate growth retardation. Among other things, these findings suggest a need for assessing types of growth retardation as well as etiologic factors when evaluating mortality risk in newborns.

Classification↗
PubMed1984

Does dehydration contribute to retarded fetal growth in rats exposed to alcohol during gestation?

An earlier study showed that pregnant rats given ethanol in drinking water exhibited a significant degree of dehydration. The objective of the present study was to determine whether dehydration alone contributes to fetal growth retardation in alcohol treated rats. Female Sprague-Dawley rats were divided into 4 dietary groups. Group 1 (alcohol) received 20% ethanol in drinking water for four weeks prior to mating and 30% alcohol in drinking water throughout pregnancy and a stock diet ad libitum. Group 2 (pair-fed) was given an amount of food equal to that consumed by the alcohol group with the alcohol isocalorically substituted by corn starch. Water was available ad libitum. Group 3 (pair-water) was given an amount of food and water equal to that consumed by the alcohol animals. Group 4 (ad libitum) was given food and water ad libitum. On day 21 of gestation body weights of the alcohol exposed fetuses were significantly lower than those of the other three treatment groups. The difference in fetal body weights between the pair-fed and pair-water groups was not significant. Placentas were significantly heavier in the alcohol group than in the pair-fed and pair-water groups. Maternal plasma osmolality was significantly higher in the alcohol treated rats when compared to the pair-fed and ad libitum controls but not the pair-water group. No significant differences were seen in fetal plasma osmolality among the four treatment groups. It is concluded that dehydration does not contribute significantly to retarded fetal growth in rats given alcohol in drinking water as the sole source of fluid prior to and during gestation.

Animals↗
PubMed1994

Umbilical vessel wall fatty acids after normal and retarded fetal growth.

In a prospective observational study, the fatty acid content of human umbilical artery and vein wall phospholipids was determined in fetuses classified according to their change in abdominal circumference during the third trimester. Three groups were identified: appropriate for gestational age (AGA; 24 infants) and small for gestational age (SGA; 38 infants) with normal antenatal growth rate, and SGA with fetal growth retardation (22 infants). The venous linoleic acid (18:2 omega 6) content (expressed as a percentage of the total fatty acids identified) was greater in growth retarded SGA fetuses (3.5 (0.6)%) than in SGA fetuses with a normal growth rate (3.1 (0.5)%) and AGA fetuses (3.0 (0.5)%), whereas the venous contents of eicosatrienoic (20:3 omega 6) and docosahexaenoic acid (22:6 omega 3) were lower. In growth retarded SGA fetuses, the venous and arterial 20:3 omega 6 content correlated with the change in abdominal circumference. In SGA fetuses with a normal growth rate, lower contents of arterial 18:2 omega 6 and 22:6 omega 3 were associated with a smaller change in abdominal circumference and birth weight. Different metabolic derangements appear to underly normal and subnormal growth rate in SGA fetuses, suggesting that different strategies of dietary intervention may be required to aid fetal growth and reduce the sequelae of fetal growth retardation.

Abdomen↗
PubMed1977

Histological observations on thymic development in fetal and newborn mammals subject to intrauterine growth retardation.

Fetal growth retardation resulting from maternal dietary protein deprivation (rats) or Coxsackie virus B3 infection in mid-pregnancy (mice) was associated with delayed thymic development. Histological examination revealed that less darkly staining small lymphocytes were present and that the thymus was not well organised into cortex and medulla as seen in the normal-weight fetuses. In preterm or neonatal piglets, the histological pattern of the thymus did not vary appreciably according to the body weight of the fetus. Hassall's corpuscles were present and the tissues were well organised into cortex and medulla regions. Although fetal growth retardation in rats and mice leads to an apparent delay in the differentiation of the thymus, functional studies are necessary to understand the immunological significance of this finding.

Animals↗
PubMed1978

Ultrasonic assessment of fetal head and body sizes in relation to normal and retarded fetal growth.

Data on consecutive ultrasonic measurements of fetal biparietal diameter (B.P.D.) and fetal chest area in 303 normal and 84 small-for-dates fetuses are presented. Duration of pregnancy varied from 24 to 41 weeks. A normal curve of the fetal B.P.D., chest area, and head-to-chest ratio was constructed. At 24 weeks mean fetal B.P.D. was 6.29 cm., mean fetal chest area was 24.9 sq. cm., and mean head-to-chest ratio was 1.59. At 41 weeks the mean values were 9.81 cm., 92.4 sq. cm., and 1.05, respectively. In the group of small-for-dates fetuses, a normal head-to-chest ratio was almost always associated with early onset of fetal growth retardation whereas in the majority of fetuses with increased head-to-chest ratios, growth retardation appeared to have started only in the third trimester of pregnancy.

Female↗
PubMed1989

Small intestinal development in growth-retarded fetal sheep.

The functional maturity of the gastrointestinal system is essential for the survival of the neonate. The effects of reducing placental size and the ensuing fetal growth retardation on the development of the small intestine (SI) of the sheep fetus were investigated. At 140 days of gestation (term is 147 days), fetal body weight, gastrointestinal weight (from the abomasum to the rectum, i.e., the gut), SI weight, and SI length in the growth-retarded fetuses (n = 6) were significantly reduced (p less than 0.05) when compared with age- and breed-matched control fetuses. The SI weight was disproportionately reduced as a fraction of the gut weight or SI length (p less than 0.01). The proximal SI showed marked reductions in the thickness of the wall, muscularis externa, mucosa, villus height, and crypt depth (p less than 0.003). Densities of villi and crypts were also reduced (p less than 0.02). The crypt-to-villus ratio was maintained. Glycogen was accumulated basally in the villus epithelial cells, and their nuclei were located apically. These characteristics are comparable to those of much younger fetuses. In the distal SI, interanimal variation was large; however, the mean thickness of the wall, the muscularis externa, the mucosa, and the villus height were all reduced (p less than 0.05). In this region, the density of villi and crypts, the pattern of glycogen accumulation, and the position of the nuclei did not markedly differ between growth-retarded and control fetuses. Villus cell density was increased (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Evaluation of the success of hemodilution therapy for fetal growth retardation by Doppler sonography.

The aim of our study was to evaluate the success of a hemodilution therapy in patients with intrauterine growth retardation (IUGR) using Doppler sonography. Therefore, 22 patients with IUGR were subjected to hemodilution therapy using infusions of 500 ml hydroxyethylstarch in combination with 500 ml Ringer solution on 14 successive days. The 22 patients were divided into two groups on the basis of the actual birth weight, whereas 13 patients gave birth to an eutrophic infant (AGA group) while 9 infants remained dystrophic (SGA group). The following parameters were determined: hematocrit, prolongation of gestation, pulsatility and resistance index of the umbilical artery, the fetal aorta, the uterine arteries and the middle cerebral artery as well as the fetal outcome. Although the hematocrit decreases in both groups were almost identical, the Doppler sonographic examinations in the AGA group revealed in all cases more favorable improvements in perfusion under therapy in comparison with the SGA group. Considering the fetal aorta we could determine a worsening of perfusion in the SGA group. In the course of our investigations we have found that hemodilution therapy with hydroxyethylstarch represents a promising approach to counteract retarded fetal growth. Doppler sonography progress monitoring appears to be highly suitable for evaluating the response to therapy, especially since it can be assumed that the absence of an improvement in flow indicates only a slight advantage for the child.

Adult↗
PubMed1996

Increased energy intake in pregnant smokers does not prevent human fetal growth retardation.

A retrospective cohort study of 729 smoking and 610 nonsmoking pregnant women participating in the Prince Edward Island Prenatal Nutritional Counselling Program (1979-1989) was undertaken to study whether lower energy intake results in lower maternal weight gain and/or a higher rate of small-for-gestational-age infants (SGA) among smokers. A second objective was to quantify, using etiological fractions, the independent contributions of cigarette smoking, maternal pregravid underweight and low pregnancy weight gain to the risk of SGA. Measurements of maternal pregravid weight, height, pregnancy weight gain, smoking status, physical activity, energy intake by a series of 3-d food records throughout the duration of pregnancy, and infant birth weight were collected for women with uncomplicated pregnancies resulting in full-term singleton infants. Multiple linear regression analyses were performed to predict the effect of smoking on maternal energy intake, weight gain and infant birth weight. The independent contributions of smoking, pregravid underweight and low pregnancy weight gain to the risk of SGA were determined using logistic regression analysis. Smoking was independently associated with a higher energy intake [+702 kJ/d (+168 kcal/d)] but with lower maternal weight gain (-2.16 kg) and infant birth weight (-205 g). Dietary energy intake was positively associated with only a small increment in birth weight [5.9 g per 418 kJ (100 kcal)]. The etiologic fraction for SGA attributable to smoking was 30.8%, pregravid underweight 16.7%, and low gestational weight gain 15.3%. We conclude that the important negative effect of smoking on retarding fetal growth cannot be adequately mitigated by simply increasing energy intake.

Adolescent↗
PubMed1994

Evidence for a direct hepatotrophic role for insulin in the fetal rat: implications for the impaired hepatic growth seen in fetal growth retardation.

Perturbations of fetal growth produce parallel but disproportionate changes in fetal liver growth that correlate with circulating fetal insulin concentration. We have studied the effects of insulin and two hepatotrophic factors, transforming growth factor-alpha (TGF alpha) and hepatocyte growth factor (HGF), on DNA synthesis by fetal and adult rat hepatocytes in primary culture. Using serum-free Minimum Essential Medium, fetal hepatocytes synthesized DNA without growth factors, unlike adult hepatocytes. Insulin augmented fetal hepatocyte DNA synthesis after 16-24 h in culture. In contrast, TGF alpha or HGF maximally stimulated fetal hepatocyte DNA synthesis after 40 h in culture. Insulin and TGF alpha were not synergistic in stimulating fetal hepatocyte DNA synthesis, but were synergistic in their action on adult hepatocytes. Brief (10-min) exposure of fetal hepatocytes to TGF alpha or HGF, but not insulin, activated mitogen-activated protein kinases 4-fold. Prolonged (24-h) exposure to TGF alpha or HGF abolished the ability of either to activate mitogen-activated protein kinases, whereas insulin had no effect. Maternal fasting for 48 h before isolation and culturing of fetal hepatocytes abolished the in vitro stimulation of DNA synthesis by insulin without affecting TGF alpha action. We conclude that insulin has growth-promoting actions on fetal hepatocytes that are distinct and independent from those of TGF alpha of HGF.

Animals↗