Marker Of Fetal Growth Research Articles

High bone turnover of type I collagen depends on fetal growth

The bone metabolic processes of proliferation and differentiation in preterm and term newborns have yet to be fully elucidated. Seventy-four umbilical cord blood samples were collected from preterm and term newborns delivered at 27 to 42 gestational weeks (GWs). Carboxy-terminal propeptide of type I procollagen (PICP), pyridinoline cross-linked telopeptide domain of type I collagen (ICTP), alkaline phosphatase (ALP), and bone-specific alkaline phosphatase (BAP) were measured. Calcitonin (CT), estrogen (E 2), intact parathyroid hormone, and insulin-like growth factor-I (IGF-I) were also examined in 20 or 23 randomly selected samples. We conducted cross-sectional regression analyses for bone metabolic markers, fetal growth markers including GWs, birth weight (BW), height (BH) and head circumference (HC), and bone related hormones. PICP and ICTP activities were very high, but decreased significantly with fetal growth based on GWs, BW, BH, and HC changes (GWs, BW, and BH to both PICP and ICTP, P < 0.0001; HC to ICTP, P < 0.0001; HC to PICP, P < 0.05), while BAP and ALP did not change significantly. E 2 and CT both showed a significant positive correlation with Ca ( P < 0.05), but neither hormone had any apparent correlation with PICP, ALP, BAP, or ICTP. These results suggest very active bone formation and resorption of type I collagen to be dependent on fetal growth and that fetal osteoblasts dominate the proliferation phase of development rather than the maturation phase. However, factors contributing to high bone turnover in the fetus remain to be elucidated.

Maternal smoking is associated with mitochondrial DNA depletion and respiratory chain complex III deficiency in placenta

Maternal smoking during pregnancy is often associated with a decrease in placental function, which might lead to intrauterine growth retardation. Because tobacco is known to alter the mitochondrial respiratory function in cardiomyocytes and lung tissue, we hypothesized that placental mitochondrial function could be altered by maternal smoking. Placental mitochondria from 9 smoking and 19 nonsmoking mothers were isolated by differential centrifugation. Mitochondrial oxygen consumption was measured by polarography, and the enzymatic activity of each complex of the electron transport chain was assessed by spectrophotometry. In addition, the relative content in mitochondrial DNA (mtDNA) was determined by real-time quantitative PCR in placentas from seven smoking and seven nonsmoking mothers. We observed a 29% reduction in the enzymatic activity of complex III in the placental mitochondria from smokers compared with nonsmokers (P = 0.03). The relative content of mtDNA (with respect to the beta-globin gene) was reduced by 37% in the placental tissue from smokers compared with nonsmokers (P < 0.02). Both the enzymatic activity of complex III and mtDNA content were inversely related with the daily consumption of cigarettes, and mtDNA content was correlated with cord blood insulin-like growth factor-binding protein-3 (r = 0.74, P < 0.01), a marker of fetal growth. These results show that maternal smoking is associated with placental mitochondrial dysfunction, which might contribute to restricted fetal growth by limiting energy availability in cells.

Adiponectin - a putative novel biochemical marker of fetal growth

Adiponectin - a putative novel biochemical marker of fetal growth

S39.1: Markers of fetal growth and prevalence of asthma, hay fever, atopic dermatitis and atopic sensitization in children at age 5‐7 years

S39.1: Markers of fetal growth and prevalence of asthma, hay fever, atopic dermatitis and atopic sensitization in children at age 5‐7 years

The relation of markers of fetal growth with asthma, allergies and serum immunoglobulin E levels in children at age 5-7 years.

It has been suggested that fetal growth and maturation have an impact on the development of allergic diseases later in life. To examine the association between measures of fetal growth and allergic disease in children at age 5-7 years. As part of the German International Study of Asthma and Allergies in Childhood phase II surveys, a random sample of school beginners (n=1138) was examined in 1995. Data on anthropometric measures at birth and gestational age were obtained from maternal copies of birth records. Data on symptoms and doctor-diagnosed asthma, atopic dermatitis and hayfever were gathered by parental questionnaires. Atopic sensitization was assessed by serum IgE and skin prick tests to common aeroallergens. Children (741) had complete data for the explanatory variables of interest and were thus eligible for this analysis. Confounder-adjusted prevalence odds ratios (PORs) and means ratios with 95% confidence intervals (CI) were calculated using multiple logistic and linear regression. Birth weight and gestational age were positively associated with atopic sensitization (Ptrend=0.025 and 0.035, respectively). Children with a low birth weight relative to head circumference had a decreased risk of sensitization (POR 0.44, 95% CI 0.21-0.91; Ptrend=0.020). Moreover, total serum IgE increased with increasing birth weight (Ptrend=0.042). No consistent relationship was observed between markers of fetal growth and wheezing, doctor-diagnosed asthma, atopic dermatitis and hayfever. These data suggest that fetal growth and maturity are associated with atopic sensitization and total serum IgE levels in childhood.

Maternal serum activin A levels in association with intrauterine fetal growth restriction

To assess maternal serum activin A as a potential marker of fetal growth restriction. A cohort study. A maternal-fetal medicine unit, university teaching hospital. Fifty-seven women with a small fetus (less than 10th centile for gestation) referred for assessment of fetal size by ultrasound biometry. At the time of presentation for fetal biometry, maternal blood was collected for activin A measurement. The case records of each woman were independently reviewed after delivery and the pregnancy grouped into one of three groups: constitutionally small fetus, intrauterine growth restricted (IUGR) fetus or IUGR fetus and maternal pre-eclampsia (IUGR-pre-eclampsia). Activin A levels in the three groups were compared. Maternal serum activin A levels. Sixteen of the 57 pregnancies were classified as constitutionally small, 17 as IUGR and 24 as IUGR-pre-eclampsia. Expressed as multiples of a normal median (MoMs), the median (95% CI) activin A level in the constitutionally small pregnancies was 1.12 (0.72-1.39) MoMs significantly lower than the level in both the IUGR pregnancies, 3.00 (1.84-4.11) MoMs, and the IUGR-pre-eclampsia pregnancies, 7.96 (5.73-10.62) MoMs (P = 0.002 and 0.0001 for IUGR vs constitutionally small and IUGR-pre-eclampsia vs constitutionally small, respectively). Maternal serum activin A may be useful in the assessment of the small for gestational age fetus.

Markers of fetal growth and serum levels of insulin-like growth factor (IGF) I, -II and IGF binding protein 3 in adults.

Fetal growth has been linked with increased risk of cancer and cardiovascular disease later in life. The insulin-like growth factor (IGF) axis has recently been proposed as a predictor of risk of subsequent cancer and cardiovascular disease. However, only few data are available on the possible association between fetal growth and levels of IGFs later in life. We examined the association between markers of fetal growth, i.e. birth weight, birth length and Ponderal Index, from birth records and serum IGF-I, IGF-II, and IGF binding protein 3 (IGFBP-3) levels in 545 middle-aged Danish men and women. We fitted separate multivariate models including birth weight, birth length, Ponderal Index and serum IGF-I, IGF-II, and IGFBP-3, respectively. After adjustment for age, alcohol intake, smoking, diabetes mellitus, systolic and diastolic blood pressure, serum total cholesterol and current height and weight, we found negative associations between birth weight and Ponderal Index, respectively, and serum IGF-II in men, i.e. the mean regression coefficients were -49.41 (95% CI: -87.06-11.77) (microg/l)/kg and -3.49 (95% CI: -6.73-0.25) (microg/l)/(kg/m3), respectively. Furthermore, in men birth weight was negatively associated with the (IGF-I + IGF-II)/IGFBP-3 and IGF-II/IGFBP-3 ratios, which are believed to be indicators of bioavailable IGF and IGF-II, respectively. However, no other associations were found in any of the models. Between 1 and 16% of the variance in serum IGF-I, IGF-II, and IGFBP-3, respectively, could be explained by the statistical models used in the analyses. We found very little support to the hypothesis of an association between fetal growth and the IGF axis throughout life.

The ratio of second to fourth digit lengths: a marker of impaired fetal growth?

Epidemiological studies showing that impaired fetal growth has long-term adverse health consequences have depended on crude measures of fetal growth such as overall weight or length. For future studies, there is a need to develop improved morphological markers of fetal growth which persist into adult life. Recent studies have suggested that the ratio of the length of the second finger relative to the length of the fourth finger (2D:4D ratio) is determined during fetal life and may be such a marker. To determine whether the 2D:4D ratio is associated with size at birth. Cohort study. 139 men and women born in Preston, Lancashire between 1935 and 1943. Measurements of the 2D:4D ratio in palm prints. Men who had an above average placental weight and a shorter neonatal crown-heel length had higher 2D:4D ratios in adult life. These preliminary findings lend support to the hypothesis that the 2D:4D ratio is determined during fetal life.

The relation between adult height and haemorrhagic and ischaemic stroke in the Renfrew/Paisley study

Adult height is a useful marker of fetal growth, growth and nutrition in childhood and childhood infections. Studies reporting inverse associations between height and stroke therefore provide support for the...

Birthweight, early environment, and genetics: a study of twins discordant for acute myocardial infarction

Epidemiological studies that used birthweight as a crude marker of fetal growth have suggested that low birthweight is associated with increased risk of coronary heart disease. Through investigation of this association within same-sexed twin pairs, confounding by genetic and early environmental factors can be greatly decreased. We undertook a case-control study in twins discordant for acute myocardial infarction (AMI). The case-control study was nested within the population-based Swedish Twin Registry and linked with the national cause-of-death and hospital-discharge registries. We manually retrieved birth records containing information on birth and maternal characteristics for 132 same-sexed twin pairs discordant for AMI and 118 individually matched control twin pairs. In comparisons between AMI cases and external matched control twins, cases had significantly lower birthweight (mean 2556 [SD 500] vs 2699 [530] g, p=0.04), birth length (47.1 [2.8] vs 47.9 [2.7] cm, p=0.04), and head circumference (33.0 [1.8] vs 33.5 [2.0] cm, p=0.03) than controls. In within-pair comparisons between AMI cases and healthy co-twins, no significant differences in birth measurements were found (birthweight 2458 [510] vs 2534 [530] g, p=0.73; birth length 47.1 [2.8] vs 47.2 [2.8] cm, p=0.91; head circumference 33.0 [1.7] vs 33.0 [1.8] cm, p=0.92). The lack of an association between birth characteristics and AMI within twin pairs suggests that previously reported associations may be influenced by genetic and early environmental factors, or possibly, by unmeasured maternal factors that operate independently of birthweight.

Fetal Growth and Urinary Albumin Excretion Among Middle-aged Danes

Impaired fetal growth has been linked with cardiovascular disease and different cardiovascular risk factors. Few studies have examined the association between fetal growth and urinary albumin excretion, an important predictor of vascular disease in both diabetic and non-diabetic subjects. We examined the association between markers of fetal growth, ie, birth weight, birth length and Ponderal Index, from birth records and urinary albumin excretion in 545 middle-aged men and women who had taken part in a population-based follow-up study in the municipality of Ebeltoft, Denmark. The outcome was the urinary albumin-creatinine ratio. Three men (1.1%) and 10 women (3.6%) had a albumin-creatinine ratio above 2.5/3.5 mg/mmol, which is considered abnormal and diagnostic of microalbuminuria. The strength of the associations between birth weight, birth length, Ponderal Index and albumin-creatinine ratio were fitted in separate multivariate models, but no associations were found in any model. Our study did not support the hypothesis of an association between fetal growth and adult albumin-creatinine ratio. Studies with larger numbers of microalbuminuric subjects are required in order to further clarify the relationship between fetal growth and later renal function.

Leptin levels in maternal and cord serum: Relationship with fetal development and placental weight

Objective To test the hypothesis that the circulating levels of leptin in the maternal and cord serum correlate with the birthweight of the newborns and with the weight of the placenta. Methods In a population of 85 women from northern Greece who gave birth to an equal number of full-term infants, we calculated the concentration of leptin in the maternal serum as well as in the cord serum, right after delivery, by using an immunoradiometric assay. The correlation between these values, the maternal BMI before pregnancy and at the time of delivery, the neonatal BMI, Ponderal Index, and the placental weight was studied. Results Mean maternal leptin showed a statistically significant difference from mean cord serum leptin (14.7 and 7.07 ng/ml, respectively) and was positively correlated to the maternal BMI at the time of delivery (r = 0.3, P = 0.016), but not to neonatal BMI. A positive correlation between the mean cord serum leptin and the BMI of the neonates (r = 0.26, P = 0.031) was found. There was no correlation between the maternal BMI at the time of delivery and the neonatal BMI. Similarly, no correlation could be established between the placental weight and the levels of leptin in the maternal or in the cord serum but a positive correlation between placental weight, neonatal BMI and weight, and mothers' BMI was observed. Finally, although a noteworthy difference between the mean leptin levels of neonates of two different sexes was observed (male 5.9 ng/ml, female 7.8 ng/ml), that difference never reached a statistically significant level. Conclusions The maternal leptin level could not be used as a reliable marker of fetal growth but a positive correlation between cord serum leptin and fetus growth is suggested. J. Matern.-Fetal Med. 2000;9:298–302. © 2000 Wiley-Liss, Inc.

Leptin levels in maternal and cord serum: relationship with fetal development and placental weight.

To test the hypothesis that the circulating levels of leptin in the maternal and cord serum correlate with the birthweight of the newborns and with the weight of the placenta. In a population of 85 women from northern Greece who gave birth to an equal number of full-term infants, we calculated the concentration of leptin in the maternal serum as well as in the cord serum, right after delivery, by using an immunoradiometric assay. The correlation between these values, the maternal BMI before pregnancy and at the time of delivery, the neonatal BMI, Ponderal Index, and the placental weight was studied. Mean maternal leptin showed a statistically significant difference from mean cord serum leptin (14.7 and 7.07 ng/ml, respectively) and was positively correlated to the maternal BMI at the time of delivery (r = 0.3, P = 0.016), but not to neonatal BMI. A positive correlation between the mean cord serum leptin and the BMI of the neonates (r = 0.26, P = 0.031 ) was found. There was no correlation between the maternal BMI at the time of delivery and the neonatal BMI. Similarly, no correlation could be established between the placental weight and the levels of leptin in the maternal or in the cord serum but a positive correlation between placental weight, neonatal BMI and weight, and mothers' BMI was observed. Finally, although a noteworthy difference between the mean leptin levels of neonates of two different sexes was observed (male 5.9 ng/ml, female 7.8 ng/ml), that difference never reached a statistically significant level. The maternal leptin level could not be used as a reliable marker of fetal growth but a positive correlation between cord serum leptin and fetus growth is suggested.

Leptin concentrations in maternal serum and cord blood: relationship to maternal anthropometry and fetal growth.

To determine 1. the relationship between maternal serum leptin concentrations and maternal anthropometry and 2. the relationship between cord serum leptin concentrations at birth and neonatal anthropometry. Prospective cohort study of fetal growth in low-risk pregnancies. University teaching hospital. Thirty-nine women and their babies taking part in a fetal growth study. Blood was taken from the women between 10-20 weeks of gestation and from the umbilical cord of their babies at delivery. Serum leptin was measured by radio-immunoassay. Maternal anthropometric measurements were recorded at booking. Neonatal anthropometric measurements were recorded within 48 hours after delivery. Linear regression analysis was used to explore the relationship between serum leptin concentrations and anthropometric measures and multiple regression analysis then applied to determine which variables remained independently associated with leptin. The median (range) leptin concentration in maternal serum was 11.8 ng/mL (1.7-39.7) and in cord blood was 4.2 ng/mL (0.6-21.4). Maternal leptin levels correlated with maternal weight, body mass index, midarm circumference and skinfold thickness, but not with birthweight, placental weight or maternal height. Body mass index and midarm circumference remained significant after multiple regression analysis. Cord leptin levels correlated with birthweight, birthlength, placental weight and skinfold thickness but not with ponderal index. Birthweight and subscapular skinfold thickness remained significant after multiple regression analysis. Cord leptin concentrations did not correlate with maternal leptin concentrations. We suggest that there are very strong associations between maternal leptin and maternal adiposity in pregnancy, and between cord leptin at delivery and birthweight, as well as other anthropometric markers of fetal growth.

Prospective cohort study of factors influencing the relative weights of the placenta and the newborn infant

Objectives: To determine the demographic, environmental, and medical factors that influence the relative weights of the newborn infant and the placenta and compare this ratio with other factors known to...

Diving into iliac bone: A 3-D trip along the Z-axis of iliac bone biopsies. A video on connectivity (with Euler numbers)

The bone metabolic processes of proliferation and differentiation in preterm and term newborns have yet to be fully elucidated. Seventy-four umbilical cord blood samples were collected from preterm and term newborns delivered at 27 to 42 gestational weeks (GWs). Carboxy-terminal propeptide of type I procollagen (PICP), pyridinoline cross-linked telopeptide domain of type I collagen (ICTP), alkaline phosphatase (ALP), and bone-specific alkaline phosphatase (BAP) were measured. Calcitonin (CT), estrogen (E2), intact parathyroid hormone, and insulin-like growth factor-I (IGF-I) were also examined in 20 or 23 randomly selected samples. We conducted cross-sectional regression analyses for bone metabolic markers, fetal growth markers including GWs, birth weight (BW), height (BH) and head circumference (HC), and bone related hormones. PICP and ICTP activities were very high, but decreased significantly with fetal growth based on GWs, BW, BH, and HC changes (GWs, BW, and BH to both PICP and ICTP, P < 0.0001; HC to ICTP, P < 0.0001; HC to PICP, P < 0.05), while BAP and ALP did not change significantly. E2 and CT both showed a significant positive correlation with Ca (P < 0.05), but neither hormone had any apparent correlation with PICP, ALP, BAP, or ICTP. These results suggest very active bone formation and resorption of type I collagen to be dependent on fetal growth and that fetal osteoblasts dominate the proliferation phase of development rather than the maturation phase. However, factors contributing to high bone turnover in the fetus remain to be elucidated.

Estradiol stimulates bone mineralization at physiological concentration in fetal mouse parietal bones

The bone metabolic processes of proliferation and differentiation in preterm and term newborns have yet to be fully elucidated. Seventy-four umbilical cord blood samples were collected from preterm and term newborns delivered at 27 to 42 gestational weeks (GWs). Carboxy-terminal propeptide of type I procollagen (PICP), pyridinoline cross-linked telopeptide domain of type I collagen (ICTP), alkaline phosphatase (ALP), and bone-specific alkaline phosphatase (BAP) were measured. Calcitonin (CT), estrogen (E2), intact parathyroid hormone, and insulin-like growth factor-I (IGF-I) were also examined in 20 or 23 randomly selected samples. We conducted cross-sectional regression analyses for bone metabolic markers, fetal growth markers including GWs, birth weight (BW), height (BH) and head circumference (HC), and bone related hormones. PICP and ICTP activities were very high, but decreased significantly with fetal growth based on GWs, BW, BH, and HC changes (GWs, BW, and BH to both PICP and ICTP, P < 0.0001; HC to ICTP, P < 0.0001; HC to PICP, P < 0.05), while BAP and ALP did not change significantly. E2 and CT both showed a significant positive correlation with Ca (P < 0.05), but neither hormone had any apparent correlation with PICP, ALP, BAP, or ICTP. These results suggest very active bone formation and resorption of type I collagen to be dependent on fetal growth and that fetal osteoblasts dominate the proliferation phase of development rather than the maturation phase. However, factors contributing to high bone turnover in the fetus remain to be elucidated.

Leptin Concentrations in Maternal and Umbilical Cord Blood in Relation to Maternal Weight, Birth Weight and Weight of the Placenta

Objective: Leptin is a hormone which regulates adipose tissue mass of the body. Substantial increase of leptin during pregnancy and detection of leptin and leptin receptor in placenta have led to the speculation that leptin is a gestational hormone with a possible role in regulation of fetal growth. The study was done to find out whether maternal and cord blood leptin correlate with birthweight and weight of the placenta. Materials and methods: A prospective cross sectional study was undertaken in the Department of Obsterics and Gynecology, Bangabandhu Sheikh Mujib Medical University from January 2005 to June 2005. The study was carried out on 39 pairs of mothers and newborns. Maternal venous blood was sampled just before delivery. Cord blood was obtained, birth weight and placental weight measurements were taken just after delivery of the baby. Serum leptin levels were measured by enzyme linked immunosorbent assay. Results: Maternal serum leptin was 24.50 ng/ml (range- 13.15-45.60 ng/ml) and cord serum leptin was 6.50 ng/ml (range- 2.02-12.30 ng/ml). There was no correlation between maternal leptin and birth weight or between maternal leptin and placental weight. Cord leptin was significantly correlated with birth weight but not with placental weight. There was no correlation between maternal and cord blood leptin. There was no significant gender differences in cord blood leptin concentrations. Conclusions: There may be an important role of leptin in regulation of fetal growth and development. Placenta may not be a major source of leptin in maternal and feto-placental circulation. Maternal leptin cannot be a reliable marker of fetal growth. Keywords: Serum leptin, birth weight, placental weight doi: 10.3329/bjog.v23i1.3049 Bangladesh J Obstet Gynaecol, 2008; Vol. 23(1) : 3-7