Umbilical Cord Leptin Levels Research Articles

Effect of gestational Mediterranean diet intervention on newborn fat mass and cord blood leptin level

BackgroundMaternal nutritional status is an important determinant of intrauterine growth and neonatal size. No published surveys exist on maternal Mediterranean diet intakes and newborn adiposity. The aim of the study was to evaluate the impact of the individual maternal Mediterranean diet on the in-utero body fat formation and cord leptin level in newborns. Pregnant women with a pre-pregnancy body mass index (BMI) between 30 and 35 kg/m2 (n = 118) were assisted for individual dietary counseling based on the Mediterranean diet healthy eating. According to diet adherence, participants (paired mother and newborn) were divided into an intervention group (n = 57) and a control group (n = 61). We examined the association between diet modification and gestational weight gain, maternal, and cord leptin level together with newborn anthropometry (weight and fat mass %).ResultsGestational weight gain, newborn birth weight, fat mass %, and cord leptin level lower in the intervention (12.22 ± 1.8 kg, 3.57 ± 0.35 kg, 9.27 ± 2.16 %, 11.78 ± 3.63 ng/ml, p = 000, respectively) than in control group (18.03 ± 3.25 kg, 4.02 ± 0.32 kg, 11.85 ± 2.30 %, 35.37 ± 11.14 ng/ml, respectively. Umbilical cord leptin levels strongly correlated with neonatal fat mass percent in both groups. However, maternal serum leptin did not correlate with the newborn parameters in the intervention group.ConclusionMaternal energy intake from healthy fat and diet intervention is probably associated with decreased fat mass and leptin levels in neonates.

Umbilical Cord SFRP5 Levels of Term Newborns in Relation to Normal and Excessive Gestational Weight Gain.

Among the new adipokines, secreted frizzled-related protein 5 (SFRP5) is considered to prevent obesity and insulin resistance. The umbilical cord SFRP5 levels have not yet been investigated. The main aim of the study was to investigate whether the umbilical cord SFRP5 concentrations are altered in term neonates born to mothers with excessive gestational weight gain (EGWG). Two groups of subjects were selected depending on their gestational weight gain, i.e. 28 controls and 38 patients with EGWG. Umbilical cord and maternal serum SFRP5 levels were lower in the EGWG group. Umbilical cord SFRP5 concentrations were directly associated with the maternal serum SFRP5, hemoglobin A1c and lean tissue index, umbilical cord leptin levels, as well as newborns’ anthropometric measurements in the EGWG subjects. In multiple linear regression models performed in all the study participants, umbilical cord SFRP5 concentrations depended positively on the maternal serum SFRP5, ghrelin, and leptin levels and negatively on the umbilical cord ghrelin levels, low-density lipoprotein cholesterol, pre-pregnancy body mass index, and gestational weight gain. EGWG is associated with disturbances in SFRP5 concentrations. Obstetricians and midwives should pay attention to nutrition and weight management during pregnancy.

Umbilical cord blood leptin concentration - What does it imply?

Objective: The significance of the placental or umbilical cord leptin levels remains unresolved in spite of their well-documented function. In the current study we investigated, whether, leptin concentration that mirrors the fetal health is influenced by type of birth, placental weight, cord length, sex, weight, pO2 and pH parameters. Methods: Umbilical cord blood samples were collected post placental delivery (n=40) from both normal and caesarian deliveries with all demographical information. Leptin concentration was determined form cord blood plasma, while fresh cord blood was used for blood gas analysis. Results: The average leptin concentrations of male and female fetal umbilical cord were 16.6 ± 1.6 and 18.2 ± 0.6 ng/ml respectively. The maximum threshold of the umbilical vein leptin concentrations were 15.3 ± 0.6 and 18.3 ± 1.2 ng/ml in male and females respectively. There was a direct relationship observed with the birthweight and leptin concentration. The mean pH 7.117 ± 0.02 and pO2 19.74 ± 2.01 mmHg did not significantly correlate with leptin levels. Discussion: Leptin concertation were significantly high in normal delivery than caesarian section. Placental weight or umbilical cord length did not affect the leptin concentration. We did not observe any significant alteration in pH or pO2 levels influencing leptin. However, the most remarkable correlation was leptin with birth weight, which explains the best utilization of the maternal fuel resources in the development of the fetus. We did observe a level in female babies. Conclusion: Overall, the placental leptin concentration mirrors the health status of the fetus and weight metabolism.

Clinical study on umbilical cord leptin levels associated with fetal growth and neonatal birth weight

Objective To study the relationship between umbilical cord leptin levels and fetal growth as well as neonatal birth weight. Methods One hundred and forty-two neonates selected from February 2009 to June 2013 in Shangqiu First People's Hospital according to the different gestational age and birth weight were divided into 3 groups.Group A included 44 cases(small for gestational age, birth weight below the average weight of the 10th percentile at the same gestational age), 23 boy cases, 21 girl cases; group B included 56 cases (appropriate for gestational age, birth weight at the average weight of the 10th to 90th percentile at the same gestational age), 30 boy cases, 26 girl cases; group C included 42 cases (large for gestational age, birth weight above the average weight of the 90th percentile at the same gestational age), 22 boy cases, 20 girl cases.Neonatal body mass index, birth weight, placenta weight and umbilical leptin levels of three groups were compared. Results Neonatal birth weight, neonatal body length, body mass index and the placenta weight leptin levels in group A were significantly lower than those of group B, having statistically significant difference (all P<0.001); Neonatal birth weight, neonatal body length, body mass index and the placenta weight leptin levels in group C were significantly higher than those in group B, with statistically significant difference (all P<0.001). Neonatal birth weight in the boy group was obviously higher than that of the girl group, and the difference was statistically significant (P<0.001). Neonatal leptin levels in the boy group were significantly lower than that of the girl group, and the difference was statistically significant (P<0.001). There were positive correlations between the umbilical cord leptin levels and the neonatal birth weight, neonatal length, neonatal weight index and the placenta weight(r=0.382, 0.276, 0.358, 0.412, all P<0.01). Conclusions The umbilical cord leptin levels are closely associated with neonatal birth weight and intrauterine growth retardation, and it can be used as one of the important indicators for reflecting neonatal birth weight and fetal growth. Key words: Infant, newborn; Birth weight; Intrauterine growth retardation; Leptin; Correlation

Multiple Correlations Between Cord Blood Leptin Concentration and Indices of Neonatal Growth

The discovery of a role for leptin in controlling fetal and neonatal growth suggests a fetal origin of some adult chronic diseases and has stimulated research into the mechanisms of action of leptin early in life. The aim of this study was to determine umbilical cord blood leptin levels and to evaluate their association with newborn growth indices. Two hundred healthy newborns (89 males, 110 females, and one of undetermined gender; gestational ages ranging from 34-43 weeks) and their healthy mothers were enrolled in this study conducted at Moovsavi Hospital in Zanjan, Iran. The body size index of each newborn was determined in terms of birth weight, birth length, head circumference, body mass index (BMI) and ponderal index. Umbilical cord blood leptin levels were measured by ELISA. Umbilical cord leptin concentration was found to positively correlate with birth weight (r=0.322; p<0.0001), neonatal BMI (r=0.247; p<0.0001), ponderal index (r=0.206; p=0.04), and gestational age (r=0.221; p=0.002). There was no significant correlation between cord leptin and birth length or umbilical glucose concentration. Umbilical cord leptin concentrations (15.20+/-12.3 vs. 12.08+/-11.7; p=0.01) were significantly greater in female as compared to male newborns, respectively. Linear regression analysis indicated that umbilical cord leptin levels correlated with birth weight, umbilical triglyceride concentration, neonatal gender, and method of delivery. Our findings confirm the association of leptin concentrations with weight gain in fetal and newborn infants.

Common SNPs in LEP and LEPR associated with birth weight and type 2 diabetes-related metabolic risk factors in twins

Children born small for gestational age are at increased risk of developing type 2 diabetes in adulthood. The satiety signal leptin that regulates food intake and energy expenditure might be a possible molecular link, as umbilical cord leptin levels are positively correlated with birth weight. In the present study, we examined whether common single nucleotide polymorphisms (SNPs) in the leptin (LEP; 19G>A) gene and its receptor (LEPR; Q223R and K109R) are associated with birth weight and adult metabolic risk factors for type 2 diabetes in twins. SNPs were genotyped in 396 monozygotic and 232 dizygotic twins (286 men and 342 women, mean age 25 years) recruited from the East Flanders Prospective Twin Survey. Data were analysed using linear mixed models. The LEPR K109R SNP was associated with birth weight (KK, KR and RR (95% confidence interval, CI): 2511 (2465-2557), 2575 (2516-2635) and 2726 (2606-2845) gram; P(additive)=0.001). Also the LEPR Q223R SNP showed a significant association with weight at birth (QQ, QR and RR (95% CI): 2492 (2431-2554), 2545 (2495-2595) and 2655 (2571-2740) gram; P(additive)=0.003). Furthermore, an interaction between the LEPR K109R and the Q223R SNP on birth weight was observed (P=0.014). G allele carriers of the LEP 19G>A SNP had higher high-density lipoprotein (HDL) cholesterol levels compared to 19A homozygotes (GX vs AA (95% CI): 1.62 (1.58-1.66) vs 1.49 (1.40-1.58) mmol l(-1); P(recessive)=0.013). This study indicates that leptin may act as a growth-promoting signal during fetal development, and suggests a possible role for the LEPR in explaining the inverse relationship between birth weight and the development of metabolic diseases in adulthood. Additionally, these results suggest that the LEP 19G>A SNP affect HDL cholesterol levels.

Maternal and Umbilical Cord Serum Leptin Concentrations in Small-for-Gestational-Age and in Appropriate-for-Gestational-Age Neonates: A Maternal, Fetal, or Placental Contribution?

Leptin is secreted during pregnancy by the placenta and by the maternal and fetal adipose tissues. The leptin levels mainly reflect the amount of fat stored and thus are indicative of the energy balance, i.e., small-for-gestational-age (SGA) neonates represent the negative metabolic balance of in utero starved babies. We chose to compare maternal and umbilical cord leptin levels in pregnancies complicated by asymmetrical SGA versus those with appropriate-for-gestational-age (AGA) neonates as well as a model of multifetal growth concordant gestations in order to establish through the ‘leptin link’ the relative contributions of mother, fetus, and placenta to fetal weight. We found that the maternal leptin levels at delivery correlated poorly with the maternal weight gain/body mass index and with neonatal birth weight. Furthermore, the umbilical cord leptin levels correlated well with neonatal and placental weights in the AGA group but not in the SGA group. As in AGA singleton pregnancies, in multifetal uncomplicated pregnancies, the umbilical cord leptin levels correlated well with the birth weight of individuals, regardless of the status of the twin or triplet in the set. Thus, we speculated that in SGA neonates the birth weight represents the lean body weight and the low adipose tissue content (as opposed to the AGA neonates who have a substantial adipose tissue content) and, therefore, reflects mainly the basic placental contribution.

Maternal and Fetal Leptin Correlate with Fetal Growth in Preeclampsia.† 1519

Serum leptin, the product of the obesity (ob) gene, correlates with adiposity and increases fat utilization. Leptin mRNA is present in the placenta, suggesting a role for leptin in fetal growth. Maternal serum leptin, triglyceride (trig) and free fatty acids (FFA) are elevated in healthy pregnancy, and are increased further in preeclampsia (PRE). Umbilical cord leptin levels correlate with birth weight, but not with maternal leptin levels in healthy pregnancy. Preeclampsia is associated with reduced perfusion of the placenta. We hypothesized that leptin production is increased in poorly perfused placenta in PRE and by increasing maternal fat utilization increases fuel availability to the fetus promoting fetal growth. Methods: Venous blood was obtained prepartum from 14 women with PRE and 15 healthy pregnant women (CNTL). Mixed arterio-venous blood was obtained from the umbilical cord of their infants at delivery. Plasma leptin concentration was measured by human antibody RIA. Lipids were measured by standard techniques. Data were analyzed using Mann-Whitney comparison of medians and Pearson correlation. Results: Median gestational age (38.1 v 37.7 wks), birth weight (BW, 3.1 v 3.2 kg), maternal leptin (52.8 v 26.7 ng/ml), cord leptin (3.7 v 5.6 ng/ml), maternal trig (263 v 239 mg/dl) and FFA (0.84 v 0.61 mmol/L) did not differ between PRE and CNTL, while BW%ile (29.3 v 59.7%) was significantly different at p=0.05. The correlation between maternal and cord leptin was highly significant in PRE (r=0.87, p=0.000) but not in CNTL(r=-0.16). Maternal trig did not correlate with leptin in PRE (r=-0.34) or CNTL (r=0.10). Maternal FFA correlated with leptin in CNTL (r=-0.72, p=0.003) but not PRE (r=-0.16). BW correlated with both maternal leptin (r=0.71, p=0.004) and cord leptin (r=0.67, p=0.012) in PRE. Only cord leptin was related to BW in CNTL (r=0.69, p=0.005). Conclusion: These data confirm the positive relationship between cord leptin and BW. We also found highly significant correlations of maternal leptin to cord leptin and to BW in preeclampsia which are not present in healthy pregnancy. Our hypothesis that maternal leptin increased in preeclampsia to increase fuel availability for the fetus is, however, not supported by these preliminary data.