Maternal Serum Leptin Concentrations Research Articles

The Effect of Maternal Overweight/Obesity on Serum and Breastmilk Leptin, and Its Associations with Body Composition, Cardiometabolic Health Indices, and Maternal Diet: The BLOOM Study.

In overweight and obese patients, elevated serum and breastmilk leptin concentrations are observed, with serum leptin also being likely affected by the diet. We analyzed serum and breastmilk leptin in normal weight (NW) and overweight/obese (OW/OB) mothers, and evaluated its associations with (1) maternal anthropometric parameters; (2) markers of cardiometabolic health; and (3) the maternal diet. The BLOOM (Breastmilk and the Link to Overweight/Obesity and Maternal diet) study was conducted among 40 women (n = 20 OW/OB; n = 20, NW) who were exclusively or predominantly breastfeeding for 15.5 ± 1.2 (OW/OB group (0.99)) weeks. We collected 24 h breastmilk and fasting blood samples for leptin analysis by ELISA. Maternal dietary habits were evaluated using a 3-day dietary record and food frequency questionnaire, which were used to calculate the Polish-adapted Mediterranean Diet score. Maternal anthropometric measurements and DEXA scans were performed, and anthropometric and cardiometabolic indices were calculated. The OW mothers had 1.4 times higher serum levels, while OB mothers had 4.5 and 6.2 higher serum and breastmilk leptin levels, respectively, in comparison to the NW mothers. The FM% was correlated with serum and breastmilk leptin levels (r = 0.878, r = 0.638). Serum leptin was associated with markers of cardiometabolic health such as AIP, CMI, and VAI in the NW mothers, and with LAP in the OW/OB mothers. Higher energy, fructose intake and adherence to the Mediterranean diet were associated with serum leptin in the NW mothers (β = 0.323, 0.039-0.608; β = 0.318, 0.065-0.572; β = 0.279, 0.031-0.528); meanwhile, higher adherence to the Mediterranean diet could protect against elevated breastmilk leptin concentrations in OW/OB mothers (β = -0.444, -0.839--0.050), even after adjustment for FM%. Our results suggest a potential association between maternal serum leptin concentrations and cardiometabolic health. In addition, we confirm the importance of healthy dietary patterns in the improvement of breastmilk composition.

Skewed fate and hematopoiesis of CD34+ HSPCs in umbilical cord blood amid the COVID-19 pandemic.

Umbilical cord blood (UCB) is an irreplaceable source for hematopoietic stem progenitor cells (HSPCs). However, the effects of SARS-CoV-2 infection and COVID-19 vaccination on UCB phenotype, specifically the HSPCs therein, are currently unknown. We thus evaluated any effects of SARS-CoV-2 infection and/or COVID-19 vaccination from the mother on the fate and functionalities of HSPCs in the UCB. The numbers and frequencies of HSPCs in the UCB decreased significantly in donors with previous SARS-CoV-2 infection and more so with COVID-19 vaccination via the induction of apoptosis, likely mediated by IFN-γ-dependent pathways. Two independent hematopoiesis assays, a colony forming unit assay and a mouse humanization assay, revealed skewed hematopoiesis of HSPCs obtained from donors delivered from mothers with SARS-CoV-2 infection history. These results indicate that SARS-CoV-2 infection and COVID-19 vaccination impair the functionalities and survivability of HSPCs in the UCB, which would make unprecedented concerns on the future of HSPC-based therapies.

Maternal Serum and Cord Blood Leptin Concentrations at Delivery in Normal Pregnancies and in Pregnancies Complicated by Intrauterine Growth Restriction

Introduction: Leptin is a polypeptide hormone, and in pregnancy, it is secreted by the placenta and maternal and fetal adipose tissues. Normal leptin production is a factor responsible for uncomplicated gestation, embryo development, and fetal growth. The study compared maternal serum and cord blood leptin concentrations at delivery in normal pregnancies and in pregnancies complicated by intrauterine growth restriction (IUGR). Methods: The study was performed in 25 pregnant women with isolated IUGR and in 194 pregnant women without any complications. Leptin concentrations in maternal serum and in cord blood samples collected at delivery were measured by ELISA and subsequently analyzed by maternal body mass index (BMI), mode of delivery, and infant gender and birth weight. For comparative analyses of normally distributed variables, parametric tests were used, that is, the Student t test and a one-way ANOVA. The nonparametric Mann-Whitney test was used when the distribution was not normal. The Pearson correlation coefficient was calculated to assess the correlation between normally distributed variables (p < 0.05). Results: In pregnancies complicated by IUGR, the mean maternal serum leptin concentration at delivery was significantly higher (52.73 ± 30.49 ng/mL) than in normal pregnancies (37.17 ± 28.07 ng/mL) (p = 0.01). The mean cord blood leptin concentration in pregnancies complicated by IUGR was 7.97 ± 4.46 ng/mL and significantly lower than in normal pregnancies (14.78 ± 15.97 ng/mL) (p = 0.04). In normal pregnancies, but not in pregnancies complicated by IUGR, a statistically significant correlation was established between maternal serum leptin concentrations and maternal BMI at delivery (r = 0.22; p = 0.00). No statistically significant correlation was found between cord blood leptin concentrations and maternal BMI in either study subjects or controls. In normal pregnancies, but not in pregnancies complicated by IUGR, a strong correlation was observed between cord blood leptin concentrations and birth weight (r = 0.23; p = 0.00). Conclusions: Elevated maternal blood leptin concentrations in pregnancies complicated by IUGR may indicate a significant adverse effect of elevated leptin on fetal growth. The differences in leptin concentrations, measured in maternal serum and in cord blood, between the study subjects and controls suggest that deregulated leptin levels may increase the risk of obstetric complications associated with placental insufficiency.

Foetal hyperinsulinaemia and increased fat mass correlate negatively with circulating fatty acid concentrations in neonates of gestational diabetic mothers with dietary-controlled glycaemia.

Higher accretion of prenatal fat is associated with a higher proportion of obesity in children. However, most of the data on regulatory factors involved in fetal adipogenesis come from animal studies; in humans there is no evidence on how fetal insulin affects fatty acid concentrations and fetal adiposity. We evaluate the relationship between fetal adipose tissue accretion with insulin and fetal consumption of circulating fatty acid (FA). In fasting maternal blood at term and cord samples, from 41 gestational diabetes mellitus women (GDM) and 68 non-diabetic controls, serum compounds were determined. Individual FA were analyzed and expressed as concentrations of FA (mmol/L). Both groups had similar maternal serum glucose, insulin, triacylglycerol (TAG), non-esterified FA (NEFA), glycerol and leptin concentrations, but most individual maternal serum FA were lower in GDM than controls. Neonatal fat mass (FM) was higher in the GDM group even though neonatal birth weights were similar. In GDM cord serum glucose, insulin, NEFA and leptin were higher than controls, but glycerol and all individual FA were lower. In GDM neonates only, a negative correlation was found between each FA and FM, and there was a strong negative correlation between the concentrations of umbilical blood insulin and five major FA. Our results show for the first time that hyperinsulinemia in fetuses of GDM women increases FA utilization, which may contribute to to their increased adiposity.

Increased maternal leptin levels may be an indicator of subclinical hypothyroidism in a newborn.

BackgroundSeveral factors may influence newborn thyroid-stimulating hormone (TSH) concentrations and cause subclinical hypothyroidism in a newborn. A sufficient level of leptin signalling is needed for the normal production of TSH and thyroid hormones by the thyroid gland. Our study aimed to investigate the correlation between maternal serum leptin concentration during the third trimester of pregnancy and newborn screening-TSH levels.MethodsThis prospective cross-sectional study was conducted in obstetrics and gynaecology clinics of a state hospital between June and August 2013. Maternal venous blood samples were collected from 270 healthy pregnant women in the third trimester just before delivery. Measurements of maternal fT3, fT4, TSH, anti-thyroid peroxidase (TPO), and anti-thyroglobulin (anti-Tg) antibodies from serum samples were performed by chemiluminescence immunoassay. Maternal serum leptin levels were determined by ELISA. Dried capillary blood spots were used to measure newborn TSH levels.ResultsSubjects were divided into two groups according to the neonatal TSH levels using a cut-point of 5.5 mIU/L. Median maternal serum leptin levels were significantly higher in newborns whose TSH levels were higher than >5.5 mIU/L [13.2 μg/L (1.3 - 46.5) vs 19.7 μg/L (2.4 - 48.5), p<0.05]. Serum leptin levels showed a negative correlation with maternal fT4 (r=0.32, p<0.05), fT3 (r=0.23, p<0.05), and a positive correlation with BMI (r=0.30, p<0.05).ConclusionsOur results suggest that high leptin levels in the third trimester of pregnancy influence maternal thyroid functions and might cause an increase in newborn TSH levels. Detection of high maternal serum leptin levels may be a reason for subclinical hypothyroidism.

The relationship between stress during pregnancy with leptin and cortisol blood concentrations and complications of pregnancy in the mother

Objective:Pregnancy is one of the most stressful periods a woman experiences in her life. The present study was an attempt to determine the relationship between maternal stress during pregnancy and cortisol plus maternal serum leptin concentrations as well as pregnancy outcomes.Material and Methods:This longitudinal study was conducted on 90 pregnant women in Miandoab city between 2015 and 2016. The samples were chosen from mothers with a gestational age of 24 to 28 weeks. The participants were asked to complete Cohen’s Perceived Stress Scale (PSS) and a demographic questionnaire and blood samples were taken from them. The mothers were then tracked with four-week intervals until the time of delivery and were asked to complete Cohen’s PSS each time along with a questionnaire related to maternal outcomes. Again, a blood sample was taken at the time of delivery. Data analysis was performed using SPSS 16. Descriptive statistics, Pearson’s correlation coefficient, and the t-test were employed for analysis.Results:A significant relationship was found between maternal stress and preeclampsia (p=0.008). The relationships between preterm childbirth and maternal cortisol concentrations in weeks 24-28 (p=0.015), and between preterm childbirth and maternal leptin concentrations at the time of delivery (p=0.007) were also found to be significant.Conclusion:Pregnancy and labor, as physically and mentally stressful events, can affect women’s physiologic and psychological indicators. As a consequence, during pregnancy, the cortisol and leptin index changes in response to the activity of the hypothalamic-pituitary axis and autonomic nervous system under stress.

Maternal serum and cord blood leptin concentrations at delivery.

IntroductionStudies have demonstrated leptin involvement in the physiology and pathophysiology of pregnancy and suggest that leptin may be a prognostic marker for some complications of pregnancy although the association remains unclear. To date no studies have reported leptin reference intervals established in normal pregnancy, which could be used for interpreting the differences in leptin levels found in normal and pathological pregnancies.ObjectiveTo determine leptin concentrations at delivery, in maternal serum in normal pregnancy and in cord blood and to establish reference intervals for leptin.Material and methodsThe study was performed in 194 pregnant women without any comorbid health conditions. Leptin concentrations in maternal serum and in cord blood were measured by ELISA and subsequently analyzed by gestational age (weeks), maternal Body Mass Index (BMI), mode of delivery and infant gender and birth weight. For comparative analyses of normally distributed variables, parametric tests such as the Student–t were used to test the assumption of homogeneity or non-homogeneity of variance and a One-Way ANOVA when more than two groups were compared. The Pearson correlation coefficient was calculated to assess the correlation between normally distributed variables (p<0.05). The reference intervals for leptin were obtained by referring to the central 95% of laboratory test values.ResultsIn normal pregnant women, the mean serum leptin concentration at delivery was 37.17 ± 28.07 ng/mL and the established reference interval was 33.19–41.14 ng/mL. The mean leptin concentration in cord blood was 14.78 ± 15.97 ng/mL and the established reference interval was 12.32–17.67 ng/mL. There was a statistically significant positive correlation between maternal serum and cord blood leptin concentrations (r = 0.37; p = 0.00). Mean leptin concentrations in cord blood increased with gestational age (p = 0.00). No statistically significant differences in maternal serum and cord blood leptin concentrations were found in regard to mode of delivery and neonatal gender. A statistically significant correlation was found between maternal serum leptin and third-trimester BMI (r = 0.22; p = 0.00), but there was no association between maternal BMI and cord blood leptin concentration. There was a statistically significant positive correlation between cord blood leptin concentration and birth weight (r = 0.23; p = 0.00).ConclusionsReference intervals for leptin in maternal serum and in cord blood established in normal pregnancy could be used in clinical practice for interpreting the differences in leptin concentrations found in normal pregnancy and in complications of pregnancy. The results indicate a strong association between maternal serum leptin levels and obesity and between cord blood leptin levels and birth weight.

Maternal and fetal Leptin and interleukin 33 concentrations in pregnancy complicated by obesity and preeclampsia

Objectives: To evaluate maternal and fetal Leptin and IL33 concentrations in pregnancy complicated by obesity and preeclampsia.Study design: A case-control study including 35 subjects with obesity (18 normotensive and 17 preeclamptic) and 47 normal weight controls (42 normotensive and 5 preeclamptic).Main outcome measures: Leptin and IL33 concentrations in maternal serum during pregnancy and in cord blood; uterine artery and umbilical artery Doppler velocimetry.Results: Subjects with obesity who developed preeclampsia had higher first trimester maternal (41.5, interquartile range (IQR) = 15.7–65.1 ng/ml) Leptin concentrations compared to either normal weight with (25, IQR = 20.4–25.8 ng/ml) and without hypertension (14.26, IQR = 8.2–22.8) (p < .05) or normotensive subjects with obesity (30.3, IQR = 10.4–38.4) (p < .05). Subjects with obesity who developed preeclampsia (2.4, IQR = 1.7–3.2 pg/ml) or not (1.4, IQR = 0.8–2 pg/ml) had lower first trimester maternal IL33 levels when compared to controls without hypertension (4.8, IQR = 2.9–5.9 pg/ml) (p < .001). Cord blood Leptin and IL33 concentrations were significantly correlated to third trimester maternal concentrations (Spearman rho = 0.51, p < .001 and Spearman rho = 0.68, p < .001, respectively). Uterine artery pulsatility index (PI) were significantly and directly correlated with maternal Leptin levels (p < .002) and inversely and statistically correlated with maternal IL33 concentrations (p < .001).Conclusions: Compared to lean controls, pregnant subjects with obesity had higher serum Leptin and lower IL33 concentrations at first trimester and during pregnancy. This difference persisted also for those who later developed preeclampsia. The relationship between maternal serum levels of Leptin and IL33 with uterine artery Doppler pulsatility index strongly suggests a role of these two markers in early placentation.

Comparison of maternal serum and umbilical cord blood leptin level in IUGR neonates

Background: Gestational weight gain is an impressive factor in the fetal outcome. Intrauterine growth restriction (IUGR) is one of the most important problems during fetal period that may lead to many perinatal and long-term complications and growing neonatal morbidities and mortalities. The aim of the study was to ascertain the relationship between umbilical cord blood leptin concentration and fetal growth in neonates born with intrauterine growth restriction. Methods: Maternal serum and umbilical cord blood leptin concentration were measured by immune radiometric assay at term gestation. The study was conducted on 22 women with uncomplicated singleton pregnancies as control group (group A) and 22 women with fetal growth restriction in singleton pregnancies as case group (group B). All subjects had normal pregravid body mass index (BMI). Results: The results of the study showed that maternal serum leptin concentrations were significantly higher in group B comparing to group A (44ng/ml [28.9-58.2] vs. 24.6ng/ml [18.8-33.3]; P<0.001). However, umbilical cord blood leptin levels were significantly lower in group B comparing to group A (8.6 ng/ml [range 4.5-12.7] vs. 14.6 ng/ml [11.7-16.7]; P<0.001). Moreover, umbilical cord blood leptin levels were directly correlated with maternal BMI and neonatal birth weight in both groups. Conclusion: In growth-restricted fetuses at term, umbilical cord blood leptin concentrations were significantly lower than normal fetuses, suggesting that fetal adipose tissue is a major source for leptin production. Maternal serum leptin concentrations were higher in the presence of a growth restricted fetuses. This increas may be due to early hypoxia or an intrinsic placental mechanism, by which small placenta produces more leptin as a compensatory mechanism. Human recombinant leptin may have some roles in the treatment of IUGR fetuses in future.

Dietary Daidzein Supplementation During Pregnancy Facilitates Fetal Growth in Rats.

Daidzein, a natural isoflavone with estrogen-like activity, has been implicated in the regulation of reproductive performance in mammals. However, little is known about the molecular mechanisms involved. Here, the effects and potential mechanisms of daidzein supplementation on fetal growth in rats have been explored. Thirty-six pregnant Sprague-Dawley rats are assigned to receive either an AIN-93M diet or an AIN-93M diet supplemented with 50mgkg-1 daidzein. Blood, placental, and fetus samples were collected on day 15 of gestation. It is shown that daidzein significantly improves the rat reproductive performance, which is associated with a higher fetus number, and the weight of the fetus and placenta (p<0.05). Daidzein also increases the maternal serum estrogen and leptin concentrations, and the activity of superoxide dismutase (SOD) (p<0.05). Notably, the isobaric tags for relative and absolute quantification (iTRAQ)-based proteomics analysis identifies 43 differentially expressed (DE) proteins in the placenta upon daidzein supplementation (p<0.05). Interestingly, critical proteins involved in amino acid transport and metabolism, embryonic development, ubiquitination processes, and immune responses are upregulated in the daidzein group (p<0.05). These results not only indicate a beneficial effect of daidzein supplementation on reproductive performance but also offer potential mechanisms behind daidzein-facilitated fetal growth in rats.

Maternal Serum Leptin at 11-13 Weeks Gestation in Normal and Pathological Pregnancies

Objective: To examine maternal serum levels of leptin at 11-13 weeks gestation in normal and pathological pregnancies. Methods: Serum leptin, PAPP-A and uterine artery pulsatility index (PI) at 11-13 weeks were measured in 480 singleton pregnancies, including 240 with normal outcome, 60 that subsequently developed preeclampsia (PE), 60 that developed Gestational Diabetes Mellitus (GDM), 60 that delivered Large for Gestational Age (LGA) neonates and 60 that delivered small(SGA) neonates. Regression analysis was used to determine factors affecting maternal serum leptin concentration and from this model each value was expressed as Multiples of the Median (MoM). The median MoM values in the outcome groups were compared. Results: In the normal group serum leptin levels increased with maternal weight and decreased with maternal height. In the PE group, the median leptin (1.18 MoM, p=0.027) and uterine artery PI (1.25 MoM, p<0.0001) were increased and serum PAPP-A (0.72 MoM, p<0.0001) was decreased. There was no significant association between serum leptin and either uterine artery PI (p=0.983) or serum PAPP-A (p=0.403). In the SGA, LGA and GDM groups serum leptin MoM was not significantly different from the controls (p=0.621, p=0.385 and p=0.722, respectively). Conclusion: In conclusion, in pregnancies that develop PE, maternal serum leptin concentration at 11-13 weeks is increased in a manner not related to altered placental perfusion or function. In pregnancies complicated by the development of GDM or delivery of SGA or LGA neonates, serum leptin is not significantly altered.

Effects of leptin supplementation to lactating Brandt’s voles (Lasiopodomys brandtii) on the developmental responses of their offspring to a high-fat diet

Maternal serum leptin concentrations have been suggested as a key factor in programming growth patterns and protecting against adult metabolic disease in human offspring. However, the role of maternal leptin in the development of wild rodent offspring is not clear. We tested the hypothesis that maternal hyperleptinemia in lactating Brandt's voles (Lasiopodomys brandtii) can protect their offspring from the risks of high-fat-diet-induced-obesity and insulin resistance. Lactating voles were supplemented with murine leptin (0.64 μg g(-1 ) day(-1)) or phosphate-buffered saline (control) on days 10-17 of lactation (peak lactation). At 12 weeks of age, the female and male offspring of the two maternal groups were randomly assigned to two groups each and fed either a high-fat diet (41% of gross energy as fat) or a control diet (14% of gross energy as fat) until the age of 23 weeks. Body mass, food intake, glucose tolerance and resting metabolic rate were determined in the four offspring groups. After animals were sacrificed, organ masses and adipose tissue distribution, and serum leptin and insulin concentrations were measured. Offspring of leptin-treated mothers showed no significant differences in body mass, energy intake or energy expenditure, body composition, glucose tolerance or serum leptin and insulin concentrations from offspring of control mothers. The high-fat diet induced increases in body mass (by 23% in female and 17% in male offspring) and reduced glucose tolerance in both female and male offspring, indicative of the emergence of insulin resistance, even though digestible energy intake of the male offspring decreased on the high-fat diet. These results indicate that maternal hyperleptinemia during peak lactation in Brandt's voles did not protect against diet-induced obesity or glucose intolerance in their offspring.

The prolonged effect of repeated maternal glucocorticoid exposure on the maternal and fetal leptin/insulin-like growth factor axis in Papio species.

Maternal obesity represents a risk factor for pregnancy-related complications. Glucocorticoids are known to promote obesity in adults. We evaluated maternal and fetal metabolic changes during and after 3 weekly courses of betamethasone administered to pregnant baboons (Papio subspecies) at doses equivalent to those given to pregnant women. Betamethasone administration during the second half of pregnancy increased maternal weight but neither maternal food intake nor fetal weight, as assessed at the end of gestation. Betamethasone increased maternal serum glucose concentration, the ratio of insulin-like growth factor-I and insulin-like growth factor binding protein-3, and serum leptin during treatment (normalized by 17, 35, and 45 days posttreatment, respectively, for each parameter). Maternal and fetal serum leptin concentrations did not differ between groups at the end of gestation. Prolonged maternal hyperleptinemia caused by betamethasone administration in the second half of gestation did not change fetal metabolic parameters measured and placental leptin distribution at the end of gestation.

Leptin in first trimester pregnancy serum: no reduction associated with small-for-gestational-age infants

Leptin is an adipocytokine that is also synthesized by the placenta. Leptin and its receptor, which is also expressed by the placenta, are believed to play an auto- and paracrine role in trophoblast invasion and placental development. The leptin concentration in first trimester maternal serum and its relation to fetal growth disturbances were examined in this study. The study is a case-control study with 36 small-for-gestational-age (SGA) (<5th percentile) pregnancies and 108 appropriate-for-gestational-age (AGA) (> or =5th percentile) pregnancies. The groups were matched by maternal age, gestational age and body mass index (BMI). All were non-smokers. Leptin was measured in maternal serum in weeks 8-13 and was normalized for BMI with concentrations expressed as multiples of the median for the actual BMI. It was found that maternal serum leptin increased strongly (r = 0.7, P < 10(-4))with maternal BMI. There was no significant difference in maternal serum leptin concentrations between SGA and AGA pregnancies. In conclusion, SGA pregnancies are not associated with a lower maternal serum leptin concentration in first trimester. The maternal serum leptin concentration is largely determined by maternal BMI. Variation in the leptin concentration in maternal serum in first trimester does not seem to be associated with impaired fetal growth.

English

Leptin is a protein secreted mainly by the adipocyte in proportion to fat mass. The serum leptin concentration reflects the amount of adipose tissue in the body and has potential role on the fat deposition in the fetus. In the present study, we investigated whether umbilical and maternal serum leptin concentrations correlate with fetal growth. In addition, we determined the relationship between leptin concentration in the maternal and cord blood. We studied 100 newborn infants (48 female and 52 male; gestational age, 34 - 40 weeks) and their mothers at Alzahra hospital in Tabriz city. Serum leptin concentrations were measured by ELISA and linear regression analysis was used to evaluate correlation. In the results, there was no significant correlation between umbilical and maternal leptin concentrations (r = 0.011; p = 0.459) in all study groups. There was a correlation between umbilical leptin concentration and birth weight of newborns (r = 0.278; p = 0.003) and correlation with body mass index (BMI) of the newborns (r = 0.249; p = 0.006). Maternal leptin concentrations correlated with maternal weight and BMI (r = 0.277; p = 0.003, r = 0.290; p = 0.002, respectively). There was no correlation between maternal leptin concentrations and birth weight (r = - 0.162; p = 0.054) and with BMI of the newborns (r = - 0.158; p = 0.058). There was gender difference in leptin concentrations in the newborns (r = 0.331; p = 0.00025) with greater level in females. In conclusion, we have shown that the association between umbilical serum leptin and birth weight in this and other studies suggests a pivotal role of fetal leptin in regulating fetal growth and development.

Maternal BMI and serum leptin concentration of infants in the first year of life

Abstract Aim: To evaluate the relationship between serum leptin concentration in infants and infant and maternal BMI. Methods: 75 healthy term infants aged 0–12 mo, 51 exclusively breastfed (BF) for at least 4 mo and 24 formula fed (FF), were included in a cross‐sectional study. Weight, length and cranial circumference of infants and their mothers were measured, body mass index (BMI) was calculated using the formula weight (kg)/height (m)2 and infant serum leptin concentration was determined. Results: A significant positive correlation between infant serum leptin concentration and maternal BMI was observed in BF infants (r = 0.389, p = 0.005), confirmed in a multiple regression model adjusted for infant age and infant BMI (β = 0.065, p = 0.006), but not in FF infants. As regards the first 4 mo of life, we have already observed a positive correlation between infant serum leptin concentration and maternal BMI in BF infants (β = 0.113, p = 0.005), but not in FF infants. Conclusion: In BF infants, serum leptin concentration correlates positively with maternal BMI. Higher maternal BMI values might increase leptin levels in breast milk, and maternal adiposity could be involved in infant energy balance.

Maternal BMI and serum leptin concentration of infants in the first year of life1

To evaluate the relationship between serum leptin concentration in infants and infant and maternal BMI. 75 healthy term infants aged 0-12 mo, 51 exclusively breastfed (BF) for at least 4 mo and 24 formula fed (FF), were included in a cross-sectional study. Weight, length and cranial circumference of infants and their mothers were measured, body mass index (BMI) was calculated using the formula weight (kg)/height (m2) and infant serum leptin concentration was determined. A significant positive correlation between infant serum leptin concentration and maternal BMI was observed in BF infants (r = 0.389, p = 0.005), confirmed in a multiple regression model adjusted for infant age and infant BMI (beta = 0.065, p = 0.006), but not in FF infants. As regards the first 4 mo of life, we have already observed a positive correlation between infant serum leptin concentration and maternal BMI in BF infants (beta = 0.113, p = 0.005), but not in FF infants. In BF infants, serum leptin concentration correlates positively with maternal BMI. Higher maternal BMI values might increase leptin levels in breast milk, and maternal adiposity could be involved in infant energy balance.

Interrelationships of Maternal Serum Leptin, Body Mass Index and Gestational Age

The aim of this study was to evaluate the interrelationships between maternal serum leptin level and body mass index (BMI) at different gestational ages or during the whole pregnancy. A total of 374 blood samples were obtained from 114 pregnant women when they visited the prenatal clinic for registration, Down syndrome screening test, 50 g oral glucose challenge test, hepatitis B markers test, and near or at the time of delivery. Serum leptin levels were measured by immunoradiometric assay. Linear regression analysis, 1-way ANOVA and post hoc tests were used to analyze the data. Throughout the course of pregnancy, maternal serum leptin concentration was significantly correlated with gestational age (p = 0.001, r = 0.179). A good correlation was also found between gestational age and maternal serum leptin level in the second trimester (p = 0.021, r = 0.158). A significant decline in maternal serum leptin was found in the third trimester (p = 0.011, r = 0.237). There were good correlations between maternal leptin and BMI in all 3 trimesters (p = 0.002 in the first trimester, p < 0.001 in the second trimester, p = 0.007 in the third trimester) and through the whole pregnancy (p < 0.001). Maternal BMI was related to gestational age in the second trimester (p < 0.001) and the whole pregnancy (p < 0.001), but not in the first (p = 0.404) and third trimesters (p = 0.053). Maternal serum leptin concentration was significantly related to gestational age (except in the first trimester) and BMI in the 3 trimesters and throughout pregnancy. Serum leptin concentration peaked during the early third trimester and declined significantly thereafter. Maternal BMI was related to gestational age in the second trimester and the whole pregnancy.

Effect of Smoking on Neonatal and Maternal Serum and Breast Milk Leptin Levels

Maternal smoking is considered to be a risk factor for low birth weight. It is hypothesized that alteration in leptin concentration may be associated with reduced fetal growth. In this study, we assess the effect of smoking during pregnancy on maternal and neonatal serum leptin concentrations, and also on breast milk leptin levels. When the infants were brought to routine physical examination at 7 days old, blood samples and breast milk specimens were taken for leptin measurement from mothers who smoked during pregnancy and their newborns. Nonsmoking mothers and their infants were recruited randomly over the same period as a control group. Maternal age, number of pregnancy, weight of the mothers, birth weight, and gestational age of the infants were similar in both groups (p > 0.05). There was no significant difference between groups in maternal serum and breast milk leptin levels (p = 0.14 and p = 0.96, respectively). However, serum leptin levels were found significantly lower in neonates born to smoking mothers compared with infants born to nonsmoking mothers (p = 0.02). Our findings suggest that maternal smoking dose not have an effect on maternal serum and breast milk leptin levels but decreases neonatal serum leptin concentration independent of birth weight.

Daily Rhythms of Serum Leptin in Ewes: Effects of Feeding, Pregnancy and Lactation

The aim of the present study was to test whether serum concentrations of leptin in ewes vary with a daily rhythm. For this purpose, we examined 24 h serum leptin profiles of ewes exposed to natural photoperiodic conditions and subjected to two different feeding schedules (regular feeding and fasting). The results show for the first time the existence of daily rhythm of plasma leptin in regularly fed ewes, with a minimum during the light phase and a peak during the dark phase. Daily rhythms of serum leptin persisted after 50 h of fasting, although fasting shifted the peak of the rhythm to the beginning of the light phase and significantly reduced daily leptin production. To gain a better understanding of the role of leptin in the temporal organization of physiological events related to pregnancy and lactation, we measured serum leptin profiles throughout 24 h in ewes either during pregnancy or lactation. Daily leptin rhythms were found to persist during pregnancy and lactation, but both physiological conditions altered leptin concentrations. Maternal serum leptin concentration rose between early and mid pregnancy, then decreased in the late pregnancy and during lactation. Daily serum leptin concentration was significantly lower in nonpregnant, nonlactating ewes, compared either to lactating or to early pregnant ewes.