Maternal Leptin Research Articles

Resveratrol partially prevents oxidative stress and metabolic dysfunction in pregnant rats fed a low protein diet and their offspring.

Protein restriction in pregnancy produces maternal and offspring metabolic dysfunction potentially as a result of oxidative stress. Data are lacking on the effects of inhibition of oxidative stress. We hypothesized that maternal resveratrol administration decreases oxidative stress, preventing, at least partially, maternal low protein-induced maternal and offspring metabolic dysfunction. In the present study, pregnant wistar rats ate control (C) (20% casein) or a protein-restricted (R) (10% casein) isocaloric diet. Half of each group received resveratrol orally, 20 mg kg(-1) day(-1), throughout pregnancy. Post-delivery, mothers and offspring ate C. Oxidative stress biomarkers and anti-oxidant enzymes were measured in placenta, maternal and fetal liver, and maternal serum corticosterone at 19 days of gestation (dG). Maternal (19 dG) and offspring (postnatal day 110) glucose, insulin, triglycerides, cholesterol, fat and leptin were determined. R mothers showed metabolic dysfunction, increased corticosterone and oxidative stress and reduced anti-oxidant enzyme activity vs. C. R placental and fetal liver oxidative stress biomarkers and anti-oxidant enzyme activity increased. R offspring showed higher male and female leptin, insulin and corticosterone, male triglycerides and female fat than C. Resveratrol decreased maternal leptin and improved maternal, fetal and placental oxidative stress markers. R induced offspring insulin and leptin increases were prevented and other R changes were offspring sex-dependent. Resveratrol partially prevents low protein diet-induced maternal, placental and sex-specific offspring oxidative stress and metabolic dysfunction. Oxidative stress is one mechanism programming offspring metabolic outcomes. These studies provide mechanistic evidence to guide human pregnancy interventions when fetal nutrition is impaired by poor maternal nutrition or placental function.

Does leptin predict successful induction of labor?

Obesity in pregnancy is becoming increasingly common and is associated with many pregnancy-related complications such as failed induction of labor (IOL). Leptin, an adipocytokine important in energy homeostasis, is found in higher levels in obese individuals. Leptin has also been demonstrated to have an inhibitory effect on myometrial contractility in vitro. We hypothesize that leptin may play a part in the mechanism of dysfunctional labor. Thus, we sought to compare the maternal plasma leptin levels in women that had a successful vaginal delivery post-IOL vs. those who had a C-section post-IOL.

Changes in Maternal Serum Leptin Levels during Pregnancy and after Labor in Preeclampsia, and Its Correlation to Neonatal Cord Leptin

Objective: The aim of this study is to determine changes in maternal serum leptin level during pregnancy and after labor in preeclamptic patients compared to healthy pregnant women. Furthermore, to investigate whether maternal serum leptin levels are correlated to the clinical characteristics and laboratory parameters of the study participants, and the possible correlation between maternal and neonatal leptin levels. Subjects and Methods: In this case control study, a total number of fifty five pregnant women in third trimester of pregnancy (≥28 weeks) were recruited. All of them were of the same age, body mass index, and gestational age. After a detailed obstetrical and medical history, they were divided into 2 groups. Group (A) 30 pregnant women with preeclampsia, and Group (B) 25 normotensive pregnant women. Results: During pregnancy, maternal serum leptin levels were significantly higher 41.0 ± 9.78 ng/ml in preeclamptic group compared to control group 24.6 ± 3.64 ng/ml (p = 0.007). After labor, it decreased significantly in both groups to 15.3 ± 3.19, and 11.2 ± 2.68 ng/ml respectively (p = 0.001, 0.002). In group (A) there were significant positive correlations between maternal serum leptin and diastolic blood pressure (r = 0.419, p = 0.021), total cholesterol (r = 0.383, p = 0.026), and uric acid (r = 0.424, p = 0.012) compared to controls, and no significant correlations were found between maternal serum leptin and body mass index, neonatal birth weight or cord leptin level in both groups. Conclusion: Maternal serum leptin is significantly increased in preeclamptic patients compared with normal pregnant women independent of body mass index. There is strong evidence that placenta, rather than maternal adipose tissue is responsible for that. In addition, maternal serum leptin levels were found to correlate positively with diastolic blood pressure, uric acid, and total cholesterol, but not correlated with body mass index, cord blood leptin and birth weight.

Materno-foetal leptin and insulin-like growth factor in low birth weight neonates

Low birth weight (LBW) is a health concern in developing countries. Leptin and insulin-like growth factor-I (IGF-I) are factors that influence LBW. A case-control study was conducted at Medani hospital, Sudan. Cases were women who had LBW deliveries (< 2,500 g) and controls were women with normal-weight babies (≥ 2.500–4,000 g). Sociodemographic and obstetrical characteristics were gathered from both groups and leptin and IGF-I levels were measured by ELISA. Cases and controls (45 in each arm) were matched in their basic data. The median (interquartile) of maternal leptin levels [9.9 (1.9–21.8) vs. 16.0 (9.6–20.8), ng/ml; P < 0.001] and IGF-I [1.6 (0.7–20.0) vs. 6.1 (4.3–7.1) ng/ml; P < 0.001] were significantly lower in cases than in controls. Likewise, cord serum leptin [5.8 (2.1–12.6) vs. 20.0 (5.1–37.8) ng/ml; P < 0.001] and cord serum IGF-I [1.7 (1.3–2.0) vs. 6.9 (5.9–7.4) ng/ml; P < 0.001] levels were significantly lower in cases than in controls. Significant positive correlation was found between birth weight and cord leptin (r = 0.398), maternal (r = 0.795) and cord (r = 0.863) IGF-I levels. Maternal and cord leptin and IGF-I levels were significantly lower in LBW babies.

Prenatal caffeine exposure induced a lower level of fetal blood leptin mainly via placental mechanism

It's known that blood leptin level is reduced in intrauterine growth retardation (IUGR) fetus, and placental leptin is the major source of fetal blood leptin. This study aimed to investigate the decreased fetal blood leptin level by prenatal caffeine exposure (PCE) and its underlying placental mechanisms. Pregnant Wistar rats were intragastrically administered caffeine (30–120mg/kgday) from gestational day 9 to 20. The level of fetal serum leptin and the expression of placental leptin-related genes were analyzed. Furthermore, we investigated the molecular mechanism of the reduced placental leptin's expression by treatment with caffeine (0.8–20μM) in the BeWo cells. In vivo, PCE significantly decreased fetal serum leptin level in caffeine dose-dependent manner. Meanwhile, placental mRNA expression of adenosine A2a receptor (Adora2a), cAMP-response element binding protein (CREB), a short-type leptin receptor (Ob-Ra) and leptin was reduced in the PCE groups. In vitro, caffeine significantly decreased the mRNA expression of leptin, CREB and ADORA2A in concentration and time-dependent manners. The addition of ADORA2A agonist or adenylyl cyclase (AC) agonist reversed the inhibition of leptin expression induced by caffeine. PCE induced a lower level of fetal blood leptin, which the primary mechanism is that caffeine inhibited antagonized Adora2a and AC activities to decreased cAMP synthesis, thus inhibited the expression of the transcription factor CREB and target gene leptin in the placenta. Meantime, the reduced transportation of maternal leptin by placental Ob-Ra also contributed to the reduced fetal blood leptin. Together, PCE decreased fetal blood leptin mainly via reducing the expression and transportation of leptin in the placenta.

Association between leptin and adverse pregnancy outcomes

A growing body of evidence indicates that leptin, a hormone that controls energy expenditure and intake and is produced by adipocytes, is important for normal reproductive function. To date, its exact role has not been elucidated. Leptin and its relationship to adverse pregnancy outcomes have not been adequately studied in fertile or infertile populations. Our objective was to evaluate the relationship between maternal leptin levels and adverse pregnancy outcomes.

The Effect of Diet Control on the Leptin Levels in Diabetic Pregnant Women

Introduction: Leptin is an adipokine that has strong correlation with the body mass index (BMI). Gestational diabetes mellitus (GDM) is a common medical complication associated with pregnancy. Leptin may lose its correlation with the body mass index (BMI) during diabetes due to hormonal rearrangement. Diet control is the first line management in GDM. Leptin reported to increase in pregnancy and further increases in diabetic patients during GDM screening. There is paucity in the reports concerning Leptin levels in GDM patients on diet control. The present study was aimed to evaluate the changes in maternal leptin in pregnancy complicated by GDM on diet control compared to the normal pregnancy in the 3rd trimesters by comparing the means and to find the correlation of Leptin with the body mass index in both groups. Methods: The study included 2 groups: normal pregnancy (n = 40) and pregnancy with GDM under diet control (n = 60) both groups are at 38-40 weeks of gestation. Leptin concentration in serum was measured in both groups and statistically tested using student t test. The BMI were measured and correlated with the Leptin level in test groups. Results: the results indicated that Leptin will nearly triple in the third trimester (38±30 ng/ml) of pregnancy compared to the standard normal non-pregnant. Leptin level was significantly lower in diabetic women on diet control (28±16 ng/ ml) when compared with the non-diabetics (38±30 ng/ml). The hormone has no correlation with the age of the patients but have a positive correlation with the body mass index before and during pregnancy in both groups. Conclusion: Leptin is increasing in pregnancy as part of the physiological changes. Dieting can decrease Leptin level in diabetics’ pregnant women. Diet can restore the hormonal dysregulation of Leptin. Assessment of Leptin level might be used as an indicator for good diet control during pregnancy.

Determinación perinatal de leptina en madres y neonatos con diagnóstico de retardo de crecimiento intrauterino (RCIU)

Recientemente se ha descrito que la leptina presenta actividad hormonal actuando sobre receptores y se ha involucrado con la regulación de la eficiencia metabólica, gasto energético e ingesta alimenticia. Se ha encontrado que es sintetizada en los sincitiotrofoblastos y es secretada dentro de la circulación materna. La leptina ha sido también relacionada con el depósito de grasa. Dado que en el último trimestre del embarazo humano, de manera característica, existe un depósito relativamente aumentado de grasa, y que éste se ve evidentemente depletado en los casos de RCIU, resulta entonces probable que la leptina guarde relación con la entidad. El objetivo de este estudio fue investigar si existen diferencias entre las mediciones de leptina obtenidas en un grupo de pacientes sanas y con RCIU. El estudio fue realizado en 12 pacientes con RCIU (casos) y 9 pacientes sin RCIU (controles). Se tomaron muestras de sangre materna, sangre de cordón y de líquido amniótico (LA). En el estudio pareado (n=9), los niveles de leptina en niños nacidos con RCIU presentaron concentraciones más bajas que los niños control (p = 0.05). Las concentraciones de leptina en sangre de cordón se correlacionaron significativamente con el peso del neonato (p = 0.0002) y peso placentario (p=0.048). No se encontró una correlación estadísticamente significativa de los niveles de leptina en sangre materna con el peso del neonato y el peso placentario. Las concentraciones de líquido amniótico mostraron una correlación inversa y estadísticamente significativa con el peso neonatal (p=0.035), pero no con el peso placentario (p = 0.071). Se observaron correlaciones inversas y estadísticamente significativas entre: concentraciones de leptina materna y leptina en sangre de cordón (p=0.034); leptina de cordón con leptina en líquido amniótico (p = 0.011) y correlación positiva entre leptina materna y leptina de líquido amniótico (p = 0.01).

Maternal high-fat diet programming of the neuroendocrine system and behavior

This article is part of a Special Issue “SBN 2014”.Maternal obesity, metabolic state, and diet during gestation have profound effects on offspring development. The prevalence of neurodevelopmental and mental health disorders has risen rapidly in the last several decades in parallel with the rise in obesity rates. Evidence from epidemiological studies indicates that maternal obesity and metabolic complications increase the risk of offspring developing behavioral disorders such as attention deficit hyperactivity disorder (ADHD), autism spectrum disorders (ASD), and schizophrenia. Animal models show that a maternal diet high in fat similarly disrupts behavioral programming of offspring, with animals showing social impairments, increased anxiety and depressive behaviors, reduced cognitive development, and hyperactivity. Maternal obesity, metabolic conditions, and high fat diet consumption increase maternal leptin, insulin, glucose, triglycerides, and inflammatory cytokines. This leads to increased risk of placental dysfunction, and altered fetal neuroendocrine development. Changes in brain development that likely contribute to the increased risk of behavioral and mental health disorders include increased inflammation in the brain, as well as alterations in the serotonergic system, dopaminergic system and hypothalamic–pituitary–adrenal (HPA) axis.

Differences in Maternal Leptin Serum Levels between Normal Pregnancy and Preeclampsia

BACKGROUND: Maternal circulating leptin, placental leptin gene expression and protein levels are increased in preeclampsia as compared with those in normal pregnancy. Increased serum leptin levels in preeclampsia which correspond with increased gestational age can be used independently or with other parameters as a marker for the severity of preeclampsia. The advantages of this examination in identifying preeclampsia severity are its simplicity, fast result, low cost and applicability.METHODS: A cross-sectional study was conducted in delivery room, polyclinic of Dr. M. Djamil Hospital, and Biomedical Laboratories of Medical Faculty of Andalas University from December 2013 to April 2014. The samples were collected from 68 women with singleton pregnancy in their third trimester (&gt;28 weeks) presenting to the polyclinic and the delivery room of Dr. M. Djamil hospital. Differences in maternal serum leptin between preeclampsia and normal pregnancy were determined using t-test and Wilcoxon test for data with and without normal distribution, respectively, where p&lt;0.05 indicating a significant results.RESULTS: The mean maternal serum leptin levels in normal pregnancy and preeclampsia were 1588.7964 ± 8.01074 ng/mL and 1608.1725 ± 6.69579 ng/mL, respectively. Thus, there is a statistically significant difference in mean maternal serum leptin levels between the normal pregnancy and preeclampsia (p&lt;0.05).CONCLUSION: There are significant differences in maternal serum leptin levels between women with normal pregnancy and preeclampsia.KEYWORDS: leptin, preeclampsia, pregnancy

Role of leptin in physiology of animal reproduction-A review

Leptin a multifarious hormone was discovered in 1994, a protein synthesized and secreted by adipose tissue has been shown to regulate feed intake in several species of animals. Although, a nimiety of information exists regarding the physiological role of leptin in animals, but the regulation and action of leptin in reproductive aspects of domestic animals is still naive. Emerging evidence in several species indicates that leptin may also affect the hypothalamo-pituitary-gonadal axis thus augmenting various reproductive processes. Leptin mRNA receptors are present in the anterior pituitary and hypothalamus of several species. Evidence to support direct action of leptin at the level of the gonad indicates that the leptin receptor and its mRNA are present in ovarian tissues of several species, including cattle. These leptin receptors are functional, since leptin inhibits insulin-induced steroidogenesis of both granulosa and thecal cells of cattle in vitro. Leptin receptors are present in buffalo corpus luteum in different stages of the estrous cycle. In both primates and animals, leptin receptors exist in placental tissues and may regulate metabolism of the fetal-placental unit. During pregnancy, placental production of leptin may be a major contributor for the increase in maternal leptin in primates. Leptin association can be made for body energy stores, dietary energy intake and reproductive functions in animals.

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Objectives A hypoxic placenta may release factors that result in maternal endothelial dysfunction, among which, leptin seems to participate. The aim of this study was evaluate the association of leptin levels in placenta, maternal and umbilical cord plasma between normotensive controls and pre-eclamptic women. Methods Placental biopsies, maternal and umbilical cord plasma were taken from 67 normotensive and 50 pre-eclamptic women. Leptin levels were quantified using MagPlexTH-C – microspheres system. The leptin concentration was analyzed by ANCOVA adjusted by BMI, gestational age and maternal age. To estimate the difference between groups, mean ratio (MR) and confidence interval (CI) of 95% was calculated. Analysis between leptin levels and maternal/fetal variables were made by Pearson correlation. The null hypothesis was rejected when p Results Higher levels of leptin were found in maternal plasma (MR = 1.40; 95%CI: 1.00–1.97, p = 0.049) and placenta (MR = 1.82; 95%CI: 1.11–2.98, p = 0.019) in patients with pre-eclampsia. A positive correlation between gestational age, birth weight vs. fetal leptin levels in pre-eclamptic group was found ( r = 0.416, r = 0.618; p r = 0.36, p r = 0.344, p = 0.021). No correlation was found between placenta vs. fetal plasma or fetal plasma vs. maternal plasma. Conclusions Leptin values in patients with pre-eclampsia were significantly increased in maternal plasma and placental tissue. Besides that, the positive correlation not observed between placentae and maternal leptin levels in pre-eclamptic group may be due to a loose of this regulation in pre-eclampsia, and should be considered for future work. Finally, a strong positive correlation in relation to clinical data and fetal leptin concentration, in pre-eclamptic group, intensify the possibility of leptin being also involved in preterm birth and birth weight, when pre-eclampsia is presented. Disclosures M.R. Hentschke: None. A.B. Comparsi: None. L.S. Lucas: None. F. Sontag: None. G. Gadonski: None. L.G. Paula: None. C.E. Poli-de-Figueiredo: None. B.E. Pinheiro da Costa: None.

Association between Maternal Urinary Arsenic Species and Infant Cord Blood Leptin Levels in a New Hampshire Pregnancy Cohort

Abstract Leptin is an important pleiotropic hormone involved in the regulation of nutrient intake and energy expenditure, and is known to influence body weight in infants and adults. High maternal levels of arsenic have been associated with reduced infant birth weight, but the mechanism of action is not yet understood. This study aimed to investigate the association between in utero arsenic exposure and infant cord blood leptin concentrations within 156 mother–infant pairs from the New Hampshire Birth Cohort Study (NHBCS) who were exposed to low to moderate levels of arsenic through well water and diet. In utero arsenic exposure was obtained from maternal second trimester urinary arsenic concentration, and plasma leptin levels were assessed through immunoassay. Results indicate that urinary arsenic species concentrations were predictive of infant cord blood leptin levels following adjustment for creatinine, infant birth weight for gestational age percentile, infant sex, maternal pregnancy-related weight gain, and maternal education level amongst 149 white mother–infant pairs in multivariate linear regression models. A doubling or 100% increase in total urinary arsenic concentration (iAs+MMA+DMA) was associated with a 10.3% (95% CI: 0.8–20.7%) increase in cord blood leptin levels. A 100% increase in either monomethylarsonic acid (MMA) or dimethylarsinic acid (DMA) was also associated with an 8.3% (95% CI: −1.0–18.6%) and 10.3% (95% CI: 1.2–20.2%) increase in cord blood leptin levels, respectively. The association between inorganic arsenic (iAs) and cord blood leptin was of similar magnitude and direction as other arsenic species (a 100% increase in iAs was associated with a 6.5% (95% CI: −3.4–17.5%) increase in cord blood leptin levels), albeit not significant. These results suggest in utero exposure to low levels of arsenic influences cord blood leptin concentration and presents a potential mechanism by which arsenic may impact early childhood growth.

RNA-seq analysis of the rat placentation site reveals maternal obesity-associated changes in placental and offspring thyroid hormone signaling

IntroductionIn animal models, maternal obesity (OB) leads to augmented risk of offspring OB. While placental function is influenced by maternal habitus, the effect of maternal obesity on the interacting zones of the placenta [the labyrinth (LZ), junctional (JZ) and metrial gland (MG)] remains unknown. MethodsUsing a rat maternal obesity model, we conducted transcriptomic profiling of the utero-placental compartments and fetal liver (FL) at dpc 18.5, in conjunction with analyses of mRNA expression of key thyroid hormone (TH) signaling genes in the placenta, fetus and weanling offspring. Results and DiscussionGene expression analysis of placenta and offspring revealed that each utero-placental compartment responds distinctly to maternal OB with changes in inflammatory signaling, lipid metabolism and hormone stimulus being the predominant effects. OB-induced alterations in 17 genes were confirmed by qPCR, including reductions in thyrotropin-releasing hormone (Trh) in JZ. We further characterized mRNA and protein expression of TH signaling regulators including deiodinases (Dio), TH receptors (Tr), and downstream targets (uncoupling proteins (Ucp)). A concerted down-regulation of multiple facets of thyroid hormone signaling in the JZ and FL was observed. JZ expression of thyroid hormone signaling components Trh, Dio2, Trα, and Ucp2 were negatively associated with maternal leptin. mRNA expression of TRH, TRβ and UCP1 were also decreased in term placenta from OB women. Finally, our studies identified persistent impairments in expression of TH related genes in tissues from offspring of obese dams. ConclusionsThe role of lower placental thyroid expression is worthy of further study as a possible pathway that leads to low energy metabolism and obesity in animals born to obese mothers.

Neonatal birth waist is positively predicted by second trimester maternal active ghrelin, a pro-appetite hormone, and negatively associated with third trimester maternal leptin, a pro-satiety hormone

IntroductionIn pregnancy physiological mechanisms activated by maternal appetite contribute to adequate energy intake for the mother and for the fetus. The role of maternal appetite-related peptides and their possible association with neonatal energy stores and glucose metabolism have not been investigated as yet. The aim was to investigate, during pregnancy, the association of fasting maternal appetite-related hormones levels [ghrelin (active), GLP1 (active), total PYY and leptin] with neonatal waist, percent total body fat and insulin levels at birth. MethodsForty-two normal and thirty eight overweight women (mean±SD; age: 26.9±2.5years; pre-pregnancy BMI 26±2.2kg/m2) were seen during each of the three trimesters, had blood sampling and a 75g oral glucose tolerance test. At birth, neonates underwent anthropometry and cord blood sampling for c-peptide, glucose, insulin. ResultsDuring all three trimesters maternal weight correlated positively with percent total neonatal body fat while during the second and third trimesters it correlated positively with birth weight. The second trimester maternal active ghrelin levels correlated positively with neonatal waist and were its best positive predictor. The third trimester maternal active ghrelin levels correlated positively with neonatal waist and negatively with percent total neonatal body fat, fetal cord blood insulin levels and were the best negative predictor of the latter. The third trimester maternal leptin levels correlated negatively with neonatal waist. ConclusionsDuring pregnancy circulating maternal active ghrelin, a pro-appetite hormone, is associated with neonatal visceral energy storage (as expressed by neonatal waist). By inhibiting glucose-driven maternal insulin secretion, ghrelin might ensure adequate fasting glucose and nutrient supplies to the fetus while limiting overall fetal adipose tissue deposition.

Obstetric and metabolic implications of excessive gestational weight gain in pregnancy

To compare maternal characteristics, obstetric outcomes and insulin resistance in a cohort of women subdivided into those who did and those who did not exceed the Institute of Medicine (IOM) gestational weight gain guidelines. This is a prospective study of 621 women without diabetes. Concentrations of glucose, insulin and leptin were measured in early pregnancy and at 28 weeks. Ultrasound at 34 weeks assessed fetal anthropometry including abdominal wall width (AAW). At delivery birthweight was recorded and fetal glucose, C-peptide and leptin measured in cord blood. Insulin resistance was calculated using the HOMA equation. Outcomes in those who did and did not exceed IOM guidelines were compared. Overall, 267 women (43%) exceeded IOM guidelines and 354 (57%) did not. On 34-week ultrasound women with excessive weight gain had higher fetal weights (2681 ± 356 g vs. 2574 ± 331, P = 0.001) and fetal adiposity (AAW) (5.29 ± 1.3 vs. 4.8 ± 1.2, P = 0.001). Infant birthweight and birthweight centiles were also higher in those who exceeded the guidelines. There was no difference between the two groups in maternal insulin resistance in early pregnancy, but by 28 weeks those with excessive weight gain had higher maternal HOMA indices and higher maternal leptin concentrations. Excessive maternal gestational weight gain has significant implications for infant growth and adiposity, with potential implications for later adult health.

Leptin, fetal growth and insulin resistance in non-diabetic pregnancies

BackgroundInterrogation of the association between leptin, insulin resistance and fetal growth may provide a biological link for the fetal programming of later metabolic health. AimsOur aim was to clarify the relationship between maternal and fetal leptin, insulin resistance and fetal growth. Study designMaternal leptin, glucose and insulin were measured in early pregnancy and at 28weeks and the HOMA index calculated. At 34weeks, ultrasound scan assessed fetal weight and adiposity (abdominal wall width). At delivery birthweight was recorded and cord blood analyzed for fetal c-peptide and leptin. Analysis was performed using a multivariate linear regression model. Subjects574 non-diabetic pregnant women. Outcome measuresFetal growth and maternal and fetal insulin resistance. ResultsOn multivariate analysis a relationship was identified between maternal and fetal leptin concentrations at each time point and maternal body mass index. Maternal leptin was related to insulin resistance in early pregnancy (β=0.15, p=0.02) and at 28week gestation (β=0.27, p<0.001). Fetal insulin resistance correlated with maternal leptin in early pregnancy (β=0.17, p=0.004); at 28weeks (β=0.12, p=0.05), and with leptin in cord blood (r=0.28, p<0.001).Fetal weight at 34weeks was related to maternal leptin in early pregnancy (β=0.16, p=0.02). Both maternal and fetal leptin correlated with infant size at birth (β=0.12, p=0.07 in early pregnancy, β=0.21, p=0.004 in cord blood), independent of all other outcome measures. ConclusionOur findings have confirmed that in a non-diabetic cohort there is a link between maternal and fetal leptin and insulin resistance. We also established a link between maternal leptin in early pregnancy and both fetal and neonatal size. These results add to the growing body of evidence suggesting a role for leptin in the fetal programming of childhood obesity and metabolic dysfunction.

Abstract P098: Maternal Insulin/Glycemic Regulation, Leptin, and Adiposity Levels are Associated with Newborn Adiposity

Introduction: Leptin is a hormone secreted by adipocytes that circulates in proportion to body fat. Placenta also produces leptin suggesting a specific role during pregnancy, maybe contributing to pregnancy-induced insulin resistance. Objective: To determine the associations between maternal levels of leptin, glucose and insulin and weight/adiposity measures in newborns. Methods: A population-based cohort of pregnant women in the region of Sherbrooke, Canada was recruited in early pregnancy (n=1040 at 1 st trimester). Maternal anthropometry was measured and blood samples were collected at the 1 st and 2 nd trimesters to measure glucose (hexokinase), leptin and insulin (ELISA Luminex, Millipore Canada). Birth weights were recorded from the medical records in 783 newborns (full term &gt;36 weeks). We measured skinfolds in 199 newborns within 72h after birth, using a standardized caliper. We measured triceps, biceps, subscapular and supra-iliac skinfolds and the sum of skinfolds was used for analysis representing overall neonatal adiposity. Correlations and linear regression analyses were performed to evaluate the associations between maternal metabolic characteristics and neonatal weight/adiposity measures. Results: Birth weight was associated with maternal body mass index (BMI; r=0.18 and r=0.20 at 1st and 2 nd trimesters respectively; both P &lt;0.001), percent body fat (%bf; r=0.25; P &lt;0.001), weight gain over pregnancy (r=0.14; P &lt;0.001), and fasting leptin (r=0.15, P &lt;0.001). Surprisingly, crude birth weight was not associated with maternal glycemic or insulin levels at 1 st or 2 nd trimesters (all P &gt;0.05). In contrast, sum of skinfolds was associated with maternal fasting glucose (r=0.17, P =0.01) and fasting insulin (r=0.24, P =0.001), in addition to fasting leptin (r=0.18, P =0.01) at 2 nd trimester. Sum of skinfolds was also associated with maternal BMI (r=0.18, P =0.008 at 1 st and r=0.21, P =0.003 at 2 nd trimester) and %bf (r=0.19; P =0.005). After adjustments for maternal BMI or %bf, sum of skinfolds remained significantly associated with maternal fasting insulin (all P &lt;0.05), but not with maternal leptin levels ( P =0.16 to 0.35) Conclusion: These results suggest that maternal insulin/glycemic regulation has a greater impact on neonatal adiposity than overall crude birth weight. Birth weight and neonatal adiposity are both associated with maternal leptin levels, likely representing maternal own adiposity levels that might influence neonatal outcomes directly or indirectly.

Maternal short-chain fatty acids are associated with metabolic parameters in mothers and newborns

During the course of pregnancy, dynamic remodeling of the gut microbiota occurs and contributes to maternal metabolic changes through an undefined mechanism. Because short chain fatty acids (SCFAs) are a major product of gut microbiome fermentation, we investigated whether serum SCFA levels during pregnancy are related to key metabolic parameters in mothers and newborns. In this prospective study, 20 pregnant women without gestational diabetes were evaluated at 36-38 weeks of gestation, and their newborns were assessed after parturition. In this cohort, which included normal (n = 10) and obese (n = 10) subjects based on prepregnancy body mass index, serum levels of SCFAs (acetate, propionate, and butyrate), maternal adipokines, maternal glucose, and C-peptide were measured at 36-38 weeks of gestation. Maternal weight gain and newborn anthropometrics were also determined. Data were analyzed using linear regression to test for associations, adjusting for prepregnancy obesity. In this cohort, serum acetate levels were associated with maternal weight gain and maternal adiponectin levels. In addition, serum propionate correlated negatively with maternal leptin levels, newborn length, and body weight. Taken together, this study observed that novel relationships exist among maternal SCFA levels and multiple interrelated maternal/newborn metabolic parameters.

754: Maternal and placental leptin in pregnancies associated with obesity

754: Maternal and placental leptin in pregnancies associated with obesity