Maternal Fat Intake Research Articles

Associations between maternal body mass index and diet composition with placental DNA methylation at term

IntroductionMaternal obesity and poor quality diets are associated with greater risk of obesity in offspring. Maternal diet and obesity influence placental gene expression and nutrient transport, but the impact of diet and obesity on global epigenetic changes in the placenta are poorly understood. We hypothesized that placental DNA methylation patterns are associated with maternal body mass index (BMI) and/or maternal diet composition. MethodsUsing reduced representation bisulfite sequencing (RRBS), we assessed genome scale DNA methylation of ~300,000 CpGs in 150 term placentas from normal weight mothers (n = 72) and overweight/obese mothers (n = 78). Maternal BMI was assessed before week 10 of gestation and maternal diet composition was assessed using 3-day food records at each trimester. ResultsIn multivariable linear regression models, maternal BMI category (normal weight or overweight/obese), BMI (kg/m2), and maternal saturated fat consumption (g/d) were associated (p < 0.0001) with methylation of 185, 103, and 302 CpGs, respectively. Of the 56 CpGs associated with both maternal BMI category and maternal BMI (p < 0.0001), GO analysis showed biological processes related to SREBP signaling, phospholipid transport, granulocyte differentiation, and RNA pol II transcription to be affected. Maternal saturated fat intake was associated with methylation of 302 CpGs (p < 0.0001). These genes were related to chromatin remodeling, IGF receptor, PI3K, and nitric oxide synthase signaling. DiscussionThese data suggest that placental DNA methylation status is associated with both maternal obesity and maternal saturated fat intake, possibly contributing to maternal obesity-associated changes in placental function.

The microbiota composition of the offspring of patients with gestational diabetes mellitus (GDM).

The microbiota composition of the offspring of women with gestational diabetes mellitus (GDM), a common pregnancy complication, is still little known. We investigated whether the GDM offspring gut microbiota composition is associated with the maternal nutritional habits, metabolic variables or pregnancy outcomes. Furthermore, we compared the GDM offspring microbiota to the microbiota of normoglycemic-mother offspring. Fecal samples of 29 GDM infants were collected during the first week of life and assessed by 16S amplicon-based sequencing. The offspring’s microbiota showed significantly lower α-diversity than the corresponding mothers. Earlier maternal nutritional habits were more strongly associated with the offspring microbiota (maternal oligosaccharide positively with infant Ruminococcus, maternal saturated fat intake inversely with infant Rikenellaceae and Ruminococcus) than last-trimester maternal habits. Principal coordinate analysis showed a separation of the infant microbiota according to the type of feeding (breastfeeding vs formula-feeding), displaying in breast-fed infants a higher abundance of Bifidobacterium. A few Bacteroides and Blautia oligotypes were shared by the GDM mothers and their offspring, suggesting a maternal microbial imprinting. Finally, GDM infants showed higher relative abundance of pro-inflammatory taxa than infants from healthy women. In conclusion, many maternal conditions impact on the microbiota composition of GDM offspring whose microbiota showed increased abundance of pro-inflammatory taxa.

An association between hypertensive disorders in pregnancy and childhood diagnosis of asthma

This cohort study examined the relationship between maternal intake of individual fatty acids, meat, and fish during pregnancy and the risk of wheeze and eczema in children aged 23–29 months because epidemiologic evidence on this topic is inconclusive.Subjects were 1354 Japanese mother-child pairs. Data on maternal intake during pregnancy were assessed with a validated diet history questionnaire. Data on symptoms of wheeze and eczema were based on criteria of the International Study of Asthma and Allergies in Childhood.Significant inverse exposure-response relationships were observed between maternal intake of eicosapentaenoic acid (EPA) and EPA plus docosahexaenoic acid (DHA) during pregnancy and infantile wheeze although the adjusted odds ratios between extreme quartiles fell just short of the significance level. No such inverse relationships were detected for infantile eczema. Maternal intake of total fat, saturated fatty acids, monounsaturated fatty acids, total n-3 polyunsaturated fatty acids (PUFA), α-linolenic acid, DHA, total n-6 PUFA, linoleic acid, arachidonic acid, cholesterol, fish, and meat and the ratio of n-3 to n-6 PUFA consumption were not significantly related to infantile wheeze or eczema.Higher maternal intake of EPA and EPA plus DHA during pregnancy may reduce the risk of infantile wheeze.

Effect of Maternal High Fructose and Offspring High Fat Intake on Programmed Hypertension in Young Adult: the Role of Nutrient Sensing Signaling in the Brain

There is now substantial epidemiological evidence suggesting the origin of susceptibility for metabolic syndromes (MetS) and associated cardiovascular dysfunctions in adulthood can be traced back to the early life. We have previously demonstrated that maternal high fructose diet (HFD) induces programmed hypertension in adult offspring; however, the cellular and molecular signaling contributing to the developmental programming of adult hypertension is not fully understood. There are a number of nutrient sensing pathways, including silent information regulator transcript (SIRT), AMP‐activated protein kinase (AMPK), and phosphatidylinositol 3‐kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) located in the central nervous system and are responsible for the detection of sugars, amino acids, lipids and the surrogate metabolite level for the maintenance of metabolic homeostasis. Perturbation of these signaling pathways could lead to MetS and the associated cardiovascular complications. This study was designed to investigate the role of these nutrient sensing pathways in the brain on developmental programming of hypertension in offspring to maternal HFD, and the influence of high fat diet (HFatD) in offspring to these nutrient sensing pathways. Female Sprague‐Dawley rats were fed with 60% HFD or normal diet (ND) during gestation and lactation periods. After weaning both HFD and ND offspring were subjected to HFatD or ND from the age of 3 to 12 weeks. Blood pressure was monitored under conscious condition via tail‐cuff method from week 6 to 12. Expression of nutrient sensing signals in the forebrain hypothalamus was examined by Western blot analysis. Tissue oxidative stress was quantified by electron spin resonance spectroscopy. Maternal HFD induced programmed MetS and hypertension that became significant at age of 9 weeks and maintained in young adult at age of 12 weeks. Changes in both metabolic and blood pressure phenotypes were appreciably enhanced in HFD offspring with additional HFatD intake after weaning. Protein expressions of SIRT1, phosphorylated AMPK (p‐AMPK), and p‐Akt in the hypothalamus were downregulated in the HFD offspring, which were further suppressed in offspring fed with HFatD. These molecular changes were associated with tissue oxidative stress in the hypothalamus.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Risk factors associated with the development of double-inlet ventricle congenital heart disease.

Congenital heart disease (CHD) is the most common birth defect group and a significant contributor to neonatal and infant death. CHD with single ventricle anatomy, including hypoplastic left heart syndrome (HLHS), tricuspid atresia (TA), and various double-inlet ventricle (DIV) malformations, is the most complex with the highest mortality. Prenatal risk factors associated with HLHS have been studied, but such data for DIV are lacking. We analyzed DIV cases and nonmalformed controls in the National Birth Defects Prevention Study, a case-control, multicenter population-based study of birth defects. Random forest analysis identified potential predictor variables for DIV, which were included in multivariable models to estimate effect magnitude and directionality. Random forest analysis identified pre-pregnancy diabetes, history of maternal insulin use, maternal total lipid intake, paternal race, and intake of several foods and nutrients as potential predictors of DIV. Logistic regression confirmed pre-pregnancy diabetes, maternal insulin use, and paternal race as risk factors for having a child with DIV. Additionally, higher maternal total fat intake was associated with a reduced risk. Maternal pre-pregnancy diabetes and history of insulin use were associated with an increased risk of having an infant with DIV, while maternal lipid intake had an inverse association. These novel data provide multiple metabolic pathways for investigation to identify better the developmental etiologies of DIV and suggest that public health interventions targeting diabetes prevention and management in women of childbearing age could reduce CHD risk.

Pre-pregnancy Body Mass Index and Maternal Nutrition in Relation to Infant Birth Size.

This cross-sectional study examined the relationship between maternal pre-pregnancy body mass index (BMI) and dietary intake on birth size in the north-east part of Iran. Maternal information including BMI and dietary intake from 453 healthy pregnant women were collected in 2013–2014. Maternal pre-pregnancy BMI were obtained from health records and dietary intakes in third trimester were collected by using a validated food frequency questionnaire (FFQ), which consisted of 160 Iranian foods. Anthropometric measurements of neonates including weight, height, and head circumference were 3.19 ± 0.49 kg, 50.24 ± 2.1 cm, and 34.61 ± 1.5 cm, respectively. A significant difference was found in neonatal birth weight (p < 0.001) and head circumference (p = 0.002) between underweight and obese mothers. Furthermore, maternal intake of fat had a direct correlation with birth size. There was a positive relationship between vitamin A and potassium intake and birth height. The article concludes that normal maternal pre-pregnancy weight and appropriate diet are likely essential for healthy babies.

Effects of Maternal Carbohydrate and Fat Intake on Fetal Telomere Length.

Telomere length can be affected by dietary factors in adults. We investigated the association between maternal carbohydrate and fat intake during pregnancy and telomere length in neonatal cord blood leukocytes. We hypothesized that high fat consumption and high carbohydrate consumption would be associated with shortened fetal telomere length. We collected umbilical cord blood at delivery from women admitted for labor and delivery in a university hospital (N = 62) and extracted genomic DNA using quantitative polymerase chain reaction. We quantified telomere length using the telomere-to-single copy gene ratio method (T:S ratio). High carbohydrate intake was defined as consumption of >175 g/day and high fat intake as >35 g/day. We performed generalized linear regression modeling and bootstrap statistical analyses to derive precise estimates of association. Of the 62 maternal-fetal dyads included in this study, 79% were classified as high carbohydrate consumers and 37% were classified as high fat consumers. High fat consumption had a significant negative effect on T:S ratio (P < 0.05). Although high carbohydrate consumption was associated with a decreased T:S ratio, this relation did not attain statistical significance. To our knowledge, this study is the first evidence of an association between maternal high fat consumption and shortened fetal telomere length. These findings could enhance our understanding of the role of maternal diet in fetal programming.

Hepatic Autophagy Gene Expression Is Induced by Post‐Weaning Diets in Sprague‐Dawley Rats fed with A Low‐Protein Diet During Lactation

BackgroundBoth maternal dietary protein restriction and excess fat intake are associated with numerous metabolic responses including the activation of transcription factor 4 (ATF4). ATF4 is one of the master regulators of stress response pathways, which potentially program autophagy genes expression in the liver of offspring rats.HypothesisThe current study tested the hypothesis that lactational low‐protein (LP) diet and postnatal high‐fat (HF) diet induce a metabolic mismatch that activates autophagy gene expression through the activation of ATF4 in the liver of offspring rats.MethodsTimed‐pregnant Sprague‐Dawley rats were fed a control diet (C, 20% protein) during gestation followed by either a LP diet (8% protein) or the control diet during lactation for 21 days. At weaning, the offspring was fed either C (16% fat) or HF (45% fat) to generate three offspring groups: C/C/C, C/LP/C and C/LP/HF. At 12 weeks of age, liver samples of male and female rats were collected for analysis.ResultsLactational LP diet and post‐weaning HF diet induce autophagy gene expression differentially in the liver of male and female offspring. mRNA expression of Beclin1, p62/sqstm1, LC3b and Atg5, crucial markers of autophagy, was significantly upregulated by lactational LP diet (C/LP/C when compared to C/C/C, p&lt;0.05) in female offspring, but not in male offspring. Consistent with that, mRNA expression of other autophagy related genes including Atg16l1, Atg12 Atg3, Gabarapl2, Atg7, Atg10 and Gabarap increased significantly in the female offspring only. Moreover, autophagy genes Atg16l1, Atg12, Atg3, Beclin1, p62/sqstm1, LC3b, Gabarapl2, Atg7, Atg10, Gabarap, and Atg5 were expressed at a higher level by post‐weaning HF diet (C/LP/HF when compared to C/LP/C, p&lt;0.05) in both male and female offspring. A master regulator of stress pathway, transcription factor ATF4, also displayed differential expression in the mismatched dietary groups.ConclusionLactational low‐protein diet induced autophagy related gene expression in female offspring and the induction was further augmented by a post‐weaning high‐fat diet. On the other hand, in the liver of male offspring, only post‐weaning high‐fat diet induced mRNA expression of autophagy related genes. The differential regulation of autophagy by diets, sex, and developmental periods could be explained by dysregulation of stress response pathway involving transcription factor ATF4. Overall, our data demonstrated that lactational low‐protein diet may impact autophagy pathway more in female offspring than in male offspring rats.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Effects of maternal high fat intake during pregnancy and lactation on total cholesterol and adipose tissue in neonatal rats.

Obesity during pregnancy is one of the most established risk factors for negative long-term programming. The aim of the present study was to investigate the effects of maternal consumption of a high-fat diet during pregnancy and lactation on the weight gain, visceral adipose tissue and cholesterolemia in neonatal rats. Wistar rats were divided into two groups according to the mother's diet during pregnancy and lactation: Control group (CG, n = 12) were the offspring of rats fed a standard diet (4% lipid) and the Test group (TG, n = 12) were pups rats fed on a high fat diet (23% lipid). The weight of the animals was measured on alternate days until the 22nd day of life, when collected visceral adipose tissue and blood were collected for biochemical analysis. For statistical analysis the Student t test, Sidak´s teste and two way ANOVA was used, with p <0.05. the test group showed differences in weight gain, visceral adipose tissue and higher cholesterol. a maternal exposure to a high-fat diet during pregnancy and lactation can promote changes in weight gain, hypercholesterolemia and an increase in adipose tissue in neonatal rats.

Maternal intake of trans-unsaturated or interesterified fatty acids during pregnancy and lactation modifies mitochondrial bioenergetics in the liver of adult offspring in mice.

The quality of dietary lipids in the maternal diet can programme the offspring to diseases in later life. We investigated whether the maternal intake of palm oil or interesterified fat, substitutes for trans-unsaturated fatty acids (FA), induces metabolic changes in the adult offspring. During pregnancy and lactation, C57BL/6 female mice received normolipidic diets containing partially hydrogenated vegetable fat rich in trans-unsaturated fatty acids (TG), palm oil (PG), interesterified fat (IG) or soyabean oil (CG). After weaning, male offspring from all groups received the control diet until day 110. Plasma glucose and TAG and liver FA profiles were ascertained. Liver mitochondrial function was accessed with high-resolution respirometry by measuring VO2, fluorimetry for detection of hydrogen peroxide (H2O2) production and mitochondrial Ca2+ uptake. The results showed that the IG offspring presented a 20 % increase in plasma glucose and both the IG and TG offspring presented a 2- and 1·9-fold increase in TAG, respectively, when compared with CG offspring. Liver MUFA and PUFA contents decreased in the TG and IG offspring when compared with CG offspring. Liver MUFA content also decreased in the PG offspring. These modifications in FA composition possibly affected liver mitochondrial function, as respiration was impaired in the TG offspring and H2O2 production was higher in the IG offspring. In addition, mitochondrial Ca2+ retention capacity was reduced by approximately 40 and 55 % in the TG and IG offspring, respectively. In conclusion, maternal consumption of trans-unsaturated and interesterified fat affected offspring health by compromising mitochondrial bioenergetics and lipid metabolism in the liver.

Abstract 4826: Maternal high butter fat intake heightens mammary cancer risk in offsprings gestationally exposed to bisphenol A at environmentally relevant dose

Abstract In utero exposure to bisphenol A (BPA) at 250ug/kg BW was shown to augment mammary cancer risk in rodent models. High fat diet is widely believed to be a major risk of breast cancer (BCa). It is therefore important to investigate whether maternal high fat intake could potentially heighten mammary cancer risk associated to gestational BPA exposure. In this study, we exposed Sprague Dawley rats with different doses of BPA (2.5-2500ug/kg BW) mixed with high butter-based diet (HBF) in the period from preconception to birth. DMBA-PND50 protocol was followed. In the presence of HBF, we observed non-monotonic effects of BPA in cancer incidence as well as in the number of terminal end buds of PND21 mammary glands. Both results were peaked at a dosage of 25ug/kg BW BPA and the effects were significant when compared with HBF alone group. We further analyzed transcriptomic data of microdissected epithelia of PND21 mammary glands from BPA (25ug/kg BW) group as well as HBF group and revealed that two specific cancer networks involving ERK and androgen receptor signaling were dysregulated. DNA methylation is one of the key mechanisms to dysregulate and impair the transcription of two selected top genes, Car7 and Kcnv2, as supported by our bisulfite-sequencing data. These data suggest that in utero BPA exposure could epigenetically modify gene expression and predispose cancer risk during early development. More importantly, some BPA genes are of high human relevance because seven selected BPA genes could dichotomize patients into two groups with significant difference in overall survival in a TCGA cancer cohort. The prognostic power of the genes was further enhanced in the survival analysis of Caucasian with ER positive patients. In conclusion, our data strongly suggest that BPA predisposes higher cancer risk by dysregulating gene expression during early mammary gland development in the presence of HBF, which could facilitate cancer development later in life. Citation Format: Yuet-Kin Leung, Vinothini Govindarajah, Ana Cheong, Dan Song, Xuegong Zhu, Jun Ying, Ady Kendler, Mario Medvedovic, Scott Belcher, Shuk-Mei Ho. Maternal high butter fat intake heightens mammary cancer risk in offsprings gestationally exposed to bisphenol A at environmentally relevant dose [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4826. doi:10.1158/1538-7445.AM2017-4826

A low-fat diet enriched in fish oil increased lipogenesis and fetal outcome of C57BL/6 mice.

There is clear evidence that nutritional strategy employed during pregnancy has profound influence on the offspring health outcomes. However, the effect of the quality and the quantity of maternal fat intake on maternal metabolic profile during different stages of pregnancy and its impact on pregnancy sustainability is not known. Female C57BL/6 mice (7 weeks old) were fed diets varying in the quantity of fat (5% vs 11%) for two weeks prior to mating and throughout pregnancy. The 5% fat diet was enriched with longer chain omega (n)-3 polyunsaturated fatty acids (PUFA) from fish oil. Maternal plasma and tissues were collected before mating and during pregnancy at days 6.5, 12.5 and 18.5. Plasma lipids, glucose, insulin, progesterone and estradiol levels were measured. Cholesterol efflux capacity of maternal plasma as well as the mRNA expression of placental steroidogenic acute regulatory protein and hepatic lipogenic genes (acetyl-CoA carboxylase-1, fatty acid synthase, diacylglycerol acyltransferase-2 and stearoyl-CoA desaturase-1) was determined. Feto-placental weight and fetuses sustained throughout gestation were recorded. A low-fat maternal diet enriched with n-3 PUFA increased maternal plasma triacylglycerol and the mRNA expression of rate-limiting lipogenic enzymes, along with increasing cholesterol efflux capacity (P < 0.05), likely to meet fetal lipid demand during pregnancy. Furthermore, diet enriched with longer chain n-3 PUFA increased the maternal plasma concentration of progesterone and estradiol during pregnancy (P < 0.05), which coincides with an increase in the number of fetuses sustained till day 18.5. These novel findings may be important when designing dietary strategies to optimize reproductive capability and pregnancy outcomes.

Maternal folate depletion during early development and high fat feeding from weaning elicit similar changes in gene expression, but not in DNA methylation, in adult offspring.

The 'Predictive Adaptive Response' hypothesis suggests that the in utero environment when mismatched with the post-natal environment can influence later life health. Underlying mechanisms are poorly understood, but may involve gene transcription changes regulated via epigenetic mechanisms. In a 2 × 2 factorial design, female C57Bl/6 mice were randomised to low or normal folate diets (0.4 mg/2 mg folic acid/kg diet) prior to and during pregnancy and lactation with offspring randomised to high- or low-fat diets at weaning. Genome-wide gene expression and promoter DNA methylation were measured using microarrays in adult male livers. Maternal folate depletion and high fat intake post-weaning influenced gene expression (1859 and 1532 genes, respectively) and promoter DNA methylation (201 and 324 loci, respectively) but changes in expression and methylation were poorly matched for both dietary interventions. Expression of 642 genes was altered in response to both maternal folate depletion and post-weaning high fat feeding, treatments imposed separately. In addition, there was evidence that the combined dietary insult (i.e. maternal folate depletion followed by high fat post-weaning) caused the largest expression change for most genes. Our observations align with, and provide evidence in support of, a potential underlying mechanism for the 'Predictive Adaptive Response' hypothesis.

Associations of maternal body composition and nutritional intake with fat content of Indonesian mothers’ breast milk

Background Breast milk is the best sole food for infants in their first six months of life. Breast milk fat content accounts for the largest part of infants’ energy and may be influenced by many factors, including maternal factors, which may vary in different settings. So far, there has been no published data about the breast milk fat content of Indonesian mothers, including whether it is affected by their body composition or nutritional intake.Objective To investigate breast milk fat content of Indonesian mothers and its associations with maternal body composition and nutritional intake. Method This cross-sectional study was conducted at Budi Kemuliaan Mothers’ and Children’s Hospital. Breast milk specimens were collected from 48 nursing mothers, centrifuged, and tested by creamatocrit for fat content. A 24-hour food recall was performed to evaluate maternal macronutrient intake. Maternal body composition was evaluated by bioelectric impedance analysis. Univariable correlations between breast milk fat content and either energy and macronutrient intake were assessed using the Spearman rho test.Results All nursing mothers had breast milk fat content within clinically normal range [mean 59.4 (SD 15.9) g/L]. There was no significant correlation between milk fat content and maternal body fat (r = -0.03, P=0.840), total body water (r = 0.09 P=0.509), or muscle mass (r = 0.08, P=0.577). Milk fat content seemed to weakly correlated with maternal fat intake, although it was not statistically significant (r = 0.27, P=0.065).Conclusion Breast milk fat content at one-month post delivery appears not associated with with maternal body composition. It seems to weakly correlate with maternal fat intake but findings need to be confirmed in larger studies with adjustment for confounding variables.

Maternal trans fat intake during pregnancy or lactation impairs memory and alters BDNF and TrkB levels in the hippocampus of adult offspring exposed to chronic mild stress

This study aimed to assess the influence of maternal dietary fat intake during pregnancy or lactation on memory of adult offspring after chronic mild stress (CMS) exposure. Female Wistar rats were supplemented daily with soybean oil/fish oil (SO/FO) or hydrogenated vegetable fat (HVF) by oral gavage (3.0g/kg body weight) during pregnancy or lactation. On post-natal day (PND) 60, half of the animals were exposed to CMS following behavioral assessments. While the adult offspring born under influence of SO/FO and HVF supplementations during pregnancy showed higher levels of n-3 and n-6 fatty acids (FA) series DHA and ARA metabolites, respectively, in the hippocampus, adult offspring born from supplemented dams during lactation showed higher levels of their precursors: ALA and LA. However, only HVF supplementation allowed TFA incorporation of adult offspring, and levels were higher in lactation period. Adult offspring born from dams supplemented with trans fat in both pregnancy and lactation showed short and long-term memory impairments before and after CMS. Furthermore, our study also showed higher memory impairment in offspring born from HVF-supplemented dams during lactation in comparison to pregnancy. BDNF expression was increased by stress exposure in offspring from both SO/FO- and HVF-supplemented dams during pregnancy. In addition, offspring from HVF-supplemented dams showed decreased TrkB expression in both supplemented periods, regardless of stress exposure. In conclusion, these findings show for the first time that the type of dietary FA as well as the period of brain development is able to change FA incorporation in brain neural membranes.

High cholesterol dietary intake during pregnancy is associated with large for gestational age in a sample of low-income women of Rio de Janeiro, Brazil.

The association between the quality of maternal dietary fat intake during pregnancy and the infant's birthweight (BW) remains controversial. Our goal was to investigate the association between maternal dietary fat intake during pregnancy and the rate of large for gestational age (LGA) newborns. This study employed a cross-sectional analysis of 297 pairs of mothers/children attending a public maternity at Rio de Janeiro, Brazil. BW for gestational age according to the Intergrowth 21st was defined as follows: adequate for gestational age (AGA ≤ 90th percentile) and LGA (>90th percentile). The statistical analysis was a Poisson regression with robust estimations of the standard errors. Maternal dietary fat intake variables comprised lipids (% total energy); saturated (mg/1000 kcal), monounsaturated (mg/1000 kcal) and polyunsaturated (mg/1000 kcal) fats; and cholesterol (mg/1000 kcal), all of which were obtained with a Food Frequency Questionnaire. The mean BW was 3338 g (SD = 446.9), and the rate of LGA newborns was 13.1%. The mean maternal total energy intake was 2880 kcal (SD = 1074), cholesterol was 154.3 mg/1000 kcal (SD = 68.1) and monounsaturated fat was 6.9 mg/1000 kcal (SD = 2). Mothers of LGA newborns reported higher cholesterol dietary intake (195.8 vs. 148 mg/1000 kcal; P < 0.001), pre-pregnancy body mass index (25.1 vs. 23.5 kg/m2 ; P = 0.026) when compared with mothers of AGA newborns. Women with cholesterol intake within the fourth quartile were 2.48 (95% confidence interval: 1.31-4.66) times more likely to have an LGA infant compared with those in the 1-3 quartiles. Dietary intake of cholesterol during pregnancy influences LGA even after adjusting for other confounders.

Maternal fat intake during pregnancy in relation to IGF2 and H19 methylation in newborns

Maternal fat intake during pregnancy in relation to IGF2 and H19 methylation in newborns

Maternal Blood Lipid Profile during Pregnancy and Associations with Child Adiposity: Findings from the ROLO Study.

BackgroundThe in-utero environment affects fetal development; it is vital to understand how maternal diet during pregnancy influences childhood body composition. While research indicates that triglycerides in hyperglycaemic women may increase birth weight, little is known about this relationship in euglycemic women. This study examines the relationship between maternal blood lipid status and infant adiposity up to 2 years of age.MethodsData from 331 mother-child pairs from the ROLO longitudinal birth cohort study was analysed. Maternal dietary intakes were recorded and fasting blood lipids, leptin and HOMA were measured in early and late pregnancy and cord blood. Infant anthropometric measurements and skin-fold thicknesses were recorded at birth, 6 months and 2 years. Correlation and regression analyses were used to explore associations between maternal blood lipid status and infant adiposity.ResultsAll maternal blood lipids increased significantly during pregnancy. Maternal dietary fat intake was positively associated with total cholesterol levels in early pregnancy. Late pregnancy triglycerides were positively associated with birth weight (P = 0.03) while cord blood triglycerides were negatively associated with birth weight (P = 0.01). Cord HDL-C was negatively associated with infant weight at 6 months (P = 0.005). No other maternal blood lipids were associated with infant weight or adiposity up to 2 years of age.ConclusionMaternal and fetal triglycerides were associated with birth weight and cord HDL-C with weight at 6 months. Thus, maternal lipid concentrations may exert in-utero influences on infant body composition. There may be potential to modulate infant body composition through alteration of maternal diet during pregnancy.

The early infant gut microbiome varies in association with a maternal high-fat diet.

BackgroundEmerging evidence suggests that the in utero environment is not sterile as once presumed. Work in the mouse demonstrated transmission of commensal bacteria from mother to fetus during gestation, though it is unclear what modulates this process. We have previously shown in the nonhuman primate that, independent of obesity, a maternal high-fat diet during gestation and lactation persistently shapes the juvenile gut microbiome. We therefore sought to interrogate in a population-based human longitudinal cohort whether a maternal high-fat diet similarly alters the neonatal and infant gut microbiome in early life.MethodsA representative cohort was prospectively enrolled either in the early third trimester or intrapartum (n = 163), with a subset consented to longitudinal sampling through the postpartum interval (n = 81). Multiple body site samples, including stool and meconium, were collected from neonates at delivery and by 6 weeks of age. A rapid dietary questionnaire was administered to estimate intake of fat, added sugars, and fiber over the past month (National Health and Examination Survey). DNA was extracted from each infant meconium/stool sample (MoBio) and subjected to 16S rRNA gene sequencing and analysis.ResultsOn average, the maternal dietary intake of fat ranged from 14.0 to 55.2 %, with an average intake of 33.1 % (σ = 6.1 %). Mothers whose diets significantly differed from the mean (±1 standard deviation) were separated into two distinct groups, a control group (n = 13, μ = 24.4 %) and a high-fat group (n = 13, μ = 43.1 %). Principal coordinate analysis revealed that the microbiome of the neonatal stool at birth (meconium) clustered differently by virtue of maternal gestational diet (PERMANOVA p = 0.001). LEfSe feature selection identified several taxa that discriminated the groups, with a notable relative depletion of Bacteroides in the neonates exposed to a maternal high-fat gestational diet (Student’s t-test, p < 0.05) that persisted to 6 weeks of age.ConclusionsSimilar to the primate, independent of maternal body mass index, a maternal high-fat diet is associated with distinct changes in the neonatal gut microbiome at birth which persist through 4–6 weeks of age. Our findings underscore the importance of counseling pregnant mothers on macronutrient consumption during pregnancy and lactation.Electronic supplementary materialThe online version of this article (doi:10.1186/s13073-016-0330-z) contains supplementary material, which is available to authorized users.

Maternal dietary intake during pregnancy and offspring body composition: The Healthy Start Study

Consistent evidence of an influence of maternal dietary intake during pregnancy on infant body size and composition in human populations is lacking, despite robust evidence in animal models. We sought to evaluate the influence of maternal macronutrient intake and balance during pregnancy on neonatal body size and composition, including fat mass and fat-free mass. The analysis was conducted among 1040 mother-offspring pairs enrolled in the prospective prebirth observational cohort: the Healthy Start Study. Diet during pregnancy was collected using repeated 24-hour dietary recalls (up to 8). Direct measures of body composition were obtained using air displacement plethysmography. The National Cancer Institute measurement error model was used to estimate usual dietary intake during pregnancy. Multivariable partition (nonisocaloric) and nutrient density (isocaloric) linear regression models were used to test the associations between maternal dietary intake and neonatal body composition. The median macronutrient composition during pregnancy was 32.2% from fat, 15.0% from protein, and 47.8% from carbohydrates. In the partition multivariate regression model, individual macronutrient intake values were not associated with birthweight or fat-free mass, but were associated with fat mass. Respectively, 418 kJ increases in total fat, saturated fat, unsaturated fat, and total carbohydrates were associated with 4.2-g (P= .03), 11.1-g (P= .003), 5.9-g (P= .04), and 2.9-g (P=.02) increases in neonatal fat mass, independent of prepregnancy body mass index. In the nutrient density multivariate regression model, macronutrient balance was not associated with fat mass, fat-free mass, or birthweight after adjustment for prepregnancy body mass index. Neonatal adiposity, but not birthweight, is independently associated with increased maternal intake of total fat, saturated fat, unsaturated fat, and total carbohydrates, but not protein, suggesting that most forms of increased caloric intake contribute to fetal fat accretion.