Influence Of Maternal Obesity Research Articles

The maternal lifestyle in pregnancy: Implications for foetal skeletal muscle development.

The world is facing a global nutrition crisis, as evidenced by the rising incidence of metabolic disorders such as obesity, insulin resistance and chronic inflammation. Skeletal muscle is the largest tissue in humans and plays an important role in movement and host metabolism. Muscle fibre formation occurs mainly during the embryonic stage. Therefore, maternal lifestyle, especially nutrition and exercise during pregnancy, has a critical influence on foetal skeletal muscle development and the subsequent metabolic health of the offspring. In this review, the influence of maternal obesity, malnutrition and micronutrient intake on foetal skeletal muscle development is systematically summarized. We also aim to describe how maternal exercise shapes foetal muscle development and metabolic health in the offspring. The role of maternal gut microbiota and its metabolites on foetal muscle development is further discussed, although this field is still in its 'infancy'. This review will provide new insights to reduce the global crisis of metabolic disorders and highlight current gaps to promote further research.

The associations of pre-pregnancy BMI and gestational weight gain with maternal gut microbiota.

Previous studies reporting the association between gut microbiota dysbiosis and maternal obesity were mostly confined at the phylum level or at postpartum period. This study aimed to investigate the dynamic changes in gut microbial communities associated with maternal obesity at different time points of pregnancy. We performed 16S rRNA gene V3-V4 amplicon sequencing on stool samples from 110 women in all three trimesters and 1-month postpartum. Maternal gut microbial communities associated with maternal pre-pregnancy body mass index (BMI) and gestational weight gain (GWG) were explored. The influence of maternal obesity on gut microbiota trajectories was determined based on longitudinal shifts in community clusters across the trimesters. The richness index of alpha diversity decreased with the progression of pregnancy, particularly in women with excessive GWG. The evenness index in 2nd trimester was found inversely associated with GWG. Various taxonomic differences in 1st trimester were associated with excessive GWG, whereas limited taxonomic differences in 2nd and 3rd trimesters were associated with pre-pregnancy BMI or GWG. Meanwhile, the gut microbiota trajectory with especially depleted genus Faecalibacterium in 1st trimester was associated with excessive GWG (adjusted odds ratio 5.7, 95% confidence interval 1.2-28.1). Moreover, the longitudinal abundances of genus Lachnospiraceae ND3007 group across gestations were depleted in women with overweight/obese pre-pregnancy BMI, while genus Bifidobacterium enriched in women with excessive GWG. Our study shows that dysbiosis of the gut microbiota in early pregnancy may have a significant impact on excess GWG. The abundance of the genus Faecalibacterium in 1st trimester may be a potential risk factor. Clinical trial number: NCT03785093 (https://classic.clinicaltrials.gov/ct2/show/NCT03785093).

Influence of maternal obesity on human trophoblast differentiation: The role of mitochondrial status

Maternal obesity is associated with complications of pregnancy and increases the infant's risk of developing obesity, diabetes and cardiovascular disease later in life. The placenta has an important role in determining the pregnancy outcome, and the syncytiotrophoblast (ST) is the main component of the placenta that supports the relationship between the mother and fetus. The differentiation of the cytotrophoblast (CT) into the ST is accompanied by changes in mitochondrial functions and dynamics. The objective of the present study was to investigate the effects of maternal obesity (without gestational diabetes) on the in vitro differentiation capacities of human CT isolated from term placenta by focusing on mitochondrial status. We found that, during human CT differentiation process, maternal obesity is associated with (i) a lower progesterone secretion, (ii) a transient impairment in the ST's fusion potential (via syncytin-2 and its receptor), (iii) a lower mitochondrial content, and (iv) weaker mRNA expression of oestrogen-related receptor-gamma (a key mitobiogenesis gene). Moreover, maternal obesity altered the time course of ATP and reactive oxygen species production throughout CT differentiation. The mitochondrial dysfunctions observed in isolated human CTs of obese women might explain the observed decrease in progesterone production. Our results demonstrated that obesity in pregnancy is associated with a functional impairment of the ST which might alter the foetal-maternal dialogue.

The Influence of Maternal Obesity on Cell-Free Fetal DNA and Blood Pressure Regulation in Pregnancies with Hypertensive Disorders.

Background and Objectives: obesity and blood pressure disorders are one of the main risk factors for antenatal, intra, postpartum, and neonatal complications. In preeclampsia (PE), the placental hypoxia leads to vascular endothelium dysfunction, cell necrosis, and apoptosis. This condition is associated with the release of free fetal DNA (cffDNA) circulating in plasma. The disturbance of the efficiency of vasodilatation and blood pressure regulation in PE can be confirmed by analyzing the apelin, salusin, and prosalusin. This study aimed to assess the influence of obesity on cffDNA, and the effectiveness of maintaining normal blood pressure in patients with preeclampsia and gestational hypertension. Material and Methods: the research material was blood serum and oral mucosa swabs, obtained from 168 patients. Pregnant women were divided into the following: a control group (C)—67 women; a gestational hypertension group (GH)—35 patients; a preeclampsia with obesity group (PE + O) (pre-gravid BMI > 30)—23 patients. The rest were lean preeclamptic women (PE)—66 patients—(pre-gravid BMI < 25 in 43 women). Results: the cffDNA was observed in 1.50% of women in the C group, in 2.45% in the GH group, but in 18.18% of lean patients with preeclampsia. The cffDNA was detected in 58% of obese pregnant women with PE. The greater the placental hypoxia was in preeclampsia, the less efficient the hypotensive mechanisms, according to an analysis of the studied adipokines. The prosalusin concentration was significantly lower in the PE group with cffDNA than in the PE group without it (p = 0.008). Apelin was higher in the PE group with cffDNA (p = 0.006) compared to other groups. The same results were also observed in the subgroup with obesity. Conclusion: in preeclamptic women, obesity seems to act as an additive factor of placental damage by means of the dysregulation of hypotensive mechanisms.

The Influence of Preeclampsia, Advanced Maternal Age and Maternal Obesity in Neonatal Outcomes Among Women with Gestational Diabetes.

The present study aims to analyze adverse fetal or neonatal outcomes in women with gestational diabetes, including fetal death, preterm deliveries, birthweight, neonatal morbidity and mortality, as well as the synergic effect of concomitant pregnancy risk factors and poor obstetric outcomes, as advanced maternal age, maternal obesity and pre-eclampsia in their worsening. The present cohort retrospective study included all pregnant women with gestational diabetes, with surveillance and childbirth at the Hospital da Senhora da Oliveira during the years of 2017 and 2018. The data were collected from the medical electronic records registered in health informatic programs Sclinico and Obscare, and statistical simple and multivariate analysis was done using IBM SPSS Statistics. The study participants included 301 pregnant women that contributed to 7.36% of the total institution childbirths of the same years, in a total of 300 live births. It was analyzed the influence of pre-eclampsia coexistence in neonatal morbidity (p = 0.004), in the occurrence of newborns of low and very low birthweight (p < 0.01) and in preterm deliveries (p < 0.01). The influence of maternal obesity (p = 0.270; p = 0.992; p = 0.684) and of advanced maternal age in these 3 outcomes was also analyzed (p = 0,806; p = 0.879; p = 0.985).Using a multivariate analysis, the only models with statistic significance to predict the three neonatal outcomes included only pre-eclampsia (p = 0.04; p < 0.01; p < 0.01). Only coexistence of pre-eclampsia showed an association with adverse neonatal outcomes (neonatal morbidity, newborns of low and very low birthweight and preterm deliveries) and can be used as a predictor of them in women with gestational diabetes.

The influence of maternal obesity on pregnancy intention: A cross-sectional analysis.

This prospective cross-sectional study of 1498 pregnant women in early pregnancy sought to investigate the prevalence of pregnancy intention between women of differing body mass index (BMI) categories. There was no difference in the risk of unintended pregnancy between women who were in the healthy weight, overweight or obesity BMI categories. The study identifies and highlights the potential missed opportunities for all women to engage in healthy reproductive life planning behaviours to support health in pregnancy and beyond.

1116: Influence of maternal obesity on risk of major congenital malformations in the US

The prevalence of obesity in the US has risen exponentially, increasing pregnancy risks in women of reproductive age. The influence of extremes of maternal obesity on risk of birth defects is not well established. We aim to estimate this risk in the offspring of mothers stratified by pre-pregnancy BMI category. Population-based retrospective cohort of live births in the US from 2012-2016 birth certificate data. Rates of newborn cardiovascular, musculoskeletal, gastrointestinal, genitourinary and central nervous system defects of normal weight women (BMI 18.5 to < 25) were compared to overweight (BMI 25 to < 30), obesity classes I (30 to < 35), II (35 to < 40), III (>/=40), as well as strata of severe obesity (BMI 40 to < 50, 50 to < 60 and >/= 60). Multivariate logistic regression quantified the relationship between maternal BMI and birth defect risk after adjustment for pregestational diabetes mellitus, late prenatal care, maternal race and maternal smoking. Of the 19,844,580 live births in the study period, maternal obesity rates were 3.4%, 23.4%, 12.5%, 23.4%, 12.5%, 6% and 4.2%, respectively for underweight, overweight, and obesity classes I, II and III. Increasing maternal BMI and particularly morbid obesity (BMI >/=40) was associated with increased rates of all birth defects except gastroschisis. The most robust relative risk increases were observed in defects of the musculoskeletal and central nervous systems, see figure. Increasing maternal BMIs were associated with decreased risk of gastroschisis. Maternal BMI had no significant influence on chromosomal abnormality. Risks of any major congenital malformation or multiple malformations, except for gastroschisis, progressively increase with increasing maternal BMIs and specifically with morbid obesity. For obese women who are planning pregnancy, efforts should be made to optimize BMI prior to pregnancy to decrease risk of birth defects.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

Influence of maternal obesity and metabolic and vascular mediators in twin-twin transfusion syndrome

Obesity is a risk factor for complications in singleton and twin pregnancies; however, there are limited data regarding maternal body mass index (BMI) in the setting of twin-twin transfusion syndrome (TTTS). We hypothesized that increased BMI in TTTS is associated with adverse perinatal outcomes and vascular pathology. A retrospective study of twin reversed arterial perfusion (n = 4), selective intrauterine growth restriction (n = 10) and TTTS (n = 33) was conducted. Treatment included fetoscopic laser photocoagulation (FLP) (n = 35) or Solomon technique (n = 12). Ex vivo placental intravascular injections, immunohistochemistry, and perinatal outcomes were compared by maternal BMI. In pregnancy complicated by TTTS, 16/33 women were obese (BMI > 30 kg/m2) and 11/33 were overweight (BMI 25–29.9 kg/m2). Women who were overweight or obese had an increased rate of premature rupture of membranes (PPROM), cesarean delivery, and/or concomitant co-morbidities when compared to the normal weight group. Duration of neonatal intensive care unit (NICU) admission was longer in neonates of overweight/obese women versus normal weight. Placental examination of FLP sites in the obese group showed larger infarcts, increased adipose triglyceride lipase, and a proangiogenic phenotype. Increased BMI is common in our TTTS cohort and it is associated with higher rate of co-morbidity, PPROM, prolonged NICU stay, and an imbalance of placental metabolic and vascular mediators.

Influence of maternal obesity on the accuracy of ultrasonography birth weight prediction

Objective: The aim of the study was to investigate whether the accuracy of ultrasound estimates of fetal weight (EFW) was dependent on maternal obesity.Study design: A prospective cross-sectional study of 1064 singleton pregnant women classified according to body mass index (BMI) into two categories: normal (BMI < 25 kg/m2, n = 863) and obese (BMI ≥ 35 kg/m2, n = 201) was conducted. EFW were calculated using Hadlock’s formula, and the difference between EFW and the actual birthweight (absolute percent error) was analyzed in both groups. Spearman’s correlation was used to assess the relationship between ultrasound performance (absolute error), maternal BMI, and actual birth weight.Results: Median absolute error of sonographic EFW was 5.90 and 6.47% for the normal and obese groups, respectively (p .38). A correlation between EFW and birth weight (BW) was found in both groups, r = 0.755 (p < .001) and r = 0.753 (p < .001), respectively. The correlation between absolute error, maternal BMI, and fetal birth weight was poor.Conclusions: Maternal obesity is unrelated to the accuracy of sonographic EFW, and regardless of maternal or fetal size, ultrasound is currently an accurate method of prediction for both obese and normal weight pregnant women.

The influence of maternal obesity on macrophage subsets in the human decidua

Obesity is seen as a low grade inflammatory state, and is associated with adverse pregnancy outcomes. Disturbed macrophage characteristics might be essential in obesity associated pregnancy pathology via effects on the regulation of angiogenesis and placental development. This study aims to address the effects of maternal obesity on macrophage subsets in the decidua of women with term uncomplicated pregnancies. Macrophages were isolated from the decidua basalis and decidua parietalis of women with pre-gravid BMI < 25 (control) and BMI > 30 (obese). Macrophages were characterized and quantified using multi-color flow cytometry. Placentas of 10 obese and 10 control women after an uncomplicated term pregnancy were included. The decidua parietalis, but not decidua basalis, showed significantly lower levels of M1-type (HLA-DR+, CD163−) macrophages (p < 0.05) in obese women (4,3% of total macrophages) compared to control women (5,3% of total macrophages). The lower levels of M1 macrophages, considered to be pro-inflammatory, might indicate a mechanism to compensate for the pro-inflammatory environment in obese women to ensure healthy pregnancy outcomes.

Influence of Maternal Obesity on Labor Induction: A Systematic Review and Meta-Analysis.

Studies have shown that women with obesity have longer labors. The purpose of this systematic review and meta-analysis is to examine existing evidence regarding labor induction in women with obesity, including processes and outcomes. The primary outcome was cesarean birth following labor induction. Secondary outcomes were the timing and dosage of prostaglandins, the success of mechanical cervical ripening methods, and synthetic oxytocin dose and timing. Searches were performed in PubMed, MEDLINE, Embase, CINAHL, EBSCO, the Cochrane Database of Systematic Reviews, the Database of Abstracts of Effects, Google Scholar, and ClinicalTrials.gov. Searches were limited to studies published in English after 1990. Ten studies published between 2009 and 2017 were included in this review. All were observational studies comparing processes and outcomes of induction of labor in relation to maternal body mass index. The primary outcome was cesarean birth following labor induction. We assessed heterogeneity using Cochran's Q test and tau-squared and I2 statistics. We also calculated fixed-effect models to estimate pooled relative risks and weighted mean differences. Ten cohort studies met inclusion criteria; 8 studies had data available for a meta-analysis of the primary outcome. Cesarean birth was more common among women with obesity compared with women of normal weight following labor induction (Mantel-Haenszel fixed-effect odds ratio, 1.82; 95% CI, 1.55-2.12; P < .001). Maternal obesity was associated with a longer time to birth, higher doses of prostaglandins, less frequent success of cervical ripening methods, and higher dose of synthetic oxytocin, as well as a longer time to birth after oxytocin use. Women with obesity are more likely than women with a normal weight to end labor induction with cesarean birth. Additionally, women with obesity require longer labor inductions involving larger, more frequent applications of both cervical ripening methods and synthetic oxytocin.

Maternal obesity and child health at different ages

In recent years, the number of obese women of childbearing age has increased significantly. The aim of this study was to reveal the influence of maternal obesity during pregnancy on the longterm health of the offspring.&#x0D; This study was performed in the outpatient clinic in St. Petersburg with 76 adolescents with chronic diseases aged from 6 to 17 years. The mean age of the examined was 12.67 ± 3.19 years; the ratio of girls to boys was 6 : 7. Children were divided into 2 groups: the main group included 26 adolescents whose mothers were obese before and during pregnancy. 50 teen agers from mothers with normal BMI during pregnancy presented comparison group. The main group and the comparison group did not differ in age and sex. The children were examined by a pediatrician. Data on the transferred diseases are obtained from an outpatient card. It has been established that maternal obesity may be considered a risk factor for miscarriage, having low birth weight babies or babies weighing more than 4 kg, as well as a risk factor for rickets, parathrophies and functional constipation in the first year of life. In adolescentes, obesity, euthyroid goiter, hypothalamic syndrome and other endocrinopathies are typical for children born from obese mothers. Several medical conditions related to obesity such as chronic pancreatitis, hiatal hernia, iron deficiency anemia and orthopaedic foot and ankle pathology are commonly seen in children of obese mothers. Maternal obesity is associated with diseases of children not only in the period of newborn, but also in adolescence.

Research roundup: October 2018

Nurse PrescribingVol. 16, No. 10 Research RoundupResearch roundup: October 2018Rita SomRita SomSearch for more papers by this authorRita SomPublished Online:17 Oct 2018https://doi.org/10.12968/npre.2018.16.10.464AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References McDonald VM, Hiles SA, Godbout K et al.. Treatable traits can be identified in a severe asthma registry and predict future exacerbations. Respirology, 19 September 2018. https://onlinelibrary.wiley.com/doi/full/10.1111/resp.13389 Google ScholarPatro Golab B, Santos S, Voerman E, Lawlor DA, Jaddoe VWV, Gaillard R, on behalf of the MOCO Study Group Authors. Influence of maternal obesity on the association between common pregnancy complications and risk of childhood obesity: an individual participant data meta-analysis. September 7, 2018. https://doi.org/https://doi.org/ doi: https://doi.org/10.1016/S2352-4642(18)30273-6 Google ScholarRamos R, Comas-Cufi M, Marti-Lluch R et al.. Statins for primary prevention of cardiovascular events and mortality in old and very old adults with and without type 2 diabetes: retrospective cohort study. BMJ 2018;362;k3359 Crossref, Google Scholar FiguresReferencesRelatedDetails 2 October 2018Volume 16Issue 10ISSN (print): 1479-9189ISSN (online): 2052-2924 Metrics History Published online 17 October 2018 Published in print 2 October 2018 Information© MA Healthcare LimitedPDF download

Influence of maternal obesity on the association between common pregnancy complications and risk of childhood obesity: an individual participant data meta-analysis

Gestational diabetes and gestational hypertensive disorders are associated with offspring obesity, but the role of maternal adiposity in these associations remains unclear. We aimed to investigate whether these pregnancy complications affect the odds of offspring obesity independently of maternal obesity. We did an individual participant data (IPD) meta-analysis of mother-offspring pairs from prospective birth cohort studies that had IPD on mothers with singleton liveborn children born from 1989 onwards and had information available about maternal gestational diabetes, gestational hypertension or pre-eclampsia, and childhood body-mass index (BMI). We applied multilevel mixed-effects models to assess associations of gestational diabetes, gestational hypertension, and pre-eclampsia with BMI SD scores and the odds of overweight and obesity throughout childhood, adjusting for lifestyle characteristics (offspring's sex, maternal age, educational level, ethnicity, parity, and smoking during pregnancy). We then explored the extent to which any association was explained by maternal pre-pregnancy or early-pregnancy BMI. 160 757 mother-offspring pairs from 34 European or North American cohorts were analysed. Compared with uncomplicated pregnancies, gestational diabetes was associated with increased odds of overweight or obesity throughout childhood (odds ratio [OR] 1·59 [95% CI 1·36 to 1·86] for early childhood [age 2·0-4·9 years], 1·41 [1·26 to 1·57] for mid childhood [5·0-9·9 years], and 1·32 [0·97 to 1·78] for late childhood [10·0-17·9 years]); however, these associations attenuated towards the null following adjustment for maternal BMI (OR 1·35 [95% CI 1·15 to 1·58] for early childhood, 1·12 [1·00 to 1·25] for mid childhood, and 0·96 [0·71 to 1·31] for late childhood). Likewise, gestational hypertension was associated with increased odds of overweight throughout childhood (OR 1·19 [95% CI 1·01 to 1·39] for early childhood, 1·23 [1·15 to 1·32] for mid childhood, and 1·49 [1·30 to 1·70] for late childhood), but additional adjustment for maternal BMI largely explained these associations (1·01 [95% CI 0·86 to 1·19] for early childhood, 1·02 [0·95 to 1·10] for mid childhood, and 1·18 [1·03 to 1·36] for late childhood). Pre-eclampsia was associated with decreased BMI in early childhood only (difference in BMI SD score -0·05 SD score [95% CI -0·09 to -0·01]), and this association strengthened following additional adjustment for maternal BMI. Although lowering maternal risk of gestational diabetes, gestational hypertension, and pre-eclampsia is important in relation to maternal and fetal pregnancy outcomes, such interventions are unlikely to have a direct impact on childhood obesity. Preventive strategies for reducing childhood obesity should focus on maternal BMI rather than on pregnancy complications. EU's Horizon 2020 research and innovation programme (LifeCycle Project).

The Influence of Maternal Obesity and Breastfeeding on Infant Appetite- and Growth-Related Hormone Concentrations: The SKOT Cohort Studies

Background/Aims: Exposure to obesity during pregnancy may lead to adverse changes in the offspring’s metabolic profile. We compared appetite- and growth-related hormones in a cohort of infants born to obese mothers (SKOT-II) with infants born mainly to nonobese mothers (SKOT-I). Methods: Infants from SKOT-I (n = 273) and SKOT-II (n = 132) were examined including anthropometric measurements and blood samples analyzed for glucose, insulin, insulin-like growth factor-I (IGF-I), adiponectin, and leptin. Information on breastfeeding and parental characteristics were also collected. Results: At 9 months of age, SKOT-II infants were 3.6% heavier and 1.2% longer than SKOT-I infants even though their mothers were shorter. There was no difference in body mass index (BMI). SKOT-II infants had higher levels of insulin, adiponectin, and leptin but lower levels of IGF-I compared to SKOT-I infants (all p ≤ 0.015). These differences remained, except for leptin, when adjusted for current weight. Breastfeeding versus nonbreastfeeding at 9 months was associated with lower concentrations of all hormones (all p ≤ 0.003). In adjusted models, maternal BMI at 9 months was positively associated with insulin and adiponectin and negatively with IGF-I. Conclusions: Pre-pregnancy obesity confers symmetrically larger infant body size and higher levels of most growth- and appetite-related hormones but surprisingly lower levels of IGF-I, suggesting other possible infant growth-promoting effects through insulin.

The Influence of Maternal Obesity on Pregnancy Complications and Neonatal Outcomes in Diabetic and Nondiabetic Women.

Introduction This study aimed to investigate the influence of obesity on pregnancy complications and neonatal outcomes in diabetic and nondiabetic women. Materials and Methods This retrospective case control study was conducted on 1193 pregnant women and their neonates at a tertiary level maternity hospital between March 2007 and 2011. The pregnant women were classified into 2 groups according to the presence of diabetes mellitus. Six hundred and seven patients with gestational diabetes or pregestational diabetes formed the diabetic group (study group) and 586 patients were in the nondiabetic group (control group). Demographic characteristics, body mass index, gestational weight gain, obstetric history, smoking status, type of delivery, gestational ages, pregnancy complications, neonatal outcomes were recorded for each patient. Multivariable logistic regression analysis was performed to evaluate the effect of obesity and diabetes on the pregnancy complications and neonatal outcomes. Results The mean age and pre-pregnancy body mass indices of women with diabetes mellitus were significantly higher than the control groupʼs (p < 0.001). Gestational weight gain and number of smokers were similar among the groups. Multiparity and obesity were more prevalent in the diabetic group compared to controls (both p < 0.001). Although gestational age at birth was earlier in the diabetic group, birth weights were higher in this group than in the control group (both p < 0.001). Cesarean delivery rates, the incidence of macrosomia, and neonatal intensive care unit admission rates were significantly higher in the diabetes group both with normal and increased body mass index (all p < 0.001). However, adverse pregnancy outcomes were comparable between the groups (p = 0.279). Multivariable logistic regression analysis showed that obesity is a significant risk factor for pregnancy complications (OR = 1.772 [95% CI, 1.283 – 2.449], p = 0.001) but not for adverse neonatal outcomes (OR = 1.068 [95% CI, 0.683 – 1.669], p = 0.773). Conclusion While obesity increases risk of developing a pregnancy complication, diabetes worsens neonatal outcomes.

Impact of donor and recipient adiposity on placental and fetal growth in adolescent sheep.

The influence of maternal obesity during oocyte development and its putative interaction with nutrient reserves at conception on pregnancy outcome were examined in an adolescent sheep model. Donor ewes were nutritionally managed to achieve contrasting adiposity (control (CD)/obese (ObD)) for 6 weeks prior to superovulation and inseminated by a non-obese sire. Morulae from 6 CD and 7 ObD were transferred in singleton into adolescent recipients of identical age but differing adiposity, classified as relatively fat or thin respectively. Thereafter, all were overnourished to promote rapid growth/adiposity (2 × 2 design, 13/14 pregnancies/group). A fifth recipient group of intermediate adiposity received embryos from another 5 CD, was offered a moderate intake to maintain adiposity throughout gestation and acted as controls for normal pregnancy outcome (optimally treated control (OTC), 19 pregnancies). Donor obesity did not influence ovulation, fertilisation or recovery rates or impact embryo morphology. Gestation length and colostrum yield were unaffected by donor or recipient adiposity and were reduced relative to OTC. Total fetal cotyledon and lamb birth weights were independent of initial donor adiposity but reduced in relatively thin vs relatively fat recipients and lower than those in the OTC group. In spite of high placental efficiency, the incidence of fetal growth restriction was greatest in the thin recipients. Thus, maternal adiposity at conception, but not pre-conception maternal obesity, modestly influences the feto-placental growth trajectory, whereas comparison with the OTC indicates that high gestational intakes to promote rapid maternal growth remain the dominant negative influence on pregnancy outcome in young adolescents. These findings inform dietary advice for pregnant adolescent girls.

Influence of Maternal Obesity and Gestational Weight Gain on Maternal and Foetal Lipid Profile.

Fatty acids (FAs) are fundamental for a foetus’s growth, serving as an energy source, structural constituents of cellular membranes and precursors of bioactive molecules, as well as being essential for cell signalling. Long-chain polyunsaturated FAs (LC-PUFAs) are pivotal in brain and visual development. It is of interest to investigate whether and how specific pregnancy conditions, which alter fatty acid metabolism (excessive pre-pregnancy body mass index (BMI) or gestational weight gain (GWG)), affect lipid supply to the foetus. For this purpose, we evaluated the erythrocyte FAs of mothers and offspring (cord-blood) at birth, in relation to pre-pregnancy BMI and GWG. A total of 435 mothers and their offspring (237 males, 51%) were included in the study. Distribution of linoleic acid (LA) and α-linolenic acid (ALA), and their metabolites, arachidonic acid, dihomogamma linoleic (DGLA) and ecosapentanoic acid, was significantly different in maternal and foetal erythrocytes. Pre-pregnancy BMI was significantly associated with maternal percentage of MUFAs (Coeff: −0.112; p = 0.021), LA (Coeff: −0.033; p = 0.044) and DHA (Coeff. = 0.055; p = 0.0016); inadequate GWG with DPA (Coeff: 0.637; p = 0.001); excessive GWG with docosaexahenoic acid (DHA) (Coeff. = −0.714; p = 0.004). Moreover, pre-pregnancy BMI was associated with foetus percentage of PUFAs (Coeff: −0.172; p = 0.009), omega 6 (Coeff: −0.098; p = 0.015) and DHA (Coeff: −0.0285; p = 0.036), even after adjusting for maternal lipids. Our findings show that maternal GWG affects maternal but not foetal lipid profile, differently from pre-pregnancy BMI, which influences both.

Maternal obesity characterized by gestational diabetes increases the susceptibility of rat offspring to hepatic steatosis via a disrupted liver metabolome.

Maternal obesity is associated with a high risk for gestational diabetes mellitus (GDM), which is a common complication of pregnancy. The influence of maternal obesity and GDM on the metabolic health of the offspring is poorly understood. We hypothesize that GDM associated with maternal obesity will cause obesity, insulin resistance and hepatic steatosis in the offspring. Female Sprague-Dawley rats were fed a high-fat (45%) and sucrose (HFS) diet to cause maternal obesity and GDM. Lean control pregnant rats received low-fat (LF; 10%) diets. To investigate the interaction between the prenatal environment and postnatal diets, rat offspring were assigned to LF or HFS diets for 12 weeks, and insulin sensitivity and hepatic steatosis were evaluated. Pregnant GDM dams exhibited excessive gestational weight gain, hyperinsulinaemia and hyperglycaemia. Offspring of GDM dams gained more weight than the offspring of lean dams due to excess adiposity. The offspring of GDM dams also developed hepatic steatosis and insulin resistance. The postnatal consumption of a LF diet did not protect offspring of GDM dams against these metabolic disorders. Analysis of the hepatic metabolome revealed increased diacylglycerol and reduced phosphatidylethanolamine in the offspring of GDM dams compared to offspring of lean dams. Consistent with altered lipid metabolism, the expression of CTP:phosphoethanolamine cytidylyltransferase, and peroxisomal proliferator activated receptor-α mRNA was reduced in the livers of GDM offspring. GDM exposure programs gene expression and hepatic metabolite levels and drives the development of hepatic steatosis and insulin resistance in young adult rat offspring.

Obesity and cardiometabolic risk factors during pregnancy

To assess cardiometabolic risk factors during normal pregnancy and the influence of maternal obesity on them. This study included 25 healthy pregnant women with a single pregnancy and a gestational age of less than twenty weeks. Longitudinal analysis of blood pressure, body weight, body mass index (BMI), serum concentrations of leptin, adiponectin, cortisol, total cholesterol and fractions, triglycerides, uric acid, fasting glucose, oral glucose tolerance test, HOMA-IR and insulin/glucose ratio was performed each trimester during pregnancy. In order to evaluate the impact of obesity, pregnant women were divided into two groups based on BMI for the first quarter of pregnancy: Gpn for pregnant women with BMI<25 kg/m2 and Gso for BMI≥25 kg/m2. One-Way ANOVA for repeated measurements or Friedman test and Student-t or Mann-Whitney tests for statistical comparisons and Pearson correlations test were used for statistical analysis. The mean values for the first quarter of pregnancy for the following parameters were: age: 22 years; weight: 66.3 kg and BMI 26.4 kg/m2, with 20.2 and 30.7 kg/m2 for the Gpn and Gso groups, respectively. Mean weight gain during pregnancy was ±12.7 kg with 10.3 kg for the Gso group and 15.2 kg for the Gpn group. Regarding plasma determinations, cortisol, uric acid and lipid profile increased during all trimesters of pregnancy, except for HDL-cholesterol, which did not change. Blood pressure, insulin and HOMA-IR only increased in the third quarter of pregnancy. The Gso group tended to gain more weight and to show higher concentrations of leptin, total cholesterol, LDL-cholesterol, VLDL-cholesterol, TG, glucose, insulin, HOMA-IR, besides lower HDL-cholesterol and greater diastolic blood pressure in the 3rd quarter of pregnancy. Three pregnant women developed gestational hypertension, presented prepregnancy obesity, excessive weight gain, hyperleptinemia and an insulin/glucose ratio greater than two. Weight and BMI were positively correlated with total cholesterol and its LDL fraction, TG, uric acid, fasting blood glucose, insulin and HOMA-IR; and were negatively correlated with adiponectin and HDL-cholesterol. Leptin level was positively correlated with blood pressure. The metabolic changes in pregnancy are more significant in obese women, suggesting, as expected, an increased risk of cardiometabolic complications. During their first visit for prenatal care, obese women should be informed about these risks, have their BMI and insulin/glucose ratio calculated along with their lipid profile to identify pregnant women at higher risk for cardiovascular diseases.