Obese Mothers Research Articles

Trends in the Prevalence and Factors Associated with Undernutrition in Tunisian Children Aged 0–23 Months

Background: In recent years, undernutrition has remained a significant public health issue in Tunisia, increasing the risk of illness and mortality in young children. Therefore, this study aims to analyse the prevalence and factors contributing to undernutrition among Tunisian children aged 0–23 months. Methods: The study included 3265 children aged 0–23 months from the 2011–2023 Tunisia Multiple Indicator Cluster Surveys (MICS). Trends and logistic regression analyses were used to determine the prevalence and predictors of undernutrition. Results: The prevalence of stunting, wasting, and underweight in infants and children aged 0–23 months has increased by 3.3%, 0.5%, and 2.1%, respectively. Stunting and underweight were more common among infants aged 0–5 months (11.8% for stunting, 8.9% for underweight, p < 0.01), and first-time mothers (8.3% for stunting, 4.1% for underweight, p < 0.01). In 2023, compared to 2011, the odds of stunting, wasting, and being underweight had increased by 22%, 16%, and 70%, respectively. Infants aged 0–5 months had higher odds of undernutrition in all three indices. Children of obese or overweight mothers, and those who started breastfeeding late, were more likely to be stunted. Boys had significantly higher odds of wasting and underweight. Children with low birth weight, and duration of breastfeeding > 12 months, had significantly higher odds of being underweight. Conclusions: This study shows that infants aged 0–5 months, first-time mothers, boys, and children from poor households in Tunisia are at a higher risk of undernutrition. To address the growing issue of undernutrition in Tunisian children, enhancing maternal and child health and nutrition services, improving parental education, and implementing community-based programs that provide breastfeeding and nutritional education to infants born to new mothers and mothers with high/low BMI is recommended.

Single-cell RNA transcriptomics in mice reveals embryonic origin of fibrosis due to maternal obesity

Over 40% of pregnant women in the USA are obese which negatively affects fetal development and offspring health. Maternal obesity (MO) leads to fibrotic infiltration in multiple tissues and organs of offspring during their adulthood although the origin and mechanisms are unclear. C57BL/6J female mice were fed a control and high-fat diet to mimic MO condition. Embryonic somatic tissues were obtained at E9.5, E11.5, and E13.5 (equivalent to 6 weeks of human pregnancy) from control (CON) and MO mice for single-cell RNA-sequencing (scRNA-seq). To explore the role of AMP-activated protein kinase (AMPK), AMPK was activated by metformin and A769662, and knocked out in embryonic mesenchymal cells (EMC) using AMPKα1 floxed mice. Using unsupervised clustering, we identified three major cell populations with fibrogenic capacity. Compared to CON, the population of fibrogenic cells increased dramatically (by ∼125%) due to MO, supporting an embryonic origin of fibrosis in the offspring. MO induced inflammatory response and elevated expression of transforming growth factor β (TGFβ) signalling and fibrogenic genes in embryos. MO inhibited AMPK and its activation by metformin and A769662 inhibited TGFβ signalling and fibrogenesis. MO profoundly enhances embryonic fibrogenesis, explaining the origin of fibrosis in the offspring of mothers living with obesity. Our data underscore the importance of early intervention, before 5-6 weeks of pregnancy, in improving embryonic development, and AMPK is an amiable target for suppressing excessive fibrogenesis in MO embryos to assist increasing populations of obese mothers having healthy children. This work was funded by National Institutes of Health Grant R01HD067449.

On the interpretability of the SVM model for predicting infant mortality in Bangladesh

BackgroundAlthough machine learning (ML) models are well-liked for their outperformance in prediction, greatly avoided due to the lack of intuition and explanation of their predictions. Interpretable ML is, therefore, an emerging research field that combines the performance and interpretability of ML models to create comprehensive solutions for complex decision-making analysis. Conversely, infant mortality is a global public health concern affecting health, social well-being, socio-economic development, and healthcare services. The study employs advanced interpretable ML techniques to anticipate and understand the factors affecting infant mortality in Bangladesh, overcoming the shortcomings of the conventional logistic regression (LR) model.MethodsBy utilizing the global surrogate model and local individual conditional expectation (ICE) interpretability technique, the interpretable support vector machine (SVM) has been used in this study to reveal significant characteristics of infant mortality using data from the Bangladesh Demographic and Health Survey (BDHS) 2017–18. To investigate intricate decision-making analysis of infant mortality, we adapted SVM and LR techniques with the hyperparameter tuning parameters. These models’ performances were initially assessed using the receiver operating characteristics (ROC) curve, run-time, and confusion matrix parameters with 100 permutations. Afterward, the SVM model’s model-agnostic explanation and the LR model’s interpretation were compared to enhance advanced comprehension for further insights.ResultsThe results of the 100 permutations demonstrated that the LR model (Average: accuracy = 0.9105, precision = NaN, sensitivity = 0, specificity = 1, F1-score = 0, area under the ROC curve (AUC) = 0.6780, run-time = 0.0832) outperformed the SVM model (Average: accuracy = 0.8470, precision = 0.1062, sensitivity = 0.0949, specificity = 0.9209, F1-score = 0.1000, AUC = 0.5632, run-time = 0.0254) in predicting infant mortality, but the LR model had a slower run-time and it was unable to predict any positive cases. The interpretation of LR analysis revealed that infant mortality rates decrease when mothers give birth after over two years, with higher educational attainment, overweight or obese mothers, working mothers, and families with polluted cooking fuel having lower rates. The local ICE interpretability technique, which depicts individual influences on the average likelihood of dying within the first birthday, explores the interpretable SVM model that mothers with normal BMIs, giving birth within two years, using less polluted cooking fuel, working mothers, and having male infant were more likely to experience infant death. The interpretable SVM model based on the global surrogate model also reveals that working mothers who used polluted cooking fuel at home and working women who used less polluted cooking fuel but had a longer period between pregnancies than two years would have higher infant death rates. Even among non-working mothers who used polluted cooking fuel and gave birth within two years of the preceding one, infant death rates were higher.ConclusionsThe interpretable SVM model reveals global interpretations help clinicians understand the entire conditional distribution, while local interpretations focus on specific instances, providing different insights into model behavior. Interpretable ML models aid policymakers, stakeholders, and families in understanding and preventing infant deaths by improving policy-making strategies and establishing effective family counseling services.

Trophoblast-specific overexpression of adiponectin receptor 2 causes fetal growth restriction in pregnant mice.

Maternal obesity in pregnancy is strongly associated with complications such as fetal overgrowth and infants of obese mothers have an increased risk to develop obesity, diabetes, and cardiovascular disease later in life. However, the underlying mechanisms are not well established. Circulating levels of adiponectin are low in obese pregnant women and maternal circulating adiponectin is negatively associated with birth weight. We have reported that normalizing maternal adiponectin in obese pregnant mice prevents placental dysfunction, fetal overgrowth, and programming of offspring cardio-metabolic disease. However, the mechanistic link between maternal adiponectin, placental function, and fetal growth remains to be established. We hypothesized that trophoblast-specific overexpression of the adiponectin receptor 2 (Adipor2) in healthy pregnant mice inhibits placental mTORC1 signaling and nutrient transport, resulting in fetal growth restriction. Using lentiviral transduction of blastocysts with a mammalian gene expression lentiviral vector for up-regulation of Adipor2 (Adipor2-OX), we achieved a ~ 3-fold increase in placenta Adipor2 mRNA levels and a 2-fold increase of the ADIPOR2 protein in the trophoblast plasma membrane. Placenta-specific Adipor2-OX increased placental peroxisome proliferator-activated receptor-α phosphorylation, ceramide synthase expression and ceramide concentrations. Furthermore, Adipor2-OX inhibited placental mTORC1 signaling and reduced invivo placental transport of glucose and amino acids. Lastly, Adipor2-OX reduced fetal weight by 11%. These data provide mechanistic evidence that placental Adipor2 signaling directly affects fetal growth. We propose that low circulating adiponectin in maternal obesity causes fetal overgrowth and programs the offspring for cardio-metabolic disease mediated by a direct effect on placental function.

Characterization of newborn gut microbiota according to the pre-gestational maternal nutritional status and delivery mode.

The aim of this study is to characterize the composition of the newborn gut microbiota based on the maternal pre-pregnancy nutritional status and the delivery mode. A biological sample was collected from the anal mucosa of the newborns between 24 and 48h after delivery, as it was not possible to collect a meconium sample at that time. A general data collection questionnaire was administered. The microbiome of the samples was analyzed by next-generation sequencing of the hypervariable regions v3-v4 of the 16S gene. Alpha diversity analyses were performed using the Observed Richness and Shannon diversity index metrics and Beta diversity analyses were conducted using Nonmetric multidimensional scaling with Weighted Unifrac, Differential abundance analysis was performed using a Negative Binomial Wald Test with maximum likelihood estimation for coefficients of Generalized Linear Models. Newborns of obese mothers exhibited lower alpha diversity compared to newborns of mothers with adequate BMI (body mass index). We observed variation in the composition of the microbial community in newborn stool samples, both from mothers with overweight/obesity and those with adequate pre-pregnancy BMI. We observed a visible correlation between the mode of delivery and the newborn's microbiota. We found variation in the overall composition of the microbial community in the stools of newborns, regardless of the delivery mode. The results of our study demonstrate differences in the microbiota of neonates born via cesarean section compared to those born vaginally as well as differences in newborns of mothers with overweight/obesity compared to those with an adequate pre-pregnancy BMI.

Investigation of the relationship between inflammation biomarkers and obesity in mother and offspring rats feeding a high-protein diet

Investigation of the relationship between inflammation biomarkers and obesity in mother and offspring rats feeding a high-protein diet

Weight gain in pregnancy and impact of obesity on the obstetric outcome: A retrospective study in a secondary care hospital in South India

ABSTRACT Objective: To evaluate the patterns of weight gain in pregnancy and the outcomes of pregnancy in overweight and obese mothers. Materials and Methods: A retrospective cohort study was performed on 1,352 mothers between October 2020 and August 2021. All pregnant women who presented for antenatal checkups from 20 weeks or earlier, with a singleton pregnancy, were included in the study. Details such as comorbidities, total duration of labor, complications during labor, and neonatal complications were included. Results: At the first antenatal visit, 16% of mothers were underweight, 51% of mothers were normal weight, and 33% of mothers were overweight or obese. Women with poor weight gain were two times more prone to give birth to a child with low birth weight than those with adequate weight gain. Excess weight gain in pregnancy in women with a normal body mass index (BMI) had an association with the development of pre-eclampsia. The odds of overweight/obese pregnant women developing gestational diabetes mellitus (GDM) were 2.1 times higher than in pregnant women with normal BMI. The odds of pregnant overweight/obese women undergoing cesarean section were 1.6 times higher than in pregnant women with normal BMI. Conclusion: Overweight/obese pregnant women had increased odds of developing GDM and undergoing a cesarean section. Excess weight gain was also seen in overweight/obese women. It is therefore important for physicians to educate women on acceptable weight gain during their pregnancy.

The Effect Of Prepregnancy Bmi And Parity On The Duration Of Breastfeeding During Exclusive Breastfeeding

Obesity Is a condition in a person who experiences overnutrition, Especially Fat Accumulation, Which cause the body to weight more than normal body weight, Indicated with A Body Mass Index (BMI) of more than 29.9 kg/M2 several International Pieces Of Research State That Obese Mothers Fail To Breastfeed Exclusively. Aside From Maternal BMI, Maternal Characteristics Also Support Exclusive Breastfeeding. Maternal Characteristic Factors Include Age, Parity, And Mother’s Education. This Study Aims To Determine The Correlation Between Prepregnancy BMI And Maternal Characteristic Factors With The Duration Of Breastfeeding During Exclusive Breastfeeding. This Research Is Quantitative Research Using A Cross-Sectional Descriptive-Correlational Method With A Retrospective Approach. The Number Of Samples In This Research Was 300 Mothers Who Met The Inclusion Criteria With The Purposive Sampling Technique. Data were collected and processed statistically using the Chi-Square Test and T-test to determine factors related to breastfeeding duration, and the linear regression test with the backward method was used to determine the most influential factors in breastfeeding.The Chi-Square Test Results Showed That All Variables Were Related To The Duration Of Breastfeeding With A P-value <0.05. The Linear Regression Test Showed That The Factors That Had A Significant Effect On The Duration Of Breastfeeding Were Prepregnancy BMI And Parity With A Significance Of 0.00; judging From The Coefficient B Factor Value Of 0.285, Parity Had A More Dominant Effect.

Maternal diet during pregnancy and adaptive changes in the maternal and fetal pancreas have implications for future metabolic health.

Fetal and neonatal development is a critical period for the establishment of the future metabolic health and disease risk of an individual. Both maternal undernutrition and overnutrition can result in abnormal fetal organ development resulting in inappropriate birth size, child and adult obesity, and increased risk of Type 2 diabetes and cardiovascular diseases. Inappropriate adaptive changes to the maternal pancreas, placental function, and the development of the fetal pancreas in response to nutritional stress during pregnancy are major contributors to a risk trajectory in the offspring. This interconnected maternal-placental-fetal metabolic axis is driven by endocrine signals in response to the availability of nutritional metabolites and can result in cellular stress and premature aging in fetal tissues and the inappropriate expression of key genes involved in metabolic control as a result of long-lasting epigenetic changes. Such changes result is insufficient pancreatic beta-cell mass and function, reduced insulin sensitivity in target tissues such as liver and white adipose and altered development of hypothalamic satiety centres and in basal glucocorticoid levels. Whilst interventions in the obese mother such as dieting and increased exercise, or treatment with insulin or metformin in mothers who develop gestational diabetes, can improve metabolic control and reduce the risk of a large-for-gestational age infant, their effectiveness in changing the adverse metabolic trajectory in the child is as yet unclear.

A combination analysis based on bioinformatics tools reveals new signature genes related to maternal obesity and fetal programming.

Maternal obesity significantly influences fetal development and health later in life; however, the molecular mechanisms behind it remain unclear. This study aims to investigate signature genes related to maternal obesity and fetal programming based on a genomic-wide transcriptional placental study using a combination of different bioinformatics tools. The dataset (GSE128381) was obtained from Gene Expression Omnibus (GEO). The data of 100 normal body mass index (BMI) and 27 obese mothers were included in the analysis. Differentially expressed genes (DEGs) were evaluated by limma package. Thereafter, functional enrichment analysis was implemented. Then, weighted gene co-expression network analysis (WGCNA) and the least absolute shrinkage and selection operator (LASSO) analysis were used to further screening of signature genes. Simple linear regression analysis was used to assess the correlation between signature genes and newborn birth weight. Gene set enrichment analysis (GSEA) was implemented to study signaling pathways related to signature genes. The expression of the signature genes was also explored in 48 overweight mothers in the same dataset. A total of 167 DEGs were obtained, of which 122 were up-regulated while 45 were down-regulated. The dataset was then clustered into 11 modules by WGCNA, and the MEbrown was found as the most significant module related to maternal obesity and fetal programming (cor = 0.2, p = 0.03). The LASSO analysis showed that PTX3, NCF2, HOXB5, ABCA6, and C1orf162 are signature genes related to maternal obesity and fetal programming, which were increased in the placenta of obese mothers compared to those with normal BMI. The area under the curve (AUC) of the signature genes in the receiver operating characteristic curve (ROC) was 0.709, 0.660, 0.674, 0.667, and 0.717, respectively. Simple linear regression analysis showed that HOXB5 was associated with newborn birth weight. GSEA analysis revealed that these signature genes positively participate in various signaling pathways/functions in the placenta. PTX3, NCF2, HOXB5, ABCA6, and C1orf162 are novel signature genes related to maternal obesity and fetal programming, of which HOXB5 is implicated in newborn birth weight.

Gestational diabetes mellitus, not obesity, triggers postpartum brain inflammation and premature aging in Sprague-Dawley rats

Previous studies showed that women with gestational diabetes mellitus (GDM) are susceptible to cognitive dysfunction. We investigated the effects of GDM on brain pathologies and premature brain aging in rats. Seven-week-old female Sprague-Dawley rats were fed a normal diet (ND) or a high-fat diet (HFD) after two weeks of acclimatization. On pregnancy day 0, HFD-treated rats received streptozotocin (GDM group) or vehicle (Obese mothers). ND-treated rats received vehicle (ND-control mothers). On postpartum day 21, brains and blood were collected. The GDM group showed increased inflammatory and premature aging markers, mitochondrial changes, and compensatory increases in the blood–brain barrier and synaptic proteins in the prefrontal cortex and hippocampus. GDM triggers maternal brain inflammation and premature aging, suggesting compensatory mechanisms may protect against these effects.

Exploring the importance of family socio-economic position on the association between parental BMI and offspring BMI trajectories

PurposeWe aimed to investigate the associations between parental BMI and offspring BMI trajectories and to explore whether the parent-offspring BMI growth trajectory association differed according to family SEP or social mobility. MethodsWe used data from the Avon Longitudinal Study of Parents and Children (ALSPAC). Children’s weight and height were collected from 1 to 18 years. Parents’ height and weight were reported pre-pregnancy. We assessed family SEP by measuring parents’ and grandparents’ educational attainment, social class, and social mobility by changes in education attainment across generations. Multilevel models were used to develop trajectories and assess patterns of change in offspring BMI, to associate parental BMI with these trajectories, and explore whether these associations differed by family SEP and social mobility. Results13,612 children were included in the analyses. The average BMI of offspring whose parents were overweight or obese was higher throughout childhood and adolescence, compared to those with parents of normal BMI. Parental and grandparental low SEP were associated with higher child BMI, but there was little evidence of modification of parent-offspring associations. For example, at age 15 years the predicted mean BMI difference between children of overweight or obese mothers versus normal-weight mothers was 12.5 % (95 %CI: 10.1 % to 14.7 %) and 12.2 % (95 %CI: 10.3 % to 13.7 %) for high and low grandparental SEP, respectively. DiscussionThese findings strengthen the evidence that higher parental BMI and lower family SEP were associated with higher offspring BMI, but we did not observe strong evidence that family SEP modifies the parental-offspring BMI association.

Metabolomic and transcriptomic remodeling of bone marrow myeloid cells in response to maternal obesity.

Maternal obesity puts the offspring at high risk of developing obesity and cardio-metabolic diseases in adulthood. Here, using a mouse model of maternal high-fat diet (HFD)-induced obesity, we show that whole body fat content of the offspring of HFD-fed mothers (Off-HFD) increases significantly from very early age when compared to the offspring regular diet-fed mothers (Off-RD). We have previously shown significant metabolic and immune perturbations in the bone marrow of newly-weaned offspring of obese mothers. Therefore, we hypothesized that lipid metabolism is altered in the bone marrow Off-HFD in newly-weaned offspring of obese mothers when compared to the Off-RD. To test this hypothesis, we investigated the lipidomic profile of bone marrow cells collected from three-week-old offspring of regular and high fat diet-fed mothers. Diacylgycerols (DAGs), triacylglycerols (TAGs), sphingolipids and phospholipids, including plasmalogen, and lysophospholipids were remarkably different between the groups, independent of fetal sex. Levels of cholesteryl esters were significantly decreased in offspring of obese mothers, suggesting reduced delivery of cholesterol to bone marrow cells. This was accompanied by age-dependent progression of mitochondrial dysfunction in bone marrow cells. We subsequently isolated CD11b+ myeloid cells from three-week-old mice and conducted metabolomics, lipidomics, and transcriptomics analyses. The lipidomic profiles of these bone marrow myeloid cells were largely similar to that seen in bone marrow cells and included increases in DAGs and phospholipids alongside decreased TAGs, except for long-chain TAGs, which were significantly increased. Our data also revealed significant sex-dependent changes in amino acids and metabolites related to energy metabolism. Transcriptomic analysis revealed altered expression of genes related to major immune pathways including macrophage alternative activation, B-cell receptor signaling, TGFβ signaling, and communication between the innate and adaptive immune systems. All told, this study revealed lipidomic, metabolomic, and gene expression abnormalities in bone marrow cells broadly, and in bone marrow myeloid cells particularly, in the newly-weaned offspring of obese mothers, which might at least partially explain the progression of metabolic and cardiovascular diseases in their adulthood.

Breast milk dominant phyla and probiotic bacteria in the obese lactating women compared with normal weights

The main purpose was to determine the abundance of dominant phyla, Bifidobacterium spp., and Lactobacillus in breast milk of obese mothers versus normal-weights in fourth month of lactation in Iranian population. Sixty health women at the fourth month of breastfeeding, aged 18–40 years, were included and categorized based on body mass index (BMI) to the obese (BMI ≥ 30 kg/m2) and normal-weights (18.5 ≤ BMI ≤ 24.9). Bacterial DNA was extracted and qPCR of the 16S region was performed after human milk donation in a sterile condition. A multiple linear mixed model was used to determine the effective factors on the phyla population. Bifidobacterium spp. was significantly higher in milk of normal-weight group than the obese. The current weight showed a significant effect on the Actinobacteria abundance in milk. The Bacteroidetes and Firmicutes were significantly lower in mother’s milk with cesarean section (p = 0.04). Pre-pregnancy obesity decreased the Firmicutes and Lactobacillus abundance in maternal milk (p = 0.04 and p = 0.01). The Actinobacteria and Bifidobacterium spp. showed a significant effect on infant’s height (p = 0.008 and p = 0.04). The maternal current and pre-pregnancy weight showed an important effect on abundance of Actinobacteria and Bifidobacterium spp., as the good phyla and genus in milk which are associated with the infant’s height.

Collagens of placenta composition in obese puerperant women who gave birth to сhildren at St. Petersburg State Pediatric Medical University in 2018–2021

BACKGROUND: The relevance of the problem of obesity is associated with the high frequency and steady growth of this pathology in the population. The epigenetic influence of maternal obesity on the course of pregnancy and childbirth, as well as on the condition of the fetus and newborn, is currently being studied. This article analyzes changes in the composition of the connective tissue of the placenta against the background of obesity in pregnant and puerperas. AIM: The aim of this study is to identify the pathomorphological features of the placenta and the composition of placental collagens in women who were obese before pregnancy and at the time of delivery at the Perinatal Center of St. Petersburg State Medical University from 2018 to 2021 to assess potential fetal risks and to predict possible complications during pregnancy and in the postnatal period for the mother. MATERIALS AND METHODS: A histological examination of the placentas of obese women (18 patients) and the ones with a normal body mass index (18 patients) who gave birth to mature newborns at the Perinatal Center of St. Petersburg State Medical University from 2018 to 2021 was performed followed by immunohistochemical examination. Staining of placenta specimens was carried out in accordance with the standard immunohistochemical protocol, using primary antibodies to type I–IV collagen. RESULTS: Microscopic examination of chorionic villi revealed no significant differences in the presence of chronic inflammation and angiogenesis disorders between the groups. When studying collagen expression levels, the following differences have been found: in the group of pregnant obese patients, the optical luminescence density and distribution area for type I–III collagen in the placenta were significantly higher, while for type IV collagen they were significantly lower compared with the control group. CONCLUSIONS: The following features of the formation of connective tissue in the placenta in obese mothers have been revealed: an increase in type I–III collagen production and a decrease in type IV collagen production. The obtained findings indicate an earlier functional and morphological change in the placenta than those detected by standard histological methods.

Maternal Obesity Induces the Meiotic Defects and Epigenetic Alterations During Fetal Oocyte Development.

It has been widely reported that obesity adversely impacts reproductive performance of females. However, the effects of maternal obesity on fetal germ cells remain poorly understood. In the present study, by employing a high-fat diet (HFD)-based mouse model, it is discovered that maternal obesity disrupts the chromosomal synapsis and homologous recombination during fetal oogenesis. Moreover, transcriptomic profiling reveales the potential molecular network controlling this process. Of note, the global hypermethylation of genomic DNA in fetal oocytes from obese mouse is detected. Importantly, time-restricted feeding (TRF) of obese mice not only ameliorate the meiotic defects, but also partly restore the epigenetic remodeling in fetal oocytes. In sum, the evidence are provided showing the deficit fetal oogenesis in obese mother, implicating a mechanism underlying the intergenerational effects of environmental insults. TRF may represent a potentially effective approach for mitigating fertility issues in obese patients.

Fetal growth restriction and placental defects in obese mice are associated with impaired decidualisation: the role of increased leptin signalling modulators SOCS3 and PTPN2

Decidualisation of the endometrium is a key event in early pregnancy, which enables embryo implantation. Importantly, the molecular processes impairing decidualisation in obese mothers are yet to be characterised. We hypothesise that impaired decidualisation in obese mice is mediated by the upregulation of leptin modulators, the suppressor of cytokine signalling 3 (SOCS3) and the protein tyrosine phosphatase non-receptor type 2 (PTPN2), together with the disruption of progesterone (P4)-signal transducer and activator of transcription (STAT3) signalling. After feeding mice with chow diet (CD) or high-fat diet (HFD) for 16 weeks, we confirmed the downregulation of P4 and oestradiol (E2) steroid receptors in decidua from embryonic day (E) 6.5 and decreased proliferation of stromal cells from HFD. In vitro decidualised mouse endometrial stromal cells (MESCs) and E6.5 deciduas from the HFD showed decreased expression of decidualisation markers, followed by the upregulation of SOCS3 and PTPN2 and decreased phosphorylation of STAT3. In vivo and in vitro leptin treatment of mice and MESCs mimicked the results observed in the obese model. The downregulation of Socs3 and Ptpn2 after siRNA transfection of MESCs from HFD mice restored the expression level of decidualisation markers. Finally, DIO mice placentas from E18.5 showed decreased labyrinth development and vascularisation and fetal growth restricted embryos. The present study revealed major defects in decidualisation in obese mice, characterised by altered uterine response to E2 and P4 steroid signalling. Importantly, altered hormonal response was associated with increased expression of leptin signalling modulators SOCS3 and PTPN2. Elevated levels of SOCS3 and PTPN2 were shown to molecularly affect decidualisation in obese mice, potentially disrupting the STAT3-PR regulatory molecular hub.

Effect of Obesity on Aquaporin5 Expression in Human Placental and Uterus Tissues.

Background: Obesity and overweight are also becoming more prevalent among women of childbearing age and pregnant women. In maternal obesity, the activation of metabolic, inflammatory, and oxidative stress pathways is proven, which appears to be a key step in the pathological changes observed in placental and uterine function. Several recent studies have evidenced that aquaporins (AQPs) are critical players in adipose tissue biology and are involved in the onset of obesity. Methods: Our studies aimed to investigate the changes in placental volume and vascularization and measure the AQP5 expression and total antioxidant capacity (TAC) in the placenta and uterus tissues in obese and typical-weight mothers. We also aim to measure the AQP5 plasma concentration. Results: We found AQP5 dominance in the uterus and plasma at 34 weeks of normal pregnancy. The placental volume increased and the vascularization decreased in obese mothers compared to the control. The AQP5 expression increased in the uterus of the obese group and did not change in the placenta. The TAC decreased in the plasma of overweight mothers. Conclusions: We hypothesize that increased AQP5 expression prolongs the length of pregnancy and inhibits the onset of contractions. Based on our findings, we can develop diagnostic tests and provide new targets for tocolytic drug development.

The Effect of Pre-Pregnancy BMI and Parity on the Duration of Breastfeeding During Exclusive Breastfeeding

Obesity is a condition of a person who experiences overnutrition, especially fat accumulation which causes the body to weigh more than normal body weight, indicated with a Body Mass Index (BMI) of more than 29.9 kg/m2. Several international pieces of research state that obese mothers fail to breastfeed exclusively. Aside from maternal BMI, maternal characteristics also support exclusive breastfeeding. Maternal characteristic factors include age, parity, and mother’s education. This study aims to determine the correlation between pre-pregnancy BMI and maternal characteristic factors with the duration of breastfeeding during exclusive breastfeeding. This research is quantitative research using a cross-sectional descriptive-correlational method with a retrospective approach. The number of samples in this research was 300 mothers who met the inclusion criteria with the purposive sampling technique. Data were collected and processed statistically using the Chi-Square test and T-test to determine factors related to breastfeeding duration and the linear regression test with the backward method to determine the most influential factor on breastfeeding duration. The Chi-Square test results showed that all variables were related to the duration of breastfeeding with a p-value <0.05. The linear regression test showed that the factors that had a significant effect on the duration of breastfeeding were pre-pregnancy BMI and parity with a significance of 0.00, judging from the coefficient B factor value of 0.285, parity had a more dominant effect. Pre-pregnancy BMI and parity are the most influential and interrelated variables in exclusive breastfeeding, where primiparous mothers with obesity are more at risk for exclusive breastfeeding failure than obese multiparous mothers.

Correlation between Obesity and Pregnancy Outcomes, Miscarriage, and Mode of Delivery

<p><strong>Introduction: </strong>The obesity pandemic is a source of problems in both developed countries. The obesity is associated with complications before and during pregnancy and even infant death. The study aims to find out the issue of obesity among women of reproductive age, particularly concerning its impact on maternal and fetal outcomes during pregnancy.</p><p><strong>Methods: </strong>This is a cross-sectional observational study using secondary data with medical records taken at Sebelas Maret University Hospital (UNS Hospital). Subjects were obese pregnant women who gave birth at UNS Hospital. Data from 284 single births were added maternal parameters, obstetric parameters, and newborn parameters were taken and then analyzed univariately, and bivariate analysis was carried out using the Kruskall-Wallis test and the Spearman test for comparison and correlation of each variable.</p><p><strong>Results: </strong>This study finds lower incidences of postdate pregnancy and instrumental deliveries among obese mothers, but a higher rate of emergency cesarean sections. Newborn anthropometric measurements increase with maternal BMI, indicating a direct association between maternal obesity and newborn health (p = 0.001), while APGAR scores show no significant differences among maternal BMI groups. The findings underscore the importance of addressing maternal obesity to improve both maternal and newborn health outcomes.</p><p><strong>Conclusion: </strong>The research indicates a correlation between maternal BMI, maternal obstetric characteristics, newborn anthropometric measurements, and APGAR scores. This suggests that interventions aimed at promoting healthy maternal BMI, beginning before conception, continuing throughout pregnancy, and extending into the post-pregnancy period, could potentially improve newborn health outcomes and give long-term health benefits.</p>