Offspring Weight Research Articles

Embryonic Exposure to Tryptophan Yields Bullying Victimization via Reprogramming the Microbiota-Gut-Brain Axis in a Chicken Model.

Maternal metabolic disorder during early pregnancy may give rise to emotional and behavioral disorders in the child, vulnerable to bullying. Placental tryptophan fluctuation consequently disrupts offspring gut microbiome and brain neurogenesis with long-lasting physiological and social behavioral impacts. The aim of this study was to examine the hypothesis that the excess gestational tryptophan may affect children’s mental and physical development via modifying the microbiota-gut-brain axis, which lays the foundation of their mental status. Chicken embryo was employed due to its robust microbiota and independence of maternal influences during embryogenesis. The results indicated that embryonic tryptophan exposure reduced body weight and aggressiveness in the male offspring before and during adolescence. Additionally, the relative gut length and crypt depth were increased, while the villus/crypt ratio was decreased in tryptophan treated roosters, which was corresponding to the changes in the cecal microbiota composition. Furthermore, the catecholamine concentrations were increased in tryptophan group, which may be associated with the alterations in the gut microbiome and the gut-brain axis’s function. These changes may underlie the sociometric status of bullying; clarify how gestational tryptophan fluctuation compromises bullying and provide a strategy to prevent bullying by controlling dietary tryptophan and medication therapy during pregnancy.

Maternal age and maternal environment affect egg composition, yolk testosterone, offspring growth and behaviour in laying hens

Maternal effects have been reported to alter offspring phenotype in laying hens. In this study, we investigated the effects of maternal environment and maternal age on egg traits and offspring development and behaviour. For this, we ran two experiments. First (E1), commercial hybrid hens were reared either in aviary or barren brooding cages, then housed in aviary, conventional cages or furnished (enriched) cages, thus forming different maternal housing treatments. Hens from each treatment were inseminated at three ages, and measures of egg composition, yolk testosterone concentration and offspring’s development, anxiety and fearfulness were assessed. In experiment 2 (E2), maternal age effects on offspring's growth and behaviour were further investigated using fertile eggs from commercial breeder flocks at three different ages. Results from E1 showed that Old hens laid heavier eggs with less yolk testosterone and produced offspring with fewer indicators of anxiety and fearfulness. Maternal rearing and housing affected egg traits, offspring weight and behaviour, but not in a consistent way. Effects of maternal age were not replicated in E2, possibly due to differences in management or higher tolerance to maternal effects in commercial breeders. Overall, our research confirms that maternal age and maternal environment affects egg composition, with maternal age specifically affecting yolk testosterone concentration, which may mediate physical and behavioural effects in offspring.

Maternal smoking status during pregnancy and low birth weight in offspring: systematic review and meta-analysis of 55 cohort studies published from 1986 to 2020.

Maternal smoking during pregnancy may be associated with low birth weight (LBW) in offspring and global risk estimates have not been summarized previously. We aimed to systematically explore evidence regarding maternal smoking and the LBW risk in offspring globally and examine possible causes of heterogeneity across relevant studies. Comprehensive search of PubMed, Ovid Embase, Ovid Medline (R), and Web of science from inception until October 2021 was carried out. A random-effects meta-analysis was used to estimate the pooled odds ratio (OR) and corresponding 95% confidence interval (CI). Restricted cubic spline analysis with three knots was used to further examine the dose-response relationship. Literature searches yielded 4940 articles, of which 53 met inclusion criteria (comprising 55 independent studies). Maternal smoking during pregnancy was significantly associated with the risk of LBW in offspring (OR = 1.89, 95% CI = 1.80-1.98). Furthermore, an obvious dose-response relationship between the amount of cigarettes daily smoked in pregnancy and the risk of LBW in offspring was observed. The results of subgroup analyses indicated that the risk of maternal smoking on LBW was larger in more recently conducted studies (P = 0.020) and longer period of active smoking during pregnancy (P = 0.002). No evidence of publication bias was found. In summary, maternal smoking in pregnancy was significantly associated with a higher risk of LBW in offspring on a global scale. The risk of maternal smoking on infant LBW seems to be increasing over time, and was higher with longer smoking duration throughout pregnancy and more cigarettes smoked daily.

Association between maternal polycystic ovary syndrome and early childhood growth: a continuous observation from 3months to 6years of age.

To investigate whether maternal PCOS could impact growth and development in offspring at an early age through continuous observation from age 3months to 6years. This prospective study was conducted in 198 children born to mothers with PCOS and 227 children born to healthy mothers in Ningbo (Zhejiang Province, China) between October 2012 and July 2015. Measurements of offspring height, weight, head circumference, and teething were examined by trained professionals through age 6years. Height, weight, and body mass index (BMI) were analysed using repeated measures analysis of variance between the PCOS and control groups. Offspring born to women with PCOS showed significantly higher BMI at age 12, 18, and 30months and 5years (P = 0.040, P = 0.000, P = 0.000, and P = 0.023, respectively). Female offspring born to women with PCOS showed significantly increased body weight at 3, 8, 12, 18, and 30months, and 3 and 6years (P = 0.027, P = 0.008, P = 0.010, P = 0.034, P = 0.047, P = 0.040, and P = 0.035, respectively) and significantly higher BMI at 3, 8, 12, 18, and 30months (P = 0.009, P = 0.016, P = 0.029, P = 0.000, and P = 0.000, respectively). After adjusting for maternal, paternal, and pregnancy confounders, PCOS status presented significant associations with weight at age 3, 8, and 12months and 3years (P = 0.005, P = 0.004, P = 0.021, P = 0.035 respectively), and with BMI at age 3 and 8months (P = 0.011 and P = 0.014) in female offspring. Maternal PCOS is associated with an increased risk of developing obesity in female offspring.

A method for identifying critical time windows of maternal air pollution exposures associated with low birth weight in offspring using massive geographic data.

Associations between maternal exposures to air pollutants and low birth weight (LBW) in offspring varied when different exposure windows were considered. Methods used in previous studies lacked flexibility in delineating exposure windows and did not consider time periods before conception, which may restrict the discoveries of critical exposure windows. This study introduces a novel method to identify critical windows of maternal air pollution exposures associated with LBW in offspring using massive georeferenced data. Through a case-control study based on birth data (94,106 LBW cases and 376,424 controls) and air quality monitoring data (367 chemicals) in Texas during 1996-2008, this study used the average ambient concentration measured by the monitoring site closest to the residence location of a mother during a time window as the maternal exposure to a specific chemical during that exposure window. Binary logistic regression was utilized to estimate air pollutant-LBW associations in different exposure windows. The odds ratios (ORs) were adjusted for child's sex, gestational weeks, maternal age, race/ethnicity, and education. The adjusted ORs were plotted against the exposure window series of different sizes for each chemical, aiming at interactively visualizing and exploring the critical exposure windows across multiple temporal scales. This study identifies ten chemicals and seventeen corresponding critical exposure windows where strong air pollutant-LBW associations are detected. The ten identified chemicals are benzaldehyde, sum of Photochemical Assessment Monitoring Stations (PAMS) target compounds, n-undecane, m-tolualdehyde, organic carbon fraction 2 (OC2), ethylene dibromide, valeraldehyde, propionaldehyde, 4-methyl-1-pentene, and zirconium. Nine critical exposure windows involving six chemicals start more than fivemonths prior to conception, seven windows involving five chemicals commence in the second and/or third trimester of pregnancy, and the remaining one window is located in other time periods. The novel method reveals a number of critical time windows of maternal exposure to ten chemicals that are positively associated with LBW in offspring. These ten chemicals were identified as LBW risk factors for the first time. Additional studies with more data are needed to validate the results in the future.

Maternal High-Fat Diet Alters the Characteristics of Astrocytes and Worsens the Outcome of Stroke in Rat Offspring, Which Improves After FGF21 Administration.

Background: Maternal high-fat diet (MHFD) has been shown to increase susceptibility to neurological disease in later offspring, but the underlying mechanism is not clear. Fibroblast growth factor 21 (FGF21) has been reported to have a neuroprotective effect in stroke, but its mechanism of action remains unknown. In this study, we investigated the mechanism of the effect of MHFD on stroke in offspring in adulthood and the mechanism by which FGF21 acts on stroke and restores neurological function. Methods: We performed transcriptome sequencing analysis on D21 neonatal rats. Bodyweight and blood indicators were recorded in the adult rats after MHFD. FGF21 was administered 7 h after photochemical modeling twice a day for three consecutive days. Results: We found numerous mRNA changes between the MHFD group and a normal maternal normal diet (MND) group at D21, including genes related to astrocyte and PI3K/Akt pathways. The body weight, blood glucose, and triglycerides of the MHFD offspring were higher, ischemic lesions were larger, the number of activated astrocytes was lower, and the neurological function score was worse than that of the MND group. After FGF21 administration, WB and qPCR analyses showed that astrocytes and the PI3K/Akt pathway were upregulated, while NF-κB and inflammatory cytokines expression were inhibited in stroke and peri-stroke regions. Conclusion: Taken together, we conclude that MHFD alters the characteristics of astrocytes and other transcriptome changes in their offspring, leading to a worse prognosis of stroke, while FGF21 plays a neuroprotective role by inhibiting NF-κB and inflammatory factors and activating the PI3K/Akt pathway and activating more astrocytes in the MND group than the MHFD group.

Maternal immunization against myostatin suppresses post-hatch chicken growth.

Myostatin (MSTN) is a negative regulator of skeletal muscle growth, thus it was hypothesized that immunization of hens against MSTN would enhance post-hatch growth and muscle mass via suppression of MSTN activity by anti-MSTN IgY in fertilized eggs. This study investigated the effects of immunization of hens against chicken MSTN (chMSTN) or a MSTN fragment (Myo2) on the growth and muscle mass of offspring. In Experiment 1, hens mixed with roosters were divided into two groups and hens in the Control and chMSTN groups were immunized with 0 and 0.5 mg of chMSTN, respectively. In Experiment 2, hens in the chMSTN group were divided into chMSTN and Myo2 groups while the Control group remained the same. The Control and chMSTN groups were immunized in the same way as Experiment 1. The Myo2 group was immunized against MSTN peptide fragment (Myo2) conjugated to KLH. Eggs collected from each group were incubated, and chicks were reared to examine growth and carcass parameters. ELISA showed the production of IgYs against chMSTN and Myo2 and the presence of these antibodies in egg yolk. IgY from the chMSTN and Myo2 groups showed binding affinity to chMSTN, Myo2, and commercial MSTN in Western blot analysis but did not show MSTN-inhibitory capacity in a reporter gene assay. In Experiment 1, no difference was observed in the body weight and carcass parameters of offspring between the Control and chMSTN groups. In Experiment 2, the body weight of chicks from the Myo2 group was significantly lower than that of the Control or chMSTN groups. The dressing percentage and breast muscle mass of the chMSTN and Myo2 groups were significantly lower than those of the Control group, and the breast muscle mass of Myo2 was significantly lower than that of the chMSTN. In summary, in contrast to our hypothesis, maternal immunization of hens did not increase but decreased the body weight and muscle mass of offspring.

Gains in body mass and body water in pregnancy and relationships to birth weight of offspring in rural and urban Pune, India.

Maternal size, weight gain in pregnancy, fetal gender, environment and gestational age are known determinants of birth weight. It is not clear which component of maternal weight or gained weight during pregnancy influences birth weight. We evaluated the association of maternal total body water measured by the deuterium dilution technique (TBW-D2O) at 17 and 34 weeks of gestation with birth weight. A secondary aim was to examine the utility of bioimpedance spectroscopy (BIS) to determine total body water (TBW-BIS) in pregnancy. At 17 and 34 weeks of pregnancy, ninety-nine women (fifty-one rural and forty-eight urban) from Pune, India had measurements of body weight, TBW-D2O, TBW-BIS and offspring birth weight. At 17 weeks of gestation, average weights for rural and urban women were 45⋅5 ± 4⋅8 (sd) and 50⋅7 ± 7⋅8 kg (P < 0⋅0001), respectively. Maternal weight gains over the subsequent 17 weeks for rural and urban women were 6⋅0 ± 2⋅2 and 7⋅5 ± 2⋅8 kg (P = 0⋅003) and water gains were 4⋅0 ± 2⋅4 and 4⋅8 ± 2⋅8 kg (P = 0⋅092), respectively. In both rural and urban women, birth weight was positively, and independently, associated with gestation and parity. Only for rural women, between 17 and 34 weeks, was an increase in dry mass (weight minus TBW-D2O) or a decrease in TBW-D2O as a percentage of total weight associated with a higher birth weight. At both 17 and 34 weeks, TBW-BIS increasingly underestimated TBW-D2O as the water space increased. Differences in body composition during pregnancy between rural and urban environments and possible impacts of nutrition transition on maternal body composition and fetal growth were demonstrated.

Neurobehavioral and neurochemical effects of perinatal arsenite exposure in Sprague-Dawley rats

Exposure to relatively high levels of inorganic arsenic (iAs) is associated with detrimental effects on human health, including cancer and diabetes. The effects of lower-level exposures are less clear, and gaps in the literature exist as to the effects of iAs exposure on neurodevelopment. The current study assessed the effects of perinatal iAs exposure on rodent neurodevelopment and behavior. Pregnant Sprague-Dawley (SD) rats were exposed to arsenite (AsIII) via oral gavage on gestational days (GD) 6 through 21, and pups were directly dosed via gavage on postnatal days (PND) 1 through 21. Dams and offspring received the same doses: 0.00, 0.10, 1.50, or 3.75 mg/kg/day. Male and female offspring underwent a battery of behavioral assessments from weaning until PND 180. Brain arsenic levels increased in a dose-dependent manner at both PND 1 and 21. Results from the behavioral tests show that pre- and postnatal AsIII exposure did not adversely affect offspring weight gain, adolescent motor and cognitive functions, or adult motor and cognitive functions in the SD rat. There were no differences in concentration of several brain proteins associated with blood-brain barrier permeability, dopamine functions, and inflammation.

A Preconception Paternal Fish Oil Diet Prevents Toxicant-Driven New Bronchopulmonary Dysplasia in Neonatal Mice.

New bronchopulmonary dysplasia is a developmental lung disease associated with placental dysfunction and impaired alveolarization. Risk factors for new BPD include prematurity, delayed postnatal growth, the dysregulation of epithelial-to-mesenchymal transition (EMT), and parental exposure to toxicants. Our group previously reported that a history of paternal toxicant exposure increased the risk of prematurity and low birth weight in offspring. A history of paternal toxicant exposure also increased the offspring’s risk of new BPD and disease severity was increased in offspring who additionally received a supplemental formula diet, which has also been linked to poor lung development. Risk factors associated with new BPD are well-defined, but it is unclear whether the disease can be prevented. Herein, we assessed whether a paternal fish oil diet could attenuate the development of new BPD in the offspring of toxicant exposed mice, with and without neonatal formula feeding. We investigated the impact of a paternal fish oil diet preconception because we previously reported that this intervention reduces the risk of TCDD associated placental dysfunction, prematurity, and low birth weight. We found that a paternal fish oil diet significantly reduced the risk of new BPD in neonatal mice with a history of paternal toxicant exposure regardless of neonatal diet. Furthermore, our evidence suggests that the protective effects of a paternal fish oil diet are mediated in part by the modulation of small molecules involved in EMT.

Prediction of Healthy Pregnancy Outcomes in Women with Overweight and Obesity: The Role of Maternal Early-Pregnancy Metabolites.

Women with obesity receive intensified antenatal care due to their increased risk of pregnancy complications, even though not all of these women develop complications. We developed a model based on maternal characteristics for prediction of healthy pregnancy outcomes in women with obesity or who are overweight. We assessed whether early-pregnancy metabolites improved prediction. In a population-based cohort study among a subsample of 1180 Dutch pregnant women with obesity or who are overweight, we developed a prediction model using 32 maternal socio-demographic, lifestyle, physical and pregnancy-related characteristics. We determined early-pregnancy amino acids, nonesterifed fatty acids, phospholipids and carnitines in blood serum using liquid chromatography-tandem mass spectrometry. A healthy pregnancy outcome was the absence of fetal death, gestational hypertension, preeclampsia, gestational diabetes, caesarian section, preterm birth, large-for-gestational-age at birth, macrosomia, postpartum weight retention and offspring overweight/obesity at 5 years. Maternal age, relationship status, parity, early-pregnancy body mass index, mid-pregnancy gestational weight gain, systolic blood pressure and estimated fetal weight were selected into the model using backward selection (area under the receiver operating characteristic curve: 0.65 (95% confidence interval 0.61 to 0.68)). Early-pregnancy metabolites did not improve model performance. Thus, in women with obesity or who are overweight, maternal characteristics can moderately predict a healthy pregnancy outcome. Maternal early-pregnancy metabolites have no incremental value in the prediction of a healthy pregnancy outcome.

Maternal B-cell depletion nor TNF-α blockade worsen offspring outcomes in a rat model of preeclampsia

Preeclampsia (PE), new onset hypertension during pregnancy, is associated with maternal death and morbidity, low birth weight in offspring, increased tumor necrosis factor alpha (TNF-α) and B cells producing autoantibodies. We have shown that Etanercept (E), a TNF-α inhibitor, improves blood pressure in the reduced uterine perfusion pressure (RUPP) rat model of PE and that Rituximab (R), used clinically for B cell depletion, lowered blood pressure and B cells in RUPP rats. Clinical use of R or E during pregnancy has not resulted in adverse outcomes for the mother, however, the effects of maternal B cell depletion or TNF-α blockade on offspring immune cells in response to placental ischemia is unknown.

Pregnancy Outcomes in Women With Autoimmune Hepatitis – A Nationwide Population-based Cohort Study With Histopathology

Autoimmune hepatitis (AIH) is a chronic inflammatory liver condition that predominantly affects women. However, pregnancy risks remain unclear. A nationwide population-based cohort study (ESPRESSO) in Sweden from 1992 to 2016 including 309 singleton births in women with AIH and 1532 matched births in women from the general population was performed. AIH was diagnosed as a combination of administrative coding from medical diagnosis of AIH and liver biopsy data from Sweden's 28 pathology departments. Using conditional logistic regression, odds ratios (ORs) for adverse pregnancy outcomes were determined. Among 306 live births to women with AIH, 51 (16.7%) were preterm, compared with 70 of 1524 (4.6%) reference births. This corresponded to an OR of 5.10 for preterm birth (95% confidence interval [CI], 3.29-7.92), with similar odds using sibling comparators. Women with AIH with and without cirrhosis had similar odds for preterm birth. The AIH association was particularly strong with medically indicated preterm birth (OR, 13.01; 95% CI, 5.50-30.79). AIH was associated with low birth weight (OR, 5.31; 95% CI, 2.82-9.99) and low 5-minute Apgar score (OR, 3.46; 95% CI, 1.14-10.49) offspring, but we found no association with congenital malformations (OR, 1.14; 95% CI, 0.68-1.91), small for gestational age (OR, 1.04; 95% CI, 0.38-2.85), stillbirth (OR, 0.59; 95% CI, 0.02-18.88), or neonatal death (OR, 7.42; 95% CI, 0.65-84.25). Maternal AIH was linked to an increased odds of cesarean section (OR, 1.44; 95% CI, 1.04-2.00) and preeclampsia (OR, 3.65; 95% CI, 2.01-6.64), but not to gestational diabetes. Maternal AIH was associated with a 5-fold higher odds of preterm birth, and cirrhosis at diagnosis did not add to the impact of AIH on preterm birth. Future studies are needed to understand how to reduce this risk.

Immune Cell and Adipose Gene Expression Reprogramming in Juvenile Monkeys Born to Health and Weight-Diverse Mothers

Over 93 million Americans are obese and 66 million suffer from metabolic disease. Roughly 40% of obese people do not have metabolic abnormalities (metabolically health obese [MHO]), while approximately 15% of lean do (metabolically unhealthy lean [MUL]). African green monkeys (AGMs) demonstrate naturally occurring obesity and metabolic syndrome (MetS) without diet manipulation, and MetS criteria are heritable. Age-matched maternal AGMs were classified by adjusted MetS criteria ([n=44]; waist >40cm, fasting glucose (FG) >100 mg/dL, SBP/DBP >135/85mmHg, and HDL-c <50mg/dL) and classified as metabolically healthy lean (MHL), MHO, MUL or metabolically unhealthy obese (MUO). Age, weight and sex-matched pre-pubertal juvenile offspring from these mothers were additionally selected (n=9-11/group; ages=1.1-3.4years) for evaluation. We assessed monocyte subtypes by flow cytometry, and subcutaneous adipose gene expression patterns by RNAseq. Non-classical monocytes were increased in obese and unhealthy mothers (MHO p=0.02, MUL p=0.003, MUO p=0.00002) compared to MHL. MUL and MUO juvenile offspring also had more non-classical monocytes compared to MHL (p=0.05 and p=0.07). Monocyte chemoattractant protein-1 (MCP)-1 was measured in plasma and found to be elevated in MUO juveniles (p=0.02). Patterns of increased cytokine and extracellular matrix gene expression were seen in MUL and MUO juveniles’ adipose (6-7/group), mirroring obese and unhealthy mothers’ adipose gene expression patterns. Maternal health and obesity influence offspring immune cells and adipose gene expression prior to weight gain and metabolic disease onset. Our data underscore maternal monocyte and adipose profiles as inherited phenotypes that present prior to adipose expansion and may be targets to improve intergenerational health trajectories.

Lack of Offspring Nrf2 Does Not Exacerbate the Detrimental Metabolic Outcomes Caused by In Utero PCB126 Exposure.

Human environmental exposures to toxicants, such as polychlorinated biphenyls (PCBs), increase oxidative stress and disease susceptibility. Such exposures during pregnancy and/or nursing have been demonstrated to adversely affect offspring health outcomes. Nuclear factor erythroid-2-related factor 2 (Nrf2) regulates the antioxidant response and is involved in the detoxification of coplanar PCBs, like PCB126. The purpose of this study was to investigate glucose tolerance and body composition in PCB-exposed offspring expressing or lacking Nrf2. We hypothesized that offspring lacking Nrf2 expression would be more susceptible to the long-term health detriments associated with perinatal PCB exposure. During gestation, whole-body Nrf2 heterozygous (Het) and whole-body Nrf2 knockout (KO) mice were exposed to vehicle or PCB126. Shortly after birth, litters were cross-fostered to unexposed dams to prevent PCB exposure during nursing. Offspring were weaned, and their body weight, body composition, and glucose tolerance were recorded. At two months of age, PCB exposure resulted in a significant reduction in the average body weight of offspring born to Nrf2 Het dams (p < 0.001) that primarily arose from the decrease in average lean body mass in offspring (p < 0.001). There were no differences in average body weight of PCB-exposed offspring born to Nrf2 KO dams (p > 0.05), and this was because offspring of Nrf2 KO dams exposed to PCB126 during pregnancy experienced a significant elevation in fat mass (p = 0.002) that offset the significant reduction in average lean mass (p < 0.001). Regardless, the lack of Nrf2 expression in the offspring themselves did not enhance the differences observed. After an oral glucose challenge, PCB-exposed offspring exhibited significant impairments in glucose disposal and uptake (p < 0.05). Offspring born to Nrf2 Het dams exhibited these impairments at 30 min and 120 min, while offspring born to Nrf2 KO dams exhibited these impairments at zero, 15, 30, 60 and 120 min after the glucose challenge. Again, the interactions between offspring genotype and PCB exposure were not significant. These findings were largely consistent as the offspring reached four months of age and demonstrate that the lack of offspring Nrf2 expression does not worsen the metabolic derangements caused by in utero PCB exposure as we expected. Future directions will focus on understanding how the observed maternal Nrf2 genotypic differences can influence offspring metabolic responses to in utero PCB exposure.

Metformin in pregnancy: a re-examination of its safety.

Metformin in pregnancy: a re-examination of its safety.

Exposure to maternal hyperglycemia and high-fat diet consumption after weaning in rats: repercussions on periovarian adipose tissue.

Clinical and epidemiological studies show that maternal hyperglycemia can change the programming of offspring leading to transgenerational effects. These changes may be related to environmental factors, such as high-fat diet (HFD) consumption, and contribute to the comorbidity onset at the adulthood of the offspring. The objective of this study was to evaluate the hyperglycemic intrauterine environment, associated or not with an HFD administered from weaning to adult life on the periovarian adipose tissue of rat offspring Maternal diabetes was chemically induced by Streptozotocin. Female offsprings were randomly distributed into four experimental groups (n = 5 animals/group): Female offspring from control or diabetic mothers and fed an HFD or standard diet. HFD was prepared with lard enrichment and given from weaning to adulthood. On day 120 of life, the rats were anesthetized and sacrificed to obtain adipose tissue samples. Then, the hyperglycemic intrauterine environment and HFD fed after weaning caused a higher body weight, total fat, and periovarian fat in adult offspring, which could compromise the future reproductive function of these females. These rats showed higher adiposity index and adipocyte area, contributing to hypertrophied adipose tissue. Therefore, maternal diabetes itself causes intergenerational changes and, in association with the HFD consumption after weaning, exacerbated the changes in the adipose tissue of adult female offspring.

Pregnancy after bariatric surgery: Effects of personalized nutrition counseling on pregnancy outcomes

Nutritional challenges following bariatric surgery can be intensified during pregnancy and may have crucial effects on the fetus, including lower birth weight. To the best of our knowledge, the effect of nutritional counseling during post-bariatric pregnancy to improve maternal diet quality and eating habits on neonatal outcome has not been evaluated. The aim of this research was to examine the effects of personal nutritional counseling during post-bariatric pregnancy on nutritional intake and neonatal outcomes. We performed a non-randomized, intervention-control clinical trial. Women (n=61) were divided into three groups; two prospective, and one retrospective: 1. An Intervention Bariatric Prospective group 2. A Control Prospective group without surgery, and 3. A Control Bariatric Retrospective group. Patient enrollment was performed from April 2016 to March 2018. The intervention program included biweekly visits with a pregnancy nutrition certified bariatric dietitian. Data collection was performed four times during pregnancy, and included demographic and eating habits questionnaires, 24h dietary recall, and information about delivery outcomes. In the retrospective group delivery outcomes and Food Frequency Questionnaire was collected once, after delivery. There were no differences between groups at baseline except for a higher pre-pregnancy BMI in the post-bariatric groups. In the prospective groups, dietary protein, energy, and iron were found to be consumed in higher amounts in the Control-Prospective group than in the Intervention Bariatric-Prospective group (p<0.05), without the addition of supplements. On the other hand, iron and calcium calculated from diet with supplements, were found to be significantly higher in the Intervention Bariatric Prospective group than in the Control Prospective group. In addition, consumption of saturated fats, oil, and salty snacks was lower in both prospective groups compared to the retrospective group (p<0.05), suggesting better food quality habits for the bariatric group with nutritional counseling. Mean birth weight was significantly lower in the Control Bariatric Retrospective group than in the Control-Prospective group (3074±368g vs. 3396±502g, respectively. p=0.023). In the Intervention Bariatric Prospective group, mean birth weight was 3168±412g, and no significant difference was observed from the Control Prospective group. Birth percentiles were also significantly lower in the Control Bariatric Retrospective group compared to the Control Prospective group (27th vs. 42nd, respectively. p<0.05). In the Intervention Bariatric Prospective group, mean birth percentile was 35th, and no significant difference was observed from the Control Prospective group. As for the weight change of the woman during pregnancy, the highest variability was noted among the Control Bariatric Retrospective group with cases of weight loss up to 37kg, due to conception close to the bariatric operation. Nevertheless, this variable was controlled, and showed no significant impact on birth weight results. Our results suggest that personalized nutritional counseling care during post bariatric pregnancy improved nutrient intake of mothers and may contribute to higher birth weight of offspring. Further research is needed to examine the effects of prenatal nutrition care intervention, in addition to repeating this trial with a larger sample size, to allow for clearer findings. IRB number: 0310-15-RMB. NCT02697981 URL: https://www.nih.gov.

Differential and Synergistic Effects of Low Birth Weight and Western Diet on Skeletal Muscle Vasculature, Mitochondrial Lipid Metabolism and Insulin Signaling in Male Guinea Pigs.

Low birth weight (LBW) offspring are at increased risk for developing insulin resistance, a key precursor in metabolic syndrome and type 2 diabetes mellitus. Altered skeletal muscle vasculature, extracellular matrix, amino acid and mitochondrial lipid metabolism, and insulin signaling are implicated in this pathogenesis. Using uteroplacental insufficiency (UPI) to induce intrauterine growth restriction (IUGR) and LBW in the guinea pig, we investigated the relationship between UPI-induced IUGR/LBW and later life skeletal muscle arteriole density, fibrosis, amino acid and mitochondrial lipid metabolism, markers of insulin signaling and glucose uptake, and how a postnatal high-fat, high-sugar “Western” diet (WD) modulates these changes. Muscle of 145-day-old male LBW glucose-tolerant offspring displayed diminished vessel density and altered acylcarnitine levels. Disrupted muscle insulin signaling despite maintained whole-body glucose homeostasis also occurred in both LBW and WD-fed male “lean” offspring. Additionally, postnatal WD unmasked LBW-induced impairment of mitochondrial lipid metabolism, as reflected by increased acylcarnitine accumulation. This study provides evidence that early markers of skeletal muscle metabolic dysfunction appear to be influenced by the in utero environment and interact with a high-fat/high-sugar postnatal environment to exacerbate altered mitochondrial lipid metabolism, promoting mitochondrial overload.

Maternal pregnancy weight or gestational weight gain and offspring's blood pressure: A systematic review

AimsAn increasing number of studies suggest that maternal weight parameters in pregnancy are associated with offspring's blood pressure (BP). The aim of this systematic review – following the updated Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) Statement – was to assess and judge the evidence for an association between maternal pregnancy weight/body mass index (BMI) or gestational weight gain (GWG) with offspring's BP in later life. Data synthesisMEDLINE, EMBASE, Cochrane Library, CINAHL and Web of Science were searched without limits. Risk of bias was assessed using the “US National Heart, Lung and Blood Institute”-tool, and an evidence grade was allocated following the “World Cancer Research Fund” criteria. Of 7,124 publications retrieved, 16 studies (all cohort studies) were included in the systematic review. Overall data from 52,606 participants (0 years [newborns] to 32 years) were enclosed. Association between maternal pregnancy BMI and offspring's BP were analyzed in 2 (both “good-quality” rated) studies, without consistent results. GWG and offspring's BP was analyzed in 14 studies (2 “good-quality”, 9 “fair-quality”, 3 “poor-quality” rated). Of these, 3 “fair-quality” studies described significant positive results for systolic BP and significant results, but partly with varying directions of effect estimates for diastolic BP. Mean arterial pressure (MAP) was analyzed in 1 “poor-quality” congress paper. Overall, based on the small number of “good-quality”-rated studies and the inconsistency of effect direction, no firm conclusion can be drawn. ConclusionEvidence for an association of maternal pregnancy weight determinants with offspring's BP was overall graded as “limited - no conclusion”.