Offspring Adiposity Research Articles

Breastfeeding moderates the association of maternal pre-pregnancy nutritional status with offspring body composition at 30 years.

Maternal pre-pregnancy body mass index is positively associated with offspring obesity, even at adulthood, whereas breastfeeding decreases the risk of obesity. The present study was aimed at assessing whether breastfeeding moderates the association of maternal pre-pregnancy body mass index with offspring body composition at adulthood, using data from 3439 subjects enrolled in a southern Brazilian birth cohort. At 30 years of age, maternal pre-pregnancy body mass index was positively associated with offspring prevalence of obesity, abdominal obesity, as well as body mass index and fat and lean mass index. Breastfeeding moderated the association of maternal pre-pregnancy obesity with offspring adiposity at 30 years of age. For those breastfed<6 months, body mass index was 4.13 kg/m2 (95% confidence interval: 2.98; 5.28) higher among offspring of obese mothers, in relation to offspring of normal weight mothers, whereas among those breastfed≥6 months the magnitude of the difference was small [2.95 kg/m2 (95% confidence interval: 1.17; 4.73)], p-value for interaction = 0.03. Concerning obesity, among those who had been breastfed < 6 months, the prevalence of obesity was 2.56 (95% confidence interval: 1.98; 3.31) times higher among offspring of obese mothers. On the other hand, among those who were breastfed ≥ 6 months, the prevalence of obesity was 1.82 (95% confidence interval: 1.09; 3.04) times higher among offspring of obese mothers. Therefore, among overweight mothers breastfeeding for more than 6 months should be supported, as it may mitigate the consequences of maternal overweight on offspring body composition.

Associations between maternal overweight/obesity during pregnancy and body composition in young adult offspring.

Maternal obesity is associated with an increased risk of large-for-gestational-age births and childhood obesity. However, evidence on its potential associations with long-term offspring body composition remains limited. This prospective cohort study examined associations between maternal body mass index (BMI) during pregnancy and body composition in the young adult offspring. Participants were the offspring from a birth cohort in Chiang Mai (Thailand). Maternal BMI was assessed at the first antenatal clinic visit (≤24 weeks of gestation) in 1989-1990. In 2010-2011, we followed up the offspring at approximately 20 years of age, assessing their body composition using whole-body dual-energy X-ray absorptiometry (DXA) scans. Associations between maternal BMI and offspring body composition were explored using unadjusted and adjusted analyses. We assessed 391 young adults (55% were females). Higher maternal BMI was associated with increased offspring fat mass and lean mass. In adjusted analyses, offspring of mothers with overweight/obesity exhibited total body fat percentages 1.5 (95% CI 0.1, 2.9; p = 0.032) and 2.3 (95% CI 0.2, 4.5; p = 0.036) percentage points higher than offspring of normal-weight and underweight mothers, respectively. Fat mass index was similarly higher: 0.9 kg/m2 (95% CI 0.3, 1.5 kg/m2; p = 0.002) and 1.4 kg/m2 (95% CI 0.5, 2.3 kg/m2; p = 0.002), respectively. However, no differences in visceral adiposity were detected. Higher maternal BMI during pregnancy was associated with increased adiposity in young adult offspring. Our findings suggest that the cross-generational transmission of maternal obesity-related traits is associated with increased offspring adiposity in the long term.

Perinatal exposures and adolescence overweight: The role of shared maternal-offspring pathways

Background and aimsEarly life exposures affect offspring health across the life-course. We aimed to examine whether prevalent perinatal exposures and obstetric complications are independently associated with offspring overweight in adolescence. We then assessed whether shared maternal-offspring pathways drive the association of perinatal exposures with offspring overweight. MethodsUsing data from the Jerusalem Perinatal Study birth cohort, two perinatal scores were constructed: obstetric complications (OC) and prevalent perinatal exposures (PPE) scores. PPE score, generated by principal component analysis, included three primary components. Logistic regressions were used to assess associations of scores with offspring overweight, with and without adjustment for maternal life-course survival. ResultsOC and PPE scores were independently associated with offspring overweight (OROC = 1.15, 95%CI:1.07,1.25; ORPPE1- SEP and lifestyle = 0.85, 95%CI:0.79,0.91; ORPPE2- Maternal body size = 1.20, 95%CI: 1.13,1.28; ORPPE3-Fetal growth = 1.18, 95%CI:1.11,1.26). Maternal survival was associated with offspring overweight (OR = 1.38, 95%CI:1.08,1.76), yet introducing PPE score to the same model attenuated this association (OR = 1.16, 95%CI:0.90, 1.49). When OC score and maternal survival were included in the same model, their associations with offspring overweight remained unchanged. ConclusionsMother-offspring shared factors, captured by maternal life-course survival, underlie the effect of prevalent perinatal exposures on offspring overweight. However, the effect of obstetric complications was independent, highlighting the contribution of additional pathways.

Maternal gestational diabetes and childhood adiposity risk from 6 to 8 years of age.

Previous studies found conflicting results on the association between maternal gestational diabetes mellitus (GDM) and childhood overweight/obesity. This study was to assess the association between maternal GDM and offspring's adiposity risk from 6 to 8 years of age. The present study longitudinally followed 1156 mother-child pairs (578 GDM and 578 non-GDM) at 5.9 ± 1.2 years postpartum and retained 912 mother-child pairs (486 GDM and 426 non-GDM) at 8.3 ± 1.6 years postpartum. Childhood body mass index (BMI), waist circumference, body fat and skinfold were measured using standardized methods. Compared with the counterparts born to mothers with normal glucose during pregnancy, children born to mothers with GDM during pregnancy had higher mean values of adiposity indicators (waist circumference, body fat, subscapular skinfold and suprailiac skinfold) at 5.9 and 8.3 years of age. There was a positive association of maternal GDM with changes of childhood adiposity indicators from the 5.9-year to 8.3-year visit, and β values were significantly larger than zero: +0.10 (95% CI: 0.02-0.18) for z score of BMI for age, +1.46 (95% CI: 0.70-2.22) cm for waist circumference, +1.78% (95% CI: 1.16%-2.40%) for body fat, +2.40 (95% CI: 1.78-3.01) mm for triceps skinfold, +1.59 (95% CI: 1.10-2.09) mm for subscapular skinfold, and +2.03 (95% CI: 1.35-2.71) mm for suprailiac skinfold, respectively. Maternal GDM was associated with higher risks of childhood overweight/obesity, central obesity, and high body fat (Odd ratios 1.41-1.57 at 5.9 years of age and 1.73-2.03 at 8.3 years of age) compared with the children of mothers without GDM. Maternal GDM was a risk factor of childhood overweight/obesity at both 5.9 and 8.3 years of age, which was independent from several important confounders including maternal pre-pregnancy BMI, gestational weight gain, children's birth weight and lifestyle factors. This significant and positive association became stronger with age.

Associations of Prenatal Per- and Polyfluoroalkyl Substance (PFAS) Exposures with Offspring Adiposity and Body Composition at 16-20 Years of Age: Project Viva.

Findings on the associations between prenatal PFAS exposures and offspring adiposity are inconsistent. Whether such associations may extend to adolescence is especially understudied. We investigated associations of prenatal PFAS exposures with offspring adiposity and body composition at 16-20 years of age. We studied 545 mother-child pairs in the prospective prebirth cohort Project Viva (Boston, Massachusetts). We measured six PFAS (PFOA, PFOS, PFNA, PFHxS, EtFOSAA, and MeFOSAA) in maternal early pregnancy (, range: 5.7-19.6 wk) plasma samples. At the late adolescence visit ( y, range: 15.9-20.0 y), we obtained anthropometric measures and assessed body composition using bioelectrical impedance analysis and dual-energy X-ray absorptiometry. We examined associations of individual PFAS with obesity [i.e., age- and sex-specific body mass index (BMI) percentile] and adiposity and body composition using multivariable Poisson and linear regression models, respectively. We assessed PFAS mixture effects using Bayesian kernel machine regression (BKMR) and quantile g-computation. We used fractional-polynomial models to assess BMI trajectories (at 3-20 years of age) by prenatal PFAS levels. Thirteen percent () of the children had obesity in late adolescence. After multivariable adjustment, higher prenatal PFAS concentrations were associated with higher obesity risk [e.g., 1.59 (95% CI: 1.19, 2.12), 1.24 (95% CI: 0.98, 1.57), and 1.49 (95% CI: 1.11, 1.99) times the obesity risk per doubling of PFOS, PFOA, and PFNA, respectively]. BKMR showed an interaction between PFOA and PFOS, where the positive association between PFOS and obesity was stronger when PFOA levels were lower. Each quartile increment of the PFAS mixture was associated with 1.52 (95% CI: 1.03, 2.25) times the obesity risk and 0.52 (95% CI: , 1.06) higher BMI. Children with higher prenatal PFOS, EtFOSAA, and MeFOSAA concentrations had higher rates of BMI increase starting from 9-11 years of age. Prenatal PFAS exposures may have obesogenic effects into late adolescence. https://doi.org/10.1289/EHP12597.

Thermoneutral Housing Enables Studies of Vertical Transmission of Obesogenic Diet-Driven Metabolic Diseases

Vertical transmission of obesity is a critical contributor to the unabated obesity pandemic and the associated surge in metabolic diseases. Existing experimental models insufficiently recapitulate “human-like” obesity phenotypes, limiting the discovery of how severe obesity in pregnancy instructs vertical transmission of obesity. Here, via utility of thermoneutral housing and obesogenic diet feeding coupled to syngeneic mating of WT obese female and lean male mice on a C57BL/6 background, we present a tractable, more “human-like” approach to specifically investigate how maternal obesity contributes to offspring health. Using this model, we found that maternal obesity decreased neonatal survival, increased offspring adiposity, and accelerated offspring predisposition to obesity and metabolic disease. We also show that severe maternal obesity was sufficient to skew offspring microbiome and create a proinflammatory gestational environment that correlated with inflammatory changes in the offspring in utero and adulthood. Analysis of a human birth cohort study of mothers with and without obesity and their infants was consistent with mouse study findings of maternal inflammation and offspring weight gain propensity. Together, our results show that dietary induction of obesity in female mice coupled to thermoneutral housing can be used for future mechanistic interrogations of obesity and metabolic disease in pregnancy and vertical transmission of pathogenic traits.

Impact of maternal cardiometabolic status after bariatric surgery on the association between telomere length and adiposity in offspring

The impact of bariatric surgery on metabolic and inflammatory status are reflected in the epigenetic profile and telomere length mediated by the changes in the metabolic status of the patients. This study compared the telomere length of children born before versus after maternal bariatric surgery as a surrogate to test the influence of the mother’s metabolic status on children’s telomere length. DNA methylation telomere length (DNAmTL) was estimated from Methylation-EPIC BeadChip array data from a total of 24 children born before and after maternal bariatric surgery in the greater Quebec City area. DNAmTL was inversely associated with chronological age in children (r = − 0.80, p < 0.001) and significant differences were observed on age-adjusted DNAmTL between children born before versus after the maternal bariatric surgery. The associations found between body mass index and body fat percentage with DNAmTL in children born after the surgery were influenced by maternal triglycerides, TG/HDL-C ratio and TyG index. This study reports the impact of maternal bariatric surgery on offspring telomere length. The influence of maternal metabolic status on the association between telomere length and markers of adiposity in children suggests a putative modulating effect of bariatric surgery on the cardiometabolic risk in offspring.

Neurodevelopmental Programming of Adiposity: Contributions to Obesity Risk.

This review analyzes the published evidence regarding maternal factors that influence the developmental programming of long-term adiposity in humans and animals via the central nervous system (CNS). We describe the physiological outcomes of perinatal underfeeding and overfeeding and explore potential mechanisms that may mediate the impact of such exposures on the development of feeding circuits within the CNS-including the influences of metabolic hormones and epigenetic changes. The perinatal environment, reflective of maternal nutritional status, contributes to the programming of offspring adiposity. The in utero and early postnatal periods represent critically sensitive developmental windows during which the hormonal and metabolic milieu affects the maturation of the hypothalamus. Maternal hyperglycemia is associated with increased transfer of glucose to the fetus driving fetal hyperinsulinemia. Elevated fetal insulin causes increased adiposity and consequently higher fetal circulating leptin concentration. Mechanistic studies in animal models indicate important roles of leptin and insulin in central and peripheral programming of adiposity, and suggest that optimal concentrations of these hormones are critical during early life. Additionally, the environmental milieu during development may be conveyed to progeny through epigenetic marks and these can potentially be vertically transmitted to subsequent generations. Thus, nutritional and metabolic/endocrine signals during perinatal development can have lifelong (and possibly multigenerational) impacts on offspring body weight regulation.

Associations of cord plasma per- and polyfluoroakyl substances (PFAS) with neonatal and child body composition and adiposity: The GUSTO study

BackgroundThe influence of prenatal exposure to per- and poly- fluoroalkyl substances (PFAS) on birth size and offspring adiposity is unclear, especially for the newer, shorter-chained replacement PFAS. MethodsIn the GUSTO multi-ethnic Singaporean mother-offspring cohort, 12 PFAS were measured in 783 cord plasma samples using ultra-performance-liquid chromatography-tandem-mass-spectrometer (UPLC-MS/MS). Outcomes included offspring anthropometry, other indicators of body composition/metabolic health, and MRI-derived abdominal adiposity (subset) at birth and 6 years of age. PFAS were modeled individually, in categories of long-chain and short-chain PFAS, and as scores of three principal components (PC) derived using PC analysis (PC1, PC2, and PC3 reflect predominant exposure patterns to “very-long-PFAS”, “long-PFAS”, and “short-PFAS”, respectively). Associations with outcomes were assessed using multivariable linear regressions, adjusted for important covariates such as maternal sociodemographic and lifestyle factors. ResultsOverall, cord PFAS levels showed either no or positive associations (mostly for long-chain PFAS) with birth weight, length and head circumference. In general, PFAS were associated with higher neonatal abdominal adiposity, driven by shorter-chain PFAS. Perfluoroheptanoic acid (PFHpA) was associated with higher volumes of superficial subcutaneous adipose tissue (sSAT) (3.75 [1.13, 6.37] mL per SD increase in PFAS) and internal adipose tissue (IAT) (1.39 [0.41, 2.38] mL). Higher levels of perfluorobutanesulfonic acid (PFBS), short-chain PFAS, and PC3 were associated with higher IAT volume (β range 1.22–1.41 mL/SD, all P < 0.02), especially in girls. Higher PC3 score was additionally associated with higher sSAT (3.12 [0.45, 5.80] mL) volume. At age 6 years, most observed associations did not persist. No consistent associations were observed between PFAS and whole-body adiposity measures. ConclusionsFetal exposure to emerging short-chain PFAS was associated with higher abdominal adiposity at birth but not at age 6 years. Further research is needed to replicate the findings and to determine if these effects may reappear beyond early childhood. Population exposure to newer PFAS and consequent health impact must be monitored.

Sex-Specific Effects of a Maternal Obesogenic Diet High in Fat and Sugar on Offspring Adiposity, Growth, and Behavior.

With rising rates of human obesity, this study aimed to determine the relationship between maternal diet-induced obesity, offspring morphometrics, and behavior in mice. Pregnant and lactating female mice fed a diet high in fat and sugar (HFHS) commonly consumed by human populations showed decreased food, calorie, and protein intake but increased adiposity at the expense of lean mass. The pre-weaning body weight of the HFHS offspring was reduced for the first postnatal week but not thereafter, with HFHS female offspring having higher body weights by weaning due to continuing higher fractional growth rates. Post-weaning, there were minor differences in offspring food and protein intake. Maternal diet, however, affected fractional growth rate and total body fat content of male but not female HFHS offspring. The maternal diet did not affect the offspring's locomotor activity or social behavior in either sex. Both the male and female HFHS offspring displayed reduced anxiety-related behaviors, with sex differences in particular aspects of the elevated plus maze task. In the novel object recognition task, performance was impaired in the male but not female HFHS offspring. Collectively, the findings demonstrate that maternal obesity alters the growth, adiposity, and behavior of male and female offspring, with sex-specific differences.

The effectiveness of resveratrol in the management of childhood obesity

Our review is focused on examining whether or not resveratrol is effective in managing and treating childhood obesity based on its beneficial health effects, while also discussing the progress made in developing functional food products containing resveratrol. Resveratrol is a natural phenolic compound found in the Veratrum grandiflorum and is known for its antioxidant properties. Resveratrol can be found in various foods like berries, grapes, pistachios, dark chocolate, peanut skins, soybeans, and pomegranates. Studies evaluating the effectiveness of resveratrol in the management and treatment of childhood obesity have been conducted both in animals and humans. Through numerous mechanisms, such as activation of AMPK, increasing lipolysis, decreasing leptin levels and leptin/soluble leptin receptor (sOB-R) ratio, managing embryonic oxidative stress biomarkers, and reducing body weight and adiposity in offspring, resveratrol has been shown to be effective in ameliorating symptoms of obesity. Thus far, researchers have established both a goal to be accomplished (treatment and management of childhood obesity) and a bioactive compound (resveratrol) to accomplish that goal, as well as appropriate dosages and times of consumption for preclinical trials, mechanisms of action, and relevant biomarkers of resveratrol. These findings have been used to conduct various preclinical trials to test the efficacy and safety of resveratrol both in vivo and on animals. To our knowledge, the following steps have not yet been completed and are required for future research; 1) clinical trials involving resveratrol supplementation to establish safety, appropriate dosage, and time of consumption in humans, 2) creation of a specialized label for resveratrol functional food products, 3) publications submitted to open access, peer-reviewed journals, 4) approval by a reliable governmental agency, 5) official establishment of the product, and 6) epidemiological studies and after-market research conducted following release of the functional food product to the general public.Keywords: Resveratrol, Obesity, Childhood, Maternal, Cardiovascular, Diabetes, Inflammation.Graphical Abstract: Effects of resveratrol on managing childhood obesity

Cord blood DNA methylation of immune and lipid metabolism genes is associated with maternal triglycerides and child adiposity.

Fetal exposures may impact offspring epigenetic signatures and adiposity. The authors hypothesized that maternal metabolic traits associate with cord blood DNA methylation, which, in turn, associates with child adiposity. Fasting serum was obtained in 588 pregnant women (27-34 weeks' gestation), and insulin, glucose, high-density lipoprotein cholesterol, triglycerides, and free fatty acids were measured. Cord blood DNA methylation and child adiposity were measured at birth, 4-6 months, and 4-6 years. The association of maternal metabolic traits with DNA methylation (429,246 CpGs) for differentially methylated probes (DMPs) and regions (DMRs) was tested. The association of the first principal component of each DMR with child adiposity was tested, and mediation analysis was performed. Maternal triglycerides were associated with the most DMPs and DMRs of all traits tested (261 and 198, respectively, false discovery rate < 0.05). DMRs were near genes involved in immune function and lipid metabolism. Triglyceride-associated CpGs were associated with child adiposity at 4-6 months (32 CpGs) and 4-6 years (2 CpGs). One, near CD226, was observed at both timepoints, mediating 10% and 22% of the relationship between maternal triglycerides and child adiposity at 4-6 months and 4-6 years, respectively. DNA methylation may play a role in the association of maternal triglycerides and child adiposity.

Determinants of Gestational Weight Gain and Its Impact on Offspring Adiposity at Age 2 Years

Determinants of Gestational Weight Gain and Its Impact on Offspring Adiposity at Age 2 Years

Growth and adiposity in newborns study (GAINS): The influence of prenatal DHA supplementation protocol

BackgroundObesity and central fat mass (FM) accrual drive disease development and are related to greater morbidity and mortality. Excessive gestational weight gain (GWG) increases fetal fat accretion resulting in greater offspring FM across the lifespan. Studies associate greater maternal docosahexaenoic acid (DHA) levels with lower offspring FM and lower visceral adipose tissue during childhood, however, most U.S. pregnant women do not consume an adequate amount of DHA. We will determine if prenatal DHA supplementation is protective for body composition changes during infancy and toddlerhood in offspring exposed to excessive GWG. Methods and designInfants born to women who participated in the Assessment of DHA on Reducing Early Preterm Birth randomized controlled trial (ADORE; NCT 02626299) will be invited to participate. Women were randomized to either a high 1000 mg or low 200 mg daily prenatal DHA supplement starting in the first trimester of pregnancy. Offspring body composition and adipose tissue distribution will be measured at 2 weeks, 6 months, 12 months, and 24 months using dual energy x-ray absorptiometry. Maternal GWG will be categorized as excessive or not excessive based on clinical guidelines. DiscussionEffective strategies to prevent obesity development are lacking. Exposures during the prenatal period are important in the establishment of the offspring phenotype. However, it is largely unknown which exposures can be successfully targeted to have a meaningful impact. This study will determine if prenatal DHA supplementation modifies the relationship between maternal weight gain and offspring FM and FM distribution at 24 months of age. Ethics and disseminationThe University of Kansas Medical Center Institutional Review Board (IRB) approved the study protocol (STUDY00140895). The results of the trial will be disseminated at conferences and in peer reviewed publications.Trial registration: ClinicalTrials.gov ID: NCT03310983

OR12-02-23 Offspring DNA Methylation of Metabolic Genes at Birth Associates With Maternal Folate and Choline Intake and Offspring Adiposity in Infancy and Childhood

OR12-02-23 Offspring DNA Methylation of Metabolic Genes at Birth Associates With Maternal Folate and Choline Intake and Offspring Adiposity in Infancy and Childhood

Maternal weight and its association with risk of overweight in offspring: a trajectory analysis from a birth cohort in China.

Most studies on the association of maternal pregnancy weight with offspring weight trajectory have a short follow-up time. This study aimed to explore the associations of maternal prepregnancy body mass index (BMI) and gestational weight gain (GWG) with childhood weight trajectories in a 7-year birth cohort. A total of 946 mother-child pairs (467 boys and 479 girls) from a longitudinal birth cohort in TianjinCity, China, were included in this study, ranging from pregnancy to offspring at 7years. The outcome variable was defined as overweight or not overweight in offspring at the last round. A group-based trajectory model was applied to identify childhood BMI trajectory groups. Five discrete BMI trajectory groups were identified and characterized as constant underweight (25.2%), constant normal weight (42.8%), and high or increasing trajectory [at risk of overweight (16.9%), progressive overweight (11.0%) and progressive obesity (4.1%)]. Maternal prepregnancy overweight was associated with 1.72 (95% CI 1.14-2.60, P = 0.01) to 4.02 (95% CI 1.94-8.36, P < 0.001) times the risk of all high or increasing trajectory groups, and excessive GWG was related to groups at risk of overweight [relative risk ratio (RRR) 2.09, 95% CI 1.27-3.46, P = 0.004] and progressive obesity (RRR 3.33, 95% CI 1.13-9.79, P = 0.029). Children in all high or increasing trajectory groups were associated with greater overweight risk at the last round [risk ratios (RRs) ranged from 3.54 (95% CI 2.53-4.95, P < 0.001) to 6.18 (95% CI 4.05-9.42, P < 0.001)]. Maternal prepregnancy overweight and excessive gestational weight gain were associated with increasing or high-level childhood body mass index trajectories as well as a greater risk of overweight at 7 years.

Maternal Pre-Pregnancy BMI, Offspring Adiposity in Late Childhood, and Age of Weaning: A Causal Mediation Analysis.

Infant feeding practices have been hypothesized to influence offspring's body mass index (BMI) later in life, and women with overweight or obesity tend to wean their infants earlier than women with healthy BMI. We, therefore, aimed to investigate how much early age of weaning mediated the maternal-offspring adiposity relationship. The study included 4920 mother-child pairs from the Avon Longitudinal Study of Parents and Children birth cohort. G-computation was applied to estimate the natural direct (NDE) and indirect (NIE) effects, via the age of weaning (<3 months, 3 months, >3 months), of maternal pre-pregnancy overweight or obesity on offspring's BMI and fat mass index. The NDE of maternal overweight or obesity on offspring BMI at 17 years old was 2.63 kg/m2 (95% CI: 2.27 to 2.99). The NIE via the age of weaning was 0.02 kg/m2 (95% CI: 0.00 to 0.04), corresponding to 0.8% of the total effect. Similar results were observed for the offspring's fat mass index. The NDE and NIE were similar to the main analyses when we looked at the relationship stratified by breastfeeding status. Our study found a minimal influence of age of weaning on the pathway between maternal and offspring adiposity, indicating the age of weaning may not be a key mediator.

Effects of different maternal diets on adipose tissue inflammation and liver tissue oxidative stress in dams and their female offspring.

Pregnancy and lactation are important stages of fetal development. Therefore, this study investigated how different maternal diets offered during gestation and lactation periods affect adipose tissue inflammation and liver tissue oxidative stress of dams and their female offspring. Female BALB/c albino mice (60days old) were randomized into three groups receiving a standard (CONT), hypercaloric (HD), or restricted (RD) diet during the pregnancy. After birth, female offspring weaned at 21days were divided into two groups that received a standard or restricted diet (CONT/CONT, CONT/RD, RD/CONT, RD/RD, HD/CONT, and HD/RD) until 100days old. Histological, oxidative parameters and inflammatory infiltrate of dams' and offspring's liver and adipose tissue were evaluated. HD dams presented non-alcoholic steatohepatitis (NASH) diagnosis and an increase in tumor necrosis factor-alpha (TNF-α) concentrations when compared to the RD and CONT dams, indicating a pro-inflammatory state. High concentrations of malondialdehyde (MDA) formation and catalase (CAT) activity in HD when compared to the CONT in the liver. SOD activity decreased in RD mice compared to CONT, and the SOD/CAT ratio was decreased in the RD and HD in comparison to the CONT. The maternal diet leads to an increase in SOD in RD/RD compared to HD/RD. RD-fed dams showed an increase in inflammatory infiltrates compared to CONT, evidencing changes caused by a restrictive diet. In the HD/CONT offspring, we verified an increase in inflammatory infiltrates in relation to the offspring fed a standard diet. In conclusion, HD, and RD, during pregnancy and lactation, altered the liver and adipose tissues of mothers. Furthermore, the maternal diet negatively impacts the offspring's adipose tissue but does not cause liver damage in these animals in adult life.

The Effects of a Western Diet vs. a High-Fiber Unprocessed Diet on Health Outcomes in Mice Offspring.

Diet influences critical periods of growth, including gestation and early development. We hypothesized that a maternal/early life diet reflecting unprocessed dietary components would positively affect offspring metabolic and anthropometric parameters. Using 9 C57BL-6 dams, we simulated exposure to a Western diet, a high-fiber unprocessed diet (HFUD), or a control diet. The dams consumed their respective diets (Western [n = 3], HFUD [n = 3], and control [n = 3]) through 3 weeks of pregnancy and 3 weeks of weaning; their offspring consumed the diet of their mother for 4.5 weeks post weaning. Measurements included dual X-ray absorptiometry (DEXA) scans, feed consumption, body weight, blood glucose, and insulin and glycated hemoglobin (HbA1c) in the offspring. Statistical analyses included one-way ANOVA with Tukey's post hoc analysis. The offspring DEXA measures at 5 and 7.5 weeks post parturition revealed higher lean body mass development in the HFUD and control diet offspring compared to the Western diet offspring. An analysis indicated that blood glucose (p = 0.001) and HbA1c concentrations (p = 0.002) were lower among the HFUD offspring compared to the Western and control offspring. The results demonstrate that diet during gestation and early life consistent with traditional diet patterns may influence hyperglycemia and adiposity in offspring.

1185-P: Maternal Exposure to Per- and Polyfluoroalkyl Substances and Risk of Adiposity in Offspring at Birth and Early Childhood—A Longitudinal Birth Cohort Study

Introduction: Per- and polyfluoroalkyl substances (FPAS) are a class of man-made chemicals that cross the placenta. We examined the associations of maternal exposure to PFAS mixture with risk of adiposity in offspring at birth and childhood. Methods: In the perspective Hyperglycaemia-and-Adverse-Pregnancy-Outcome (HAPO) study, we measured serum concentrations of six PFAS biomarkers using high-performance LC-MS-MS in 1601 mothers who had joined the Hong Kong centre in 2002-2004 and 922 children at seven years old. We estimated PFAS burden score for each mother and child using concentrations of individual PFAS and exposure patterns of PFAS mixture. Adiposity in the offspring was defined by the ponderal-index (PI) at birth and sum-of-skinfold-thickness in mm at birth and childhood. We used linear regression to estimate associations of maternal exposure to PFAS mixture with adiposity risk. Results: PFAS burden score in pregnancy was positively associated with PI (β=0.50, 95% CI: 0.02, 0.97) and negatively associated with skinfold thickness (β=-0.61, 95% CI: -0.96, -0.27) in offspring at birth. The correlation of PFAS burden score in mothers and children at seven years old was weak (r=0.07). After adjusting for PFAS burden score of childhood, maternal PFAS burden score was negatively associated with skinfold-thickness in childhood (β=-2.29, 95% CI: -3.97, -0.62). Sex-specific analyses showed similar associations with PI in boys and girls at birth. In contrast, significant negative associations with skinfold thickness were observed in girls but not in boys at childhood. Conclusions: Maternal exposure to PFAS mixture is independently associated with risk of adiposity in offspring at birth. Its effect on childhood adiposity was apparent only in girls, not boys. Disclosure A.Yang: None. C.H.Tam: None. R.Ozaki: None. W.L.Lowe: None. B.E.Metzger: None. W.H.Tam: None. C.K.Wong: None. R.C.Ma: Advisory Panel; AstraZeneca, Merck &amp; Co., Inc., Other Relationship; Bayer Inc., Boehringer-Ingelheim, Research Support; Tricida, Inc., Roche Diagnostics, Novo Nordisk. Funding Health and Medical Research Fund (13140761); Eunice Kennedy Shriver National Institute of Child Health and Human Development/National Institute of Diabetes and Digestive and Kidney Diseases (R01HD34242, R01HD34243); Research Grants Council of Hong Kong (473408, 471713)