Perfluorooctanesulfonic acid (PFOS) is a persistent environmental contaminant previously found in consumer surfactants and industrial fire-fighting foams. PFOS has been widely implicated in metabolic dysfunction across the lifespan, including diabetes and obesity. However, the contributions of the embryonic environment to metabolic disease remain uncharacterized. This study seeks to identify perturbations in embryonic metabolism, pancreas development, and adiposity due to developmental and subchronic PFOS exposures and their persistence into later larval and juvenile periods. Zebrafish embryos were exposed to 16 or 32 μM PFOS developmentally (1–5 days post fertilization; dpf) or subchronically (1–15 dpf). Embryonic fatty acid and macronutrient concentrations and expression of peroxisome proliferator-activated receptor (PPAR) isoforms were quantified in embryos. Pancreatic islet morphometry was assessed at 15 and 30 dpf, and adiposity and fish behavior were assessed at 15 dpf. Concentrations of lauric (C12:0) and myristic (C14:0) saturated fatty acids were increased by PFOS at 4 dpf, and PPAR gene expression was reduced. Incidence of aberrant islet morphologies, principal islet areas, and adiposity were increased in 15 dpf larvae and 30 dpf juvenile fish. Together, these data suggest that the embryonic period is a susceptible window of metabolic programming in response to PFOS exposures, and that these early exposures alone can have persisting effects later in the lifecourse.

Polychlorinated biphenyls (PCBs), one type of lipophilic pollutant, are ubiquitous in daily life. PCBs exposure has been implicated in the alterations of gut microbial community which is profoundly associated with diverse metabolic disorders, including obesity. High-fat diet (H) is a dietary pattern characterized by a high percentage of fat. According to the theory that similarities can be easily solvable in each other, PCBs and H exposures are inevitably and objectively coexistent in a real living environment, prompting great concerns about their individual and combined effects on hosts. However, the effects of PCBs-H interactions on gut microbiota and obesity are still incompletely understood. In the present study, the effects of PCBs and/or H on the gut microbiota alteration and obesity risk in mice were examined and the interactions between PCBs and H were investigated. Obtained results showed that PCBs and/or H exposure induced prominent variations in the gut microbiota composition and diversity. Exposure to PCBs also resulted in higher body fat percentage, greater size of abdominal subcutaneous adipocytes and increased expression of proinflammatory cytokines including TNF-α, iNOS and IL-6. Such PCBs-induced changes could be further enhanced upon the co-exposure of H, implying that obese individuals may be vulnerable to PCBs exposure. Taken together, the present study is helpful for a better understanding of the gut microbiota variation influenced by PCBs and/or H exposure, and furthermore, provides a novel insight into the mechanism of PCBs-H interactions on host adiposity.

For most birds, energy efficiency and conservation are paramount to balancing the competing demands of self-maintenance, reproduction, and other demanding life history stages. Yet the ability to maximize energy output for behaviors like predator escape and migration is often also critical. Environmental perturbations that affect energy metabolism may therefore have important consequences for fitness and survival. Methylmercury (MeHg) is a global pollutant that has wide-ranging impacts on physiological systems, but its effects on the metabolism of birds and other vertebrates are poorly understood. We investigated dose-dependent effects of dietary MeHg on the body composition, basal and peak metabolic rates (BMR, PMR), and respiratory quotients (RQ) of zebra finches (Taeniopygia guttata). Dietary exposure levels (0.0, 0.1, or 0.6 ppm wet weight) were intended to reflect a range of mercury concentrations found in invertebrate prey of songbirds in areas contaminated by atmospheric deposition or point-source pollution. We found adiposity increased with MeHg exposure. BMR also increased with exposure while PMR decreased, together resulting in reduced metabolic scope in both MeHg-exposed treatments. There were differences in RQ among treatments that suggested a compromised ability of exposed birds to rapidly metabolize carbohydrates during exercise in a hop-hover wheel. The elevated BMR of exposed birds may have been due to energetic costs of depurating MeHg, whereas the reduced PMR could have been due to reduced oxygen carrying capacity and/or reduced glycolytic capacity. Our results suggest that environmentally relevant mercury exposure is capable of compromising the ability of songbirds to both budget and rapidly exert energy.

Exposure to endocrine disrupting chemicals during the first 1000 days of life may have long-lasting adverse effects on cardio-metabolic risk in later life. This study aimed to examine the associations between maternal prenatal Bisphenol A (BPA) exposure and child cardio-metabolic risk factors at age 2 years in a prospective cohort. During 2012–2013, 218 pregnant women were enrolled at late pregnancy from Shanghai, China. Urinary BPA concentration was measured in prenatal and child 2-year spot urine samples, and classified into high, medium and low tertiles. Child adiposity anthropometric measurements, random morning plasma glucose, serum insulin, and lipids (high-density lipoprotein, low-density lipoprotein, cholesterol, triglyceride), systolic (SBP) and diastolic blood pressure (DBP) were measured. Linear regression was used to evaluate the associations between prenatal BPA and each of the cardio-metabolic risk factors in boys and girls, respectively, adjusting for pertinent prenatal, perinatal and postnatal factors. BPA was detectable (>0.1 μg/L) in 98.2% of mothers prenatally and 99.4% of children at age 2 years. Compared to those with low prenatal BPA, mean SBP was 7.0 (95%CI: 2.9–11.2) mmHg higher, and DBP was 4.4 (95%CI: 1.2–7.5) mmHg higher in girls with high prenatal BPA levels, but these associations were not found in boys. In boys, medium maternal prenatal BPA level was associated with 0.36 (95% CI: 0.04–0.68) mmol/L higher plasma glucose. No associations were found between prenatal BPA and child BMI, skinfold thicknesses, serum lipids, or insulin in either girls or boys. There were no associations between concurrent child urinary BPA and cardio-metabolic risk factors. These results support that BPA exposure during prenatal period, susceptible time for fetal development, may be associated with increase in child BP and plasma glucose in a sex-specific manner. Further independent cohort studies are needed to confirm the findings.

Bisphenol S (BPS) has replaced bisphenol A (BPA), a known non-persistent endocrine disrupting chemical, in several products. Considering that little is known regarding BPS effects, especially during critical windows of ontogenetic development, and that BPA, which is quite similar to BPS, is know to be transferred to the offspring via the placenta and milk, in the present study we investigated the behavioral, biochemical and endocrine profiles of Wistar rats born from dams that were BPS-exposed [groups: BPS10 (10 μg/kg/day), BPS50 (50 μg/kg/day)] during pregnancy and lactation. Due to the non-monotonic dose-response effect of bisphenol, the data of both BPS groups were directly compared with those of the controls, not to each other. Males and females were analyzed separately. At weaning, male BPS50 offspring had hypotriglyceridemia and hyperthyroxinemia, whereas BPS50 females showed higher 25(OH)D levels. At adulthood, BPS offspring of both sexes had lower food intake. BPS males showed lower visceral adiposity. BPS50 females had smaller fat droplets in brown adipocytes. BPS males showed higher anxiety and higher locomotor activity, while BPS10 females showed lower exploration. During a food challenge test at adulthood, BPS males consumed more high-fat diet at 30 min. BPS10 females initially (at 30 min) consumed more high-fat diet but, after 12 h, less of this diet was consumed. BPS50 males had hypertriglyceridemia and lower plasma T3, while BPS females showed lower plasma T4. BPS10 females had lower progesterone, whereas BPS50 females had higher plasma 25(OH)D. Maternal BPS exposure has adverse effects on the triacylglycerol, hormones levels and behavior of the progeny. Furthermore, the increased preference for the fat-enriched diet suggests an increased risk for obesity and its health consequences in the long term.

Traffic noise has attracted much attention as a significant and intractable public health threat. This study was designed as a systematical review to explore the association of traffic noise with different indicators of obesity, thus providing updated quantitative estimates for the pooled effect estimates of the existing literature. We conducted an extensive search for epidemiological studies that investigated the association of traffic noise with obesity in three electronic databases till February 23, 2021. We used random-effects meta-analysis to calculate the summary effect estimates for each 10-dB(A) increase in noise and compared the highest with the lowest category of noise in relation to seven obesity indicators. Meanwhile, we assessed the risk of bias and the overall quality of the evidence of each study as well as the level of evidence for each exposure–outcome pair. The initial search identified 30 studies, 13 of which were ultimately included. The meta-analysis for the highest versus the lowest category of noise exposure was generally associated with higher waist circumfluence (WC) ranging from 0.326 cm (95% confidence interval (CI) = 0.078, 0.574) to 0.705 cm (95% CI = 0.071, 1.340) and higher odds of central obesity ranging from 1.055 (95% CI = 1.000, 1.109) to 1.167 (95% CI = 1.037, 1.298). When the continuous exposure (each 10 dB(A) increase in noise) was introduced, similar results were found. This study indicated positive associations of traffic noise with WC and central obesity. However, in consideration of some limitations, there is an urgent need for future studies to increase the sample size, discriminate the etiological differences in different noise and obesity indicators, and thoroughly consider socioeconomic status.

The effect of caffeine exposure on children’s health remains poorly understood. We aimed to characterize the associations of caffeine and caffeine metabolites with adiposity outcomes among children and adolescents. We performed cross-sectional analyses of 1,447 children and adolescents aged 6–19 years from the 2009–2014 National Health and Nutrition Examination Survey. The linear regression and weighted quantile sum (WQS) regression were used to explore the associations of urinary caffeine and 14 caffeine metabolites with adiposity outcomes, including body mass index (BMI) z-score, waist circumference (WC), obesity, and overweight. In linear regression models, compared with the participants who consumed low caffeine, higher BMI z-score, WC, and risks of obesity and overweight were more likely among those who consumed high caffeine (P < 0.05). In WQS regression models, an interquartile range increase in the weighted caffeine index was significantly associated with increased BMI z-score (β = 0.10, 95% CI = 0.01, 0.17) and WC (β = 1.20, 95% CI = 0.31, 2.09), and risks of obesity (OR = 1.09, 95% CI = 1.02, 1.17). Totally, no modification effect of age or gender was observed in the linear regression model. Nonetheless, in WQS models, the positive associations of caffeine exposure with WC and risks of obesity and overweight were significant in children aged 6–11 years rather than 12–19 years. When stratified by gender, caffeine exposure was significantly associated with BMI z-score and WC in both boys and girls. These results add novel evidence that caffeine exposure might be associated with adverse adiposity outcomes among children and adolescents.

Paraben esters and their salts are widely used as preservatives in cosmetics, personal care products, pharmaceuticals, and foods. We and others have reported that parabens promote adipogenesis in vitro. Here, we investigated the effects of post-weaning exposure to parabens (methylparaben and butylparaben) on body weight, white adipose tissue mass, and obesity associated metabolic biomarkers in female obesity-prone C57BL/6J mice fed with a chow diet or a high fat diet. Methylparaben exposure by daily oral gavage (100 mg/kg/day) increased adiposity and serum leptin levels compared to the controls when fed the chow diet, but not the high fat diet. In contrast, butylparaben exposure did not induce such effects. Exposure to either paraben induced changes in gene expression related to adipocyte differentiation and lipogenesis in the white adipose tissue (WAT) and the liver, regardless of diet. Moreover, exposure to both parabens under the chow diet significantly decreased serum procollagen type 1 N-terminal propeptide (P1NP) but had no effects on C-terminal telopeptide of type I collagen (CTX-I) levels, suggesting that post-weaning exposure to paraben may negatively affect bone formation, but not bone resorption. Taken together, our results demonstrate that post-weaning exposure to paraben, methylparaben in particular, promotes adipogenesis but suppresses serum marker of bone formation in vivo. Our results add to the growing body of literature indicating potential negative health outcomes associated with paraben exposure. Further study of early life exposure to paraben on the development of fat and bone is warranted.