Sea fish contain omega-3 polyunsaturated fatty acids (omega-3 PUFAs) which have been found to reduce triglyceride (TG) levels. However, sea fish may contain pollutants such as mercury which cause oxidative stress and increase TG levels. Therefore, the relationship between sea fish and TG remains unclear. We aimed to explore whether blood mercury (BHg) can affect the effect of sea fish consumption frequency on TG level among Chinese adults. A total of 10,780 participants were included in this study. BHg levels were measured using inductively coupled plasma mass spectrometry (ICP-MS). The associations of sea fish consumption frequency with BHg and TG levels as well as the association of BHg with TG levels were evaluated using multiple linear regression. Causal mediation analysis was used to evaluate the mediation effect of BHg levels on the association of sea fish consumption frequency with TG levels. The frequency of sea fish consumption showed a negative association with TG level. Compared with the participants who never ate sea fish, the TG level decreased by 0.193 mmol/L in those who ate sea fish once a week or more [β (95%CI): −0.193 (−0.370, −0.015)]. Significant positive associations were observed of BHg with TG levels. With one unit increase of log2-transformed BHg, the change of TG level was 0.030 mmol/L [0.030 (0.009, 0.051)]. The association between sea fish consumption and TG was mediated by log2-transformed BHg [total effect = −0.037 (−0.074, −0.001); indirect effect = 0.009 (0.004, 0.015)], and the proportion mediated by log2-transformed BHg was 24.25%. BHg may reduce the beneficial effect of sea fish consumption frequency on TG levels among Chinese adults. Overall, sea fish consumption has more benefits than harms to TG.

Bisphenol A (BPA) is a representative endocrine disrupting compound used in a vast array of consumer products, and are being frequently substituted by its analogues, bisphenol S (BPS) and bisphenol F (BPF). We aimed to examine the association between urinary bisphenol levels with obesity and lipid profiles in the general population to comprehensively evaluate its potential of metabolic disturbance. A representative sample of 1046 US adults from the National Health and Nutrition Examination Survey (2013–2016) and 3268 Korean adults from the Korean National Environmental Health Survey (2015–2017) was analyzed. We examined the exposure levels of bisphenols and determined their associations with obesity, high-density lipoprotein cholesterol (HDL-C) and triglyceride (TG) levels, and hypercholesterolemia prevalence through multiple linear, and binary/ordinal logistic regression models. In both populations, high BPA levels (lowest tertile vs. 2nd, 3rd tertiles) showed corresponding associations with lipid profile and obesity. BPA levels were associated with decreased HDL-C levels (Q3: β = −0.053, p = 0.08 (US); Q2: β = −0.030, p-0.03), increased TG levels (Q3: β = 0.121, p = 0.029 (US); Q3: β = 0.089, p = 0.021, and higher odds for obesity (Q3: OR = 1.58, 95% CI: 1.06, 2.35 (US); Q3: OR = 1.41, 95% CI: 1.11, 1.78). Higher BPS levels were positively associated with obesity status, especially in US men (Q2: OR = 1.84, 95% CI: 1.15, 2.96) and Korean women (Q3: OR = 1.27, 95% CI: 0.99, 1.64). A significant decrease in HDL-C (Q3: β = −0.088, p = 0.01) and elevated odds for obesity at higher BPF levels (Q3: OR = 1.60, 95% CI: 1.00, 2.56) was observed in US women. The findings of our study indicate that BPA and its analogues, BPS and BPF, are associated with lipid metabolism disorders in addition to obesity in adults. Given the increase in exposure to BPA alternatives, continuous biomonitoring, and further investigation of their health effects through prospective cohort studies are warranted.

Environmental obesogens contributed significantly to the obesity prevalence. Recently, antibiotics joined the list of environmental obesogens, while the underlying mechanisms remained to be explored. In the present study, effects of erythromycin (ERY), one widely used macrolide antibiotic, were measured on C. elegans to investigate the obesogenic mechanism. Results showed that ERY at 0.1 μg/L significantly increased the fat content by 17.4% more than the control and also stimulated triacylglycerol (TAG) levels by 25.7% more than the control. Regarding the obesogenic mechanisms, ERY provoked over-eating by stimulation on the pharyngeal pumping and reduction on the satiety quiescence percentage and duration. Such effects were resulted from stimulation on the neurotransmitters including serotonin (5-HT), dopamine (DA) and acetylcholine (ACh). The nervous responses involved the up-regulation of Gsα (e.g., ser-7, gsa-1, acy-1 and kin-2) signaling pathway and the down-regulation of TGFβ (daf-7) but not via cGMP-dependent regulations (e.g., egl-4). Moreover, ERY stimulated the activities of fatty acid synthase (FAS) and glycerol-3-phosphateacyl transferases (GPAT) that catalyze lipogenesis, while ERY inhibited those of acyl-CoA synthetase (ACS), carnitine palmitoyl transferase (CPT) and acyl-CoA oxidase (ACO) that catalyze lipolysis. The unbalance between lipogenesis and lipolysis resulted in the fat accumulation which was consistent with up-regulation on mgl-1 and mgl-3 which are the down-steam of TGFβ regulation. Such consistence supported the close connection between nervous regulation and lipid metabolism. In addition, ERY also disturbed insulin which connects lipid with glucose in metabolism.

DEHP is commonly found in the environment, biota, food, and humans, raising significant health concerns. Whether developmental stage and exposure duration modify the obesogenic effects of DEHP is unclear, especially the underlying mechanisms by which chronic exposure to DEHP as well as its metabolites remain largely unknown. This study investigated the obesogenic effects of chronic DEHP exposure, with levels below environmentally-relevant amounts and provide the mechanism in Caenorhabditis elegans. We show that early-life DEHP exposure resulted in an increased lipid and triglyceride (TG) accumulation mainly attributed to DEHP itself, not its metabolite mono-2-ethylhexyl phthalate (MEHP). In addition, developmental stage and exposure timing influence DEHP-induced TG accumulation and chronic DEHP exposure resulted in the most significant effect. Analysis of fatty acid composition shows that chronic DEHP exposure altered fatty acid composition and TG, resulting in an increased ω-6/ω-3 ratio. The increased TG content by chronic DEHP exposure required lipogenic genes fat-6, fat-7, pod-2, fasn-1, and sbp-1. Moreover, chronic DEHP exposure induced XBP-1-mediated endoplasmic reticulum (ER) stress which might lead to up-regulation of sbp-1. This study suggests the possible involvement of ER stress and SBP-1/SREBP-mediated lipogenesis in chronic DEHP-induced obesogenic effects. Results from this study implies that chronic exposure to DEHP disrupts lipid metabolism, which is likely conserved across species due to evolutionary conservation of molecular mechanisms, raising concerns in ecological and human health.

Various microplastics (MPs) are found in the environment and organisms. MP residues in organisms can affect health; however, their impacts on metabolism in aquatic organisms remain unclear. In this study, zebrafish embryos were exposed to polyethylene MPs with sizes ranging from 1 to 4 μm at concentrations of 0, 10, 100, and 1000 μg/L for 7 days. Through qPCR technology, the results indicated that zebrafish exposed to polyethylene MPs exhibited significant change in microbes of the phyla Firmicutes, Bacteroidetes, Proteobacteria, and Verrucomicrobia, etc. Moreover, 16S RNA gene sequencing revealed that there was a significant difference in alpha diversity between the control and 1000 μg/L MP-treated groups. At the genus level, the abundance of Aeromonas, Shewanella, Microbacterium, Nevskia and Methyloversatilis have increased remarkably. Conversely, the abundance of Pseudomonas, Ralstonia and Stenotrophomonas were significant reduction after MPs exposure. In addition, the levels of TG (triglyceride), TCHO (total cholesterol), NEFA (nonesterified fatty acid), TBA (total bile acid), GLU (glucose) and pyruvic acid significantly changed in MP-treated larval zebrafish, indicating that their metabolism was disturbed by MPs. Transcriptional levels of glucose and lipid metabolism-related genes showed a decreasing trend. Furthermore, LC/MS-based nontargeted metabolomics analysis demonstrated that a total of 59 phospholipid-related substances exhibited significant changes in larval fish treated with 1000 μg/L MPs. The mRNA levels of phospholipid metabolism-related genes were also obviously changed. Pearson correlation analysis indicated that the abundance of Aeromonas, Shewanella and Chitinibacter bacteria showed a negative correlation with most phospholipids, while Nevskia, Parvibacter and Lysobacter showed a positive correlation with most phospholipids. Based on these results, it is suggested that 1–4 μm PE-MPs could impact the microbiome and metabolism of larval zebrafish. All of these results indicated that the health risk of MPs cannot be ignored.

Bisphenol S is an endocrine disruptor exhibiting metabolic disturbances, especially following perinatal exposures. To date, no data are available on the obesogen effects of BPS in a mutligenerational issue.We investigated obesogen effects of BPS in a multigenerational study by focusing on body weight, adipose tissue and plasma parameters in male and female mice.Pregnant C57BL6/J mice were exposed to BPS (1.5 μg/kg bw/day ie a human equivalent dose of 0.12 μg/kg bw/day) by drinking water from gestational day 0 to post natal day 21. All offsprings were fed with a high fat diet during 15 weeks. Body weight was monitored weekly and fat mass was measured before euthanasia. At euthanasia, blood glucose, insuline, triglyceride, cholesterol and no esterified fatty acid plasma levels were determined and gene expressions in visceral adipose tissue were assessed. F1 males and females were mated to obtain the F2 generation. Likewise, the F2 mice were cross-bred to obtain F3. The same analyses were performed.In F1 BPS induced an overweight in male mice associated to lipolysis gene expressions upregulation. In F1 females, dyslipidemia was observed. In F2, BPS exposure was associated to an increase in body weight, fat and VAT masses in males and females. Several plasma parameters were increased but with a sex related pattern (blood glucose, triglycerides and cholesterol in males and NEFA in females). We observed a down-regulation in mRNA expression of gene involved in lipogenesis and in lipolysis for females but only in the lipogenesis for males. In F3, a decrease in VAT mass and an upregulation of lipogenesis gene expression occurred only in females.BPS perinatal exposure induced sex-dependent obesogen multigenerational effects, the F2 generation being the most impacted. Transgenerational disturbances persisted only in females.

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.

Despite growing concern about the occurrence of microplastics in aquatic ecosystems there is only rudimentary understanding of the pathways through which any adverse effects might occur. Here, we assess the effects of polystyrene microplastics (PS-MPs; <70 μm) on a common and widespread algal species, Chlorella sorokiniana. We used laboratory exposure to test the hypothesis that the lipids and fatty acids (FAs) are important molecules in the response reactions of algae to this pollutant. Cultivation with PS-MPs systematically reduced the concentration of essential linoleic acid (ALA, C18:3n-3) in C. sorokiniana, concomitantly increasing oleic acid (C18:1n-9). Among the storage triacylglycerols, palmitoleic and oleic acids increased at the expenses of two essential fatty acids, linoleic (LIN, C18:2n-6) and ALA, while PS-MPs had even more pronounced effects on the fatty acid and hydrocarbon composition of waxes and steryl esters. The FA composition of two major chloroplast galactolipids, monogalactosyldiacylglycerol (MGDG) and digalactosyldiacylglycerol (DGDG), were affected implying changes in the conformational structure of photosynthetic complexes in ways that can impair the photosynthesis. These data reveal how exposure to polystyrene microplastics can modify the concentrations of lipid molecules that are important intrinsically in cell membranes, and hence the lipid bilayers that could form an important barrier between algal cellular compartments and plastics in the aquatic environment. Changes in lipid synthesis and fatty acid composition in algae could also have repercussions for food quality, growth and stressor resistance in primary consumers. We advocate further studies of microplastics effects on the lipid composition of primary producers, and of their potential propagation through aquatic food webs.

As a Chinese-specific alternative to perfluorooctane sulfonate (PFOS), 6:2 chlorinated polyfluorinated ether sulfonate (commercial name: F-53B) has been used in the metal plating industry for over 40 years. This prevalence of use has resulted in its subsequent detection within the environment, wildlife, and humans. Despite this, however, its hepatotoxic effects on aquatic organisms remain unclear. Here, we characterized the impacts of long-term F-53B exposure on adult zebrafish liver and their offspring. Results showed that the concentration of F-53B was greater in the F0 liver than that in the gonads and blood. Furthermore, males had significantly higher liver F-53B levels than females. Hepatomegaly and obvious cytoplasmic vacuolation indicated that F-53B exposure induced liver injury. Compared to control, liver triglyceride levels decreased by 30% and 33.5% in the 5 and 50 μg/L-exposed males and 22% in 50 μg/L-exposed females. Liver transcriptome analysis of F0 adult fish found 2175 and 1267 differentially expressed genes (DEGs) in the 5 μg/L-exposed males and females, respectively. Enrichment analyses further demonstrated that the effects of F-53B on hepatic transcripts were sex-dependent. Gene Ontology showed that most DEGs were involved in multicellular organism development in male fish, whereas in female fish, most DEGs were related to metabolic processes and gene expression. qRT-PCR analysis indicated that the PPAR signaling pathway likely contributed to F-53B-induced disruption of lipid metabolism in F0 adult fish. In F1 larvae (5 days post fertilization), the transcription of pparα increased, like that in F0 adult fish, but most target genes showed the opposite expression trends as their parents. Taken together, our research demonstrated chronic F-53B exposure adversely impacts zebrafish liver, with disruption of PPAR signaling pathway dependent on sex and developmental stage.