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.

Denitrification, as both origins and sinks of N₂O, occurs extensively, and is of critical importance for regulating N₂O emissions in acidified soils. However, whether soil acidification stimulates N₂O emissions, and if so for what reason contributes to stimulate the emissions is uncertain and how the N₂O fractions from fungal (ffD) and bacterial (fbD) denitrification change with soil pH is unclear. Thus, a pH gradient (6.2, 7.1, 8.7) was set via manipulating cropland soils (initial pH 8.7) in North China to illustrate the effect of soil acidification on fungal and bacterial denitrification after the addition of KNO₃ and glucose. For source partitioning, we used and compared SP/δ¹⁸O mapping approach (SP/δ¹⁸O MAP) and acetylene inhibition technique combined isotope two endmember mixing model (AIT-IEM). The results showed significantly higher N₂O emissions in the acidified soils (pH 6.2 and pH 7.1) compared with the initial soil (pH 8.7). The cumulative N₂O emissions during the whole incubation period (15 days) ranged from 7.1 mg N kg⁻¹ for pH 8.7–18.9 mg N kg⁻¹ for pH 6.2. With the addition of glucose, relative to treatments without glucose, this emission also increased with the decrement of pH values, and were significantly stimulated. Similarly, the highest N₂O emissions and N₂O/(N₂O + N₂) ratios (rN₂O) were observed in the pH 6.2 treatment. But the difference was the highest cumulative N₂O + N₂ emissions, which were recorded in the pH 7.1 treatment based on SP/δ¹⁸O MAP. Based on both approaches, ffD values slightly increased with the acidification of soil, and bacterial denitrification was the dominant pathway in all treatments. The SP/δ¹⁸O MAP data indicated that both the rN₂O and ffD were lower compared to AIT-IEM. It has been known for long that low pH may lead to high rN₂O of denitrification and ffD, but our documentation of a pervasive pH-control of rN₂O and ffD by utilizing combined SP/δ¹⁸O MAP and AIT-IEM is new. The results of the evaluated N₂O emissions by acidified soils are finely explained by high rN₂O and enhanced ffD. We argue that soil pH management should be high on the agenda for mitigating N₂O emissions in the future, particularly for regions where long-term excessive nitrogen fertilizer is likely to acidify the soils.

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.

Liming is a safe and effective remediation practice for Cd contaminated acid paddy soil. The fate of Cd can also be strongly influenced by redox chemistry of sulfur. But it is unclear if, to what extent and how the combination of liming and sulfur mediation could further control Cd uptake by paddy rice. A rice cultivation pot experiment was conducted to evaluate the impact of different sulfur forms (S⁰ and SO₄²⁻ in K₂SO₄) on the solubility, uptake and accumulation of Cd in the soil-paddy rice system and how liming and reducing organic carbon mediate the process. Results showed that under neutral soil circumstances achieved by liming, co-application of K₂SO₄ and glucose significantly reduced brown rice Cd by 33%, compared to liming alone. They made it more readily for Cd²⁺ to be precipitated into CdS/CdS₂ or co-precipitate with newly formed FeS/FeS₂/iron oxides. The higher pH balancing capability of K₂SO₄ as well as liming kept the newly formed sulfide or iron containing minerals negatively charged to be more prone to adsorb Cd²⁺, that kept the porewater Cd²⁺ the lowest among all the treatments. Individual K₂SO₄ showed significant promoting effect on soil Cd solubility due to SO₄²⁻ chelation effect. Furthermore, K₂SO₄ had much weaker inhibiting effect on Cd translocation from root to grain, it showed no significant attenuating effect on brown rice Cd. S⁰ containing treatments displayed weaker or no attenuating effect on brown rice Cd due to its strong soil acidification effect. On the basis of liming, organic carbon induced sulfur (K₂SO₄) mediation showed great application potential for safe production on large areas of acid paddy soil contaminated by Cd.

Constructed wetlands integrated with microbial fuel cells (MFC-CWs) have been recently developed and tested for removing antibiotics. However, the effects of carbon source availability, electron transfer flux and cathode conditions on antibiotics removal in MFC-CWs through co-metabolism remained unclear. In this study, four experiments were conducted in MFC-CW microcosms to investigate the influence of carbon source species and concentrations, external resistance and aeration duration on sulfamethoxazole (SMX) and tetracycline (TC) removal and bioelectricity generation performance. MFC-CWs supplied with glucose as carbon source outperformed other carbon sources, and moderate influent glucose concentration (200 mg L⁻¹) resulted in the best removal of both SMX and TC. Highest removal percentages of SMX (99.4%) and TC (97.8%) were obtained in MFC-CWs with the external resistance of 700 Ω compared to other external resistance treatments. SMX and TC removal percentages in MFC-CWs were improved by 4.98% and 4.34%, respectively, by increasing the aeration duration to 12 h compared to no aeration. For bioelectricity generation performance, glucose outperformed sodium acetate, sucrose and starch, with the highest voltages of 386 ± 20 mV, maximum power density (MPD) of 123.43 mW m⁻³, and coulombic efficiency (CE) of 0.273%. Increasing carbon source concentrations from 100 to 400 mg L⁻¹, significantly (p < 0.05) increased the voltage and MPD, but decreased the internal resistance and CE. The highest MPD was obtained when the external resistance (700 Ω) was close to the internal resistance (600.11 Ω). Aeration not only improved the voltage and MPD, but also reduced the internal resistance. This study demonstrates that carbon source species and concentrations, external resistances and aeration duration, all play vital roles in regulating SMX and TC removal in MFC-CWs.

The presence of chemicals and the destruction of freshwater habitats have been addressed as one of the reasons for the decline in the amphibians’ populations worldwide. Considering the threat that these animals have been suffering in tropical regions, the present study tested if the Brazilian legislation, concerning the permissive levels of lithium and selenium in water bodies and effluents, warrants the protection of aquatic life. To do so, we assessed the metabolic, immunologic, and histopathologic alterations in liver samples of American bullfrog (Lithobates catesbeianus), at the premetamorphic stage, through biomarkers indicative of general energetic status, i.e., glucose, lipid, and protein metabolism using biochemical and histochemical approaches. The immunologic responses were assessed by the quantification of melanomacrophage centres (MMCs); the histopathologic evaluation of the liver sections was also performed. The assay was carried out over 21 days with two periods of sampling (after 7 and 21 days) to assess the effects of exposure over time. The animals were exposed to the considered safe levels of lithium (2.5 mg L⁻¹) and selenium (10 μg L⁻¹), both, isolated and mixed. The exposed animals showed alterations in glucose and lipid metabolism throughout the experiment. The intense presence of MMCs and histopathological responses are compatible with hepatotoxicity. The toxicity expressed by the employed animal model indicates that the Brazilian environmental legislation for the protection of aquatic life needs to be updated. With this study, we intend to provide data for better environmental policies and bring attention to sublethal effects triggered by the presence of contaminants in the aquatic environment.

The mediating influence of thyroid function on the association of phthalate exposure with glucose metabolism, including insulin resistance, remains unclear. We explored the mediating influence of thyroid hormone levels on the phthalate exposure–insulin resistance association. This cross-sectional study of 217 Taiwanese adults assessed insulin resistance (Homeostatic Model Assessment for Insulin Resistance, HOMA-IR scores) and the levels of 11 urinary phthalate metabolites and 5 thyroid hormones. Multiple regression models were used to analyze the associations among serum thyroid hormone levels, urinary phthalate metabolite levels, and HOMA-IR scores. The mediation analysis assessed the influence of thyroid function on the phthalate exposure–HOMA-IR association. Our data indicated urinary mono-ethylhexyl phthalate (MEHP) levels was negatively associated with free thyroxine (T₄) (β = −0.018; 95% confidence interval [CI]: −0.031, −0.005) and positively associated with HOMA-IR scores (β = 0.051, 95% CI: 0.012, 0.090). The study also revealed urinary mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP) levels was negatively associated with free T₄ (β = −0.036, 95% CI: −0.056, −0.017) and HOMA-IR (β = 0.070, 95% CI: 0.013, 0.126). Free T₄ and HOMA-IR had a negative association (β = −0.757, 95% CI: −1.122, −0.392). In the mediation analysis, free T₄ mediated 24% and 35% of the associations of urinary MEHP and MEOHP with HOMA-IR, respectively. Our findings revealed the mediating role of thyroid function in the phthalate exposure–glucose metabolism association in adults.

Carbon disulfide (CS₂) has been reported to induce disorder of glucose metabolism. However, the associations of CS₂ exposure with plasma glucose levels and risk of diabetes have not been explored in general population, and the underlying mechanisms remain unclear. We aim to examine the relationships between CS₂ exposure and fasting plasma glucose (FPG) levels, as well as diabetes, and assess the potential role of oxidative stress among the abovementioned relationships in Chinese general adults. The concentrations of urinary biomarkers of CS₂ exposure (2-thiothiazolidin-4-carboxylic acid, TTCA), and biomarkers for lipid peroxidation (8-isoprostane, 8-iso-PGF₂α) and DNA oxidative damage (8-oxo-7,8-dihydro-20-deoxyguanosine, 8-OHdG) were measured among 3338 urban adults from the Wuhan-Zhuhai cohort. Additionally, FPG levels were tested promptly. Generalized linear models and logistic regression models were used to quantify the associations among urinary TTCA, oxidative damage markers, FPG levels and diabetes risk. Mediation analysis was employed to estimate the role of oxidative damage markers in the association between urinary TTCA and FPG levels. We discovered a significant relationship between urinary TTCA and FPG levels with regression coefficient of 0.080 (95% CI: 0.002,0.157). Besides, the risk of diabetes was positively related to urinary TTCA (OR:1.282, 95% CI: 1.055,1.558), particularly among those who did not exercise regularly. Each 1% increase of urinary TTCA concentration was associated with a 0.096% and 0.037% increase in urinary 8-iso-PGF₂α and 8-OHdG, respectively. Moreover, we found an upward trend of FPG level as urinary 8-iso-PGF₂α gradually increased (Pₜᵣₑₙd<0.05), and urinary 8-iso-PGF₂α mediated 21.12% of the urinary TTCA-associated FPG increment. Our findings indicated that urinary CS₂ metabolite was associated with increased FPG levels and diabetes risk in general population. Lipid peroxidation partly mediated the association of urinary CS₂ metabolite with FPG levels.

The influence of pollutants on metabolic diseases such as type 2 diabetes mellitus is an emerging field in environmental medicine. Here, we explored the effects of a low-dose endosulfan sulfate (ES), a major metabolite of the pesticide endosulfan and a bio-persistent contaminant detected in environmental and human samples, on the progress of obesity and metabolic disorders. Pregnant CD-1 mice were given ES from gestational day 6 to postnatal day 21 (short-term). After weaning, male pups of exposed dams were provided with a low-fat or a high-fat diet (LFD or HFD) and assessed after an additional 12 weeks. At the same time, one group of male pups continuously received ES (long-term). Treatment with low-dose ES, short or long-term, alleviated the development of obesity and accumulation of hepatic triglycerides induced by HFD. Analysis of gene expression, metabolic profile and gut microbiome indicates that ES treatment inhibits adipogenesis induced by HFD due to enhanced lipid catabolism, fatty acid oxidation and disturbance of gut microbiota composition. However, impaired glucose and insulin homeostasis were still conserved in HFD-fed mice exposed to ES. Furthermore, ES treatment impaired glucose tolerance, affected hepatic gene expression, fatty acids composition and serum metabolic profile, as well as disturbed gut microbiota in LFD-fed mice. In conclusion, ES treatment at levels close to the accepted daily intake during fetal development directly impact glucose homeostasis, hepatic lipid metabolism, and gut microbiome dependent on the type of diet consumed. These findings provide a better understanding of the complex interactions of environmental pollutants and diet at early life stages also in the context of metabolic disease.