Suppression of high-fat-diet-induced obesity in mice by dietary folic acid supplementation is linked to changes in gut microbiota.

PURPOSE: To investigate whether the effects of dietary folic acid supplementation on body weight gain are mediated by gut microbiota in obesity. METHODS: Male C57 BL/6J conventional (CV) and germ-free (GF) mice both aged three to four weeks were fed a high-fat diet (HD), folic acid-deficient HD (FD-HD), folic acid-supplement HD (FS-HD) and a normal-fat diet (ND) for 25 weeks. Faecal microbiota were analyzed by 16S rRNA high-throughput sequencing, and the mRNA expression of genes was determined by the real-time RT-PCR. Short-chain fatty acids (SCFAs) in faeces and plasma were measured using gas chromatography-mass spectrometry. RESULTS: In CV mice, HD-induced body weight gain was inhibited by FS-HD, accompanied by declined energy intake, smaller white adipocyte size, and less whitening of brown adipose tissue. Meanwhile, the HD-induced disturbance in the expression of fat and energy metabolism-associated genes (Fas, Atgl, Hsl, Ppar-α, adiponectin, resistin, Ucp2, etc.) in epididymal fat was diminished, and the dysbiosis in faecal microbiota was lessened, by FS-HD. However, in GF mice with HD feeding, dietary folic acid supplementation had almost no effect on body weight gain and the expression of fat- and energy-associated genes. Faecal or plasma SCFA concentrations in CV and GF mice were not altered by either FD-HD or FS-HD feeding. CONCLUSION: Dietary folic acid supplementation differently affected body weight gain and associated genes' expression under HD feeding between CV and GF mice, suggesting that gut bacteria might partially share the responsibility for beneficial effects of dietary folate on obesity.

Early-life antibiotic exposure increases the risk of childhood overweight and obesity in relation to dysbiosis of gut microbiota: a birth cohort study.

BACKGROUND: Early-life antibiotic exposure is associated with the development of later obesity through the disruption of gut microbiota in the animal models. However, the related epidemiological evidence is still conflicting. METHODS: A birth cohort was consisted of 2140 mother-infant pairs in Chaoyang District Maternal and Child Health Care Hospital in this study. Here, their available antibiotic exposure during the first one year of life was ascertained using a open-ended questionnaire and related anthropometric parameters from the health screening program. The compositions of gut microbiota were comprehensively analyzed by16S rRNA high throughput sequencing. Then the spearman correlations were performed by the multiple covariance-adjusted regressions between the antibiotic exposure with anthropometric parameters and compositions of gut microbiota. RESULTS: Among the 2140 subjects, the antibiotic exposure during the first one year of life was 53.04%, mainly by Cephalosporins (53.39%) and Erythromycins(27.67%) for the treatment of respiratory tract infection (79.56%), which were not significantly different among the subgroups. Compared to the control group, both childhood overweight and obesity at two and a half years were higher in the antibiotic exposed group, with higher percents of Faecalibacterium, Agathobacter and Klebsiella, and lower percentage of Bifidobacterium. Moreover, there were positively potential associations between early-life antibiotic exposure with the accelerated anthropometric parameters and disruption of Faecalibacterium, Agathobacter, Klebsiella and Bifidobacterium at two and a half years. CONCLUSION: These above results proved that early-life antibiotic exposure was positively associated with the accelerated childhood overweight and obesity from one year to two and a half years by impacting the disorders of Faecalibacterium, Agathobacter, Klebsiella and Bifidobacterium, which would propose the theoretical basis for rationalizing the personalized antibiotic exposure among the infants to truly reflect the fairness of public health.

Association of fish oil containing lipid emulsions with retinopathy of prematurity: a retrospective observational study.

BACKGROUND: Retinopathy of prematurity (ROP) remains a leading cause of childhood blindness worldwide. This study aimed to investigate whether supplementation of n-3 polyunsaturated fatty acids (n-3 PUFAs) in parenteral nutrition may have beneficial effects on ROP in preterm infants. METHODS: A total of 89 preterm infants, admitted to Neonatal Intensive Care Unit (NICU) in Anhui Provincial Children's Hospital from September 2017 to August 2020, were recruited in the study. Based on the medical documents, the subjects were categorised into two groups: administration of the fish oil emulsion (n=43) containing soy oil, medium-chain-triglycerides (MCT), olive oil and fish oil (6g/dL, 6g/dL, 5g/dL and 3g/dL respectively), and the soy oil emulsion (n=46) containing 10g/dL of soy oil and MCT each. At 4 weeks of hospitalization, ROP was screened and diagnosed. Fatty acids in erythrocytes were determined using gas chromatography. RESULTS: The averaged birth weight and gestational age were 1594±296 g and 31.9±2.3 wk, 1596±263 g and 31.6±2.3 wk respectively for preterm infants in the fish oil group and soy oil group. After 4 to 6 weeks of hospitalization, among all the preterm infants, 52 developed ROP (all stages) indicating an incidence of ROP at 58.43%. Although the incidence of ROP with any stages showed no differences between the two groups, the severe ROP incidence in the group with fish oil emulsions (2.33%) was significantly lower than that in the group with soy oil emulsions (23.91%) (P<0.05). After 14 days of nutrition support, the preterm infants administered fish oil emulsions had an increase in erythrocyte DHA content, with a reduction in ratio of arachidonic acid (AA) to DHA and an increase of n-3 index. CONCLUSION: Supplementation of n-3 PUFAs through parenteral fish oil containing lipid emulsions resulted in an increase in erythrocyte DHA, and this might have beneficial effects on prevention of severe ROP in preterm infants.

An insight into the exploration of proliferation of antibiotic resistance genes in high-fat diet induced obesity mice.

Using mice as an animal model, we first demonstrated the significant proliferation of ARGs and the change of mobile genetic elements (MGEs) in high-fat diet induced obesity (DIO) mice, which the ermB and tnpA-03 genes mostly increased, illuminating that DIO could enrich the abundance of ARGs. Additionally, Lactobacillus sharply increased in the DIO mice and might contribute to the proliferation of ARGs and dramatical change of MGEs in the HFD groups. Finally, procrustes analysis showed the explanatory variables of the MGEs, the metabolites, and the microbial communities for the ARGs accounted for 94.3%, 53.4%, and 68.1%, respectively, and implying that MGEs might be the most direct factor affecting ARGs, and microbiota could be the main driver of the proliferation of ARGs in the DIO mice.

Association of telomere length and telomerase methylation with n-3 fatty acids in preschool children with obesity.

BACKGROUND: Telomeres play a crucial role in cellular survival and its length is a predictor for onset of chronic non-communicable diseases. Studies on association between telomeres and obesity in children have brought discrepant results and the underlying mechanisms and influential factors are to be elucidated. This study aimed to investigate changes in telomere length and telomerase reverse transcriptase (TERT) DNA methylation, and further to determine their correlation with n-3 polyunsaturated fatty acids (PUFAs) in preschool children with obesity. METHODS: Forty-six preschool children with obesity aged 3 to 4 years were included in the study, with equal numbers of age- and gender-matched children with normal weight as control. Leukocyte telomere length was determined by the ratio of telomeric product and single copy gene obtained using real-time qPCR. DNA methylation of TERT promoter was analyzed by bisulfite sequencing. Fatty acids in erythrocytes were measured by gas chromatography with a total of 15 fatty acids analyzed. The total saturated fatty acids (SFAs), total n-6 PUFAs, total n-3 PUFAs, and the ratio of arachidonic acid (AA) to docosahexaenoic acid (DHA) were calculated. Then the correlation between leukocyte telomere length, TERT promoter methylation and fatty acids was determined. RESULTS: In preschool children with obesity, leukocyte telomeres were shortened and had a negative association with the body mass index. The methylated fractions in 13 of 25 CpG sites in the TERT promoter were increased by approximately 3 to 35% in the children with obesity compared to the normal weight children. Erythrocyte lauric acid and total SFAs, lenoleic acid and total n-6 PUFAs were higher, and DHA was lower in the children with obesity than those in the children with normal weight. Correlative analysis showed that leukocyte telomere length had a positive association with total SFAs and DHA, and a negative association with the AA/DHA ratio. However, no association between erythrocyte DHA and the TERT promoter methylation was found. CONCLUSION: These data indicate that the reduced body DHA content and increased AA/DHA ratio may be associated with shortened leukocyte telomeres in child obesity, which is probably not involved in the TERT promoter methylation.

A preliminary study on the differential expression of long noncoding RNAs and messenger RNAs in obese and control mice.

Obesity has become one of the public health problems that threatens children's health, but its specific etiology and pathogenesis are still unclear. Recently, many long noncoding RNAs (lncRNAs) have been shown to be involved in the occurrence of obesity. However, their roles are still poorly understood. Thus, the aim of this study was to discover the profiles of the lncRNAs and messenger RNAs (mRNAs) altered in obesity. Epididymal fat samples were collected from mice fed with control and high-fat diets (HFD) for 16 weeks to investigate the differentially expressed lncRNAs and mRNAs by lncRNA microarray, after which seven lncRNAs and nine mRNAs were validated using reverse-transcription polymerase chain reaction (RT-PCR). Bioinformatics analysis and predictions were used to determine the potential biofunctions of these differentially expressed lncRNAs. Then a coexpression network was constructed to determine the transcriptional regulatory relationship of the differentially expressed lncRNAs and mRNAs between the control and HFD groups. The body weight of the HFD group was much higher than that of the control group, as a result of the increased energy intake. In total, 8421 differentially expressed lncRNAs and 6840 mRNAs were profiled using the lncRNAs microarray. Bioinformatics predictions and the coexpression network all indicated that the occurrence of obesity was attributed to those differentially expressed lncRNAs and mRNAs associated with energy metabolism, cell differentiation, and oxidative phosphorylation. The expression levels of Cyp2e1, Atp5b, Hibch, Cnbp, Frmd6, Ptchd3, ENSMUST00000155948, AK140152, ENSMUST00000135194, and ENSMUST00000180861 were significantly different between the control and HFD groups. All these Results suggested that obesity was partially attributed to those lncRNAs associated with energy metabolism, cell differentiation, and oxidative phosphorylation.

Effects of gut microbiota on leptin expression and body weight are lessened by high-fat diet in mice.

Aberration in leptin expression is one of the most frequent features in the onset and progression of obesity, but the underlying mechanisms are still unclear and need to be clarified. This study investigated the effects of the absence of gut microbiota on body weight and the expression and promoter methylation of the leptin. Male C57 BL/6 J germ-free (GF) and conventional (CV) mice (aged 4-5 weeks) were fed either a normal-fat diet (NFD) or a high-fat diet (HFD) for 16 weeks. Six to eight mice from each group, at 15 weeks, were administered exogenous leptin for 7 d. Leptin expression and body weight gain in GF mice were increased by NFD with more CpG sites hypermethylated at the leptin promoter, whereas there was no change with HFD, compared with CV mice. Adipose or hepatic expression of genes associated with fat synthesis (Acc1, Fas and Srebp-1c), hydrolysis and oxidation (Atgl, Cpt1a, Cpt1c, Ppar-α and Pgc-1α) was lower, and hypothalamus expression of Pomc and Socs3 was higher in GF mice than levels in CV mice, particularly with NFD feeding. Exogenous leptin reduced body weight in both types of mice, with a greater effect on CV mice with NFD. Adipose Lep-R expression was up-regulated, and hepatic Fas and hypothalamic Socs3 were down-regulated in both types of mice. Expression of fat hydrolysis and oxidative genes (Atgl, Hsl, Cpt1a, Cpt1c, Ppar-α and Pgc-1α) was up-regulated in CV mice. Therefore, the effects of gut microbiota on the leptin expression and body weight were affected by dietary fat intake.

Effects of SCFA on the DNA methylation pattern of adiponectin and resistin in high-fat-diet-induced obese male mice.

Specific adipokines, such as adiponectin and resistin, are secreted from adipose tissue and are associated with the development of obesity. Supplementation of dietary SCFA can prevent and reverse high-fat-diet (HFD)-induced obesity. However, it is not clear whether SCFA ameliorate abnormal expression of adiponectin and resistin in the obese state. The aim of this study was to investigate the effects of SCFA on adiponectin and resistin's expressions in diet-induced obese mice, as well as the potential mechanisms associated with DNA methylation. C57BL/6J male mice were fed for 16 weeks with five types of HFD (34·9 % fat by wt., 60 % kJ) - a control HFD and four HFD with acetate (HFD-A), propionate (HFD-P), butyrate (HFD-B) and their admixture (HFD-SCFA). Meanwhile, a low-fat diet (4·3 % fat by wt., 10 % kJ) was used as the control group. The reduced mRNA levels of adiponectin and resistin in the adipose tissue of the HFD-fed mice were significantly reversed by dietary supplementation of acetate, propionate, butyrate or their admixture to the HFD. Moreover, the expressional changes of adiponectin and resistin induced by SCFA were associated with alterations in DNA methylation at their promoters, which was mediated by reducing the expressions of enzyme-catalysed DNA methyltransferase (DNMT1, 3a, 3b) and the methyl-CpG-binding domain protein 2 (MBD2) and suppressing the binding of these enzymes to the promoters of adiponectin and resistin. Our results indicate that SCFA may correct aberrant expressions of adiponectin and resistin in obesity by epigenetic regulation.

NLRP3 Inflammasome Activation During Acute Negative Pressure Injury in the Middle Ear of Mice.

HYPOTHESIS: The present study was conducted to explore the role of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome in mouse otic barotrauma models. BACKGROUND: Previous studies suggest that the NLRP3 inflammasome plays an important role in the pathogenesis of middle ear disease. However, whether middle ear negative pressure injury underlies NLRP3 inflammasome activation remains unclear. METHODS: Wild-type and Nlrp3 -/- mice were randomly assigned to control and pressure injury groups, respectively. Pressure loading was performed using a pressure cabin with the pressure level set to 20 kPa higher than that of the ambient atmosphere. This was achieved in approximately 15 seconds and maintained for 10 minutes. Hematoxylin and eosin staining was performed to detect morphological changes of the middle ear mucosa, tissue IL-1ß was measured via an enzyme-linked immunosorbent assay, and cleaved caspase-1 was detected by Western blot. RESULTS: We found that the maturation of caspase-1 and IL-1ß production in the middle ear significantly increased after otic barotrauma. In Nlrp3 -/- mice, inflammasome activation is downregulated and mucosal hyperplasia is reduced compared with those of wild-type mice during recovery. CONCLUSION: The NLRP3 inflammasome likely plays an important role in the pathogenesis of otic barotrauma. Controlling activation of the NLRP3 inflammasome may promote middle ear recovery after negative pressure injury.

Imbalance of early-life vitamin D intake targets ROS-mediated crosstalk between mitochondrial dysfunction and differentiation potential of MSCs associated the later obesity.

BACKGROUND: Obesity is characterized by excessive fat accumulation, which is related with abnormal pluripotency of mesenchymal stem cells (MSCs). Recently, there is growing evidence that the disorder of maternal vitamin D (VD) intake is a well-known risk factor for long-term adverse health outcomes to their offspring. Otherwise, less is known of its repercussion and underlying mechanisms on the different differentiation potential of MSCs. METHODS: Four-week-old female C57BL/6J mice were fed with different VD reproductive diets throughout the whole pregnancy and lactation. The characteristics of BMSCs from their seven-day male offspring, VDR knockdown establishment of HuMSCs and HuMSCs under the different VD interventions in vitro were confirmed by flow cytometry, RT-PCR, and immunofluorescence. The roles of VD on their mitochondrial dysfunction and differentiation potential were also investigated. Then their remaining weaned male pups were induced by administrating high-fat-diet (HFD) for 16 weeks and normal fat diet was simultaneously as controls. Their lipid accumulation and adipocytes hypertrophy were determined by histological staining and related gene expressions. RESULTS: Herein, it was proved that imbalance of early-life VD intake could significantly aggravate the occurrence of obesity by inducing the adipogenesis through affecting the VD metabolism and related metabolites (P < 0.05). Moreover, abnormally maternal VD intake might be involved on the disorders of differentiation potential to inhibit the maintenance of MSCs stemness through increasing the productions of ROS, which was accompanied by impairing the expression of related genes on the adipo-osteogenic differentiation (P < 0.05). Moreover, it was along with increasing potential of adipogenic differentiation of MSCs as higher ROS in the state of VD deficiency, while excessive maternal VD status could conversely enhance the osteogenic differentiation with slightly lower ROS (P < 0.05). Furthermore, the underlying mechanisms might be involved on the mitochondria dysfunctional, especially the mitophagy, by activating the LC3b, P62 and etc. using in vivo and in vitro studies (P < 0.05). CONCLUSION: These findings demonstrated that imbalance of early-life VD intake could target ROS-mediated crosstalk between mitochondrial dysfunction and differentiation potential of MSCs, which was significantly associated with the later obesity. Obviously, our results could open up an attractive modality for the benefits of suitable VD intake during the pregnancy and lactation.

Decreased vitamin D bio-availability with altered DNA methylation of its metabolism genes in association with the metabolic disorders among the school-aged children with degree I, II, and III obesity.

Obesity is strongly associated with disturbances of vitamin D (VD) metabolites in the animal models. However, the related epidemiological evidence is still controversial, especially the different degrees of obesity children. Hence, in this present representative case-control study, 106 obesity school-age children aged 7-12 years were included and divided into different subgroups as degree I (the age- and sex-specific BMI≥95th percentile, n=45), II (BMI ≥120% percentile, n=34) and III (BMI ≥140% percentile, n=27) obesity groups across the ranges of body mass index (BMI). While the age- and sex-matched subjects without obesity were as the control group. Notably, it was significantly different of body composition, anthropological and clinical characteristics among the above four subgroups with the dose-response relationships (P<.05). Moreover, comparing with the control group, the serum VD concentrations were higher, VD metabolites like 25(OH)D, 25(OH)D3 and 1,25(OH)2D, and related hydroxylases as CYP27A1, CYP2R1 and CYP27B1 were lower in the degree I, II, and III obesity subgroups (P<.05), which were more disorder with the anthropological and clinical characteristics as the obesity was worsen in a BMI-independent manner (P<.05). However, there was a significant increase of CYP27B1 in the degree III obesity group than those in the degree I and II obesity subgroups. Furthermore, the methylation patterns on the genome-wide (Methylation/Hydroxymethylation) and VD metabolism genes (CYP27A1, CYP2R1 and CYP27B1) were negatively correlated with the worse obesity and their related expressions (P<.05). In summary, these results indicated that obesity could affect the homeostasis of VD metabolism related genes such as CYP27A1, CYP2R1, CYP27B1 and etc through abnormal DNA methylation, resulting in the disorders of VD related metabolites to decrease VD bio-availability with the BMI-independent manner. In turn, the lower levels of VD metabolites would affect the liver function to exacerbate the progression of obesity, as the Degree II and III obesity subgroups.

An international multidisciplinary consensus on pediatric metabolic dysfunction-associated fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is highly prevalent in children and adolescents, particularly those with obesity. NAFLD is considered a hepatic manifestation of the metabolic syndrome due to its close associations with abdominal obesity, insulin resistance, and atherogenic dyslipidemia. Experts have proposed an alternative terminology, metabolic dysfunction-associated fatty liver disease (MAFLD), to better reflect its pathophysiology. This study aimed to develop consensus statements and recommendations for pediatric MAFLD through collaboration among international experts. METHODS: A group of 65 experts from 35 countries and six continents, including pediatricians, hepatologists, and endocrinologists, participated in a consensus development process. The process encompassed various aspects of pediatric MAFLD, including epidemiology, mechanisms, screening, and management. FINDINGS: In round 1, we received 65 surveys from 35 countries and analyzed these results, which informed us that 73.3% of respondents agreed with 20 draft statements while 23.8% agreed somewhat. The mean percentage of agreement or somewhat agreement increased to 80.85% and 15.75%, respectively, in round 2. The final statements covered a wide range of topics related to epidemiology, pathophysiology, and strategies for screening and managing pediatric MAFLD. CONCLUSIONS: The consensus statements and recommendations developed by an international expert panel serve to optimize clinical outcomes and improve the quality of life for children and adolescents with MAFLD. These findings emphasize the need for standardized approaches in diagnosing and treating pediatric MAFLD. FUNDING: This work was funded by the National Natural Science Foundation of China (82070588, 82370577), the National Key R&D Program of China (2023YFA1800801), National High Level Hospital Clinical Research Funding (2022-PUMCH-C-014), the Wuxi Taihu Talent Plan (DJTD202106), and the Medical Key Discipline Program of Wuxi Health Commission (ZDXK2021007).

n-3 fatty acids modulate adipose tissue inflammation and oxidative stress.

PURPOSE OF REVIEW: Dietary n-3 polyunsaturated fatty acids (n-3 PUFAs) may be related to a number of chronic metabolic abnormalities, including metabolic syndrome. This review presents an update on the effects of n-3 PUFAs on risk factors of metabolic syndrome, especially adipose tissue inflammation, oxidative stress and underlying mechanisms of these effects. RECENT FINDINGS: Anti-inflammatory actions of n-3 PUFAs are thought to be mediated by the formation of their active metabolites (eicosanoids and other lipid mediators) as well as their regulation of the production of inflammatory mediators (e.g., adipocytokines, cytokines) and immune cell infiltration into adipose tissue. n-3 PUFAs mediate these effects by modulating several pathways, such as those involving nuclear factor-κB, peroxisome proliferator-activated receptors and Toll-like receptors. The antioxidative effects of n-3 PUFAs in adipocytes appear to inhibit reactive oxygen species production and alter mitochondrial function. SUMMARY: This review summarizes the evidence for beneficial effects of n-3 PUFAs on adipose tissue inflammation and oxidative stress. More studies are necessary to investigate the mechanisms underlying these effects and to relate this topic to human health.

Developmental origins of health and disease: Impact of paternal nutrition and lifestyle.

Most epidemiological and experimental studies have focused on maternal influences on offspring's health. The impact of maternal undernutrition, overnutrition, hypoxia, and stress is linked to adverse offspring outcomes across a range of systems including cardiometabolic, respiratory, endocrine, and reproduction among others. During the past decade, it has become evident that paternal environmental factors are also linked to the development of diseases in offspring. In this article, we aim to outline the current understanding of the impact of male health and environmental exposure on offspring development, health, and disease and explore the mechanisms underlying the paternal programming of offspring health. The available evidence suggests that poor paternal pre-conceptional nutrition and lifestyle, and advanced age can increase the risk of negative outcomes in offspring, via both direct (genetic/epigenetic) and indirect (maternal uterine environment) effects. Beginning at preconception, and during utero and the early life after birth, cells acquire an epigenetic memory of the early exposure which can be influential across the entire lifespan and program a child's health. Potentially not only mothers but also fathers should be advised that maintaining a healthy diet and lifestyle is important to improve offspring health as well as the parental health status. However, the evidence is mostly based on animal studies, and well-designed human studies are urgently needed to verify findings from animal data.

Effects of agricultural land types on microplastic abundance: A nationwide meta-analysis in China.

Microplastics (MPs) accumulation in agricultural land that possibly poses threats to food security and human health has recently attracted increasing attention. Land use type probably is a key factor that drives the contamination level of soil MPs. Nevertheless, few studies have performed large-scale systematic analysis of the effects in different agricultural land soils on the MPs abundance. In this study, we constructed a national MPs dataset comprising 321 observations from 28 articles, summarised the current status of microplastic pollution in five agricultural land types in China through meta-analysis, and investigated the effects and key factors of agricultural land types on microplastic abundance. The results showed that among the existing soil microplastic research, vegetable soils maintained a higher environmental exposure distribution than other agricultural lands, and with the most common trend being vegetable land > orchard land > cropland > grassland. By combining agricultural practices, demographic economic factors and geographical factors, a potential impact identification method based on subgroup analysis was established. The findings demonstrated that agricultural film mulch significantly increased soil MPs abundance, especially in orchards. Increased population and economy (carbon emissions and PM2.5 concentrations) add MPs abundance in all kinds of agricultural lands. And the significant changes of effect sizes in high-latitude and mid-altitude areas suggested that geographical space differences exerted a certain degree of impact on the soil distribution of MPs. By the proposed method, different levels of MPs risk areas in agricultural soils can be more reasonably and effectively identified, which will provide type-specific policies technical and theoretical support for the precise management of MPs in agricultural land soils.

Novel insights into the temporal molecular fractionation of dissolved black carbon at the iron oxyhydroxide - water interface.

As the most reactive and mobile fraction of black carbon, dissolved black carbon (DBC) inexorably interacts with minerals in the biosphere. Nevertheless, the research on the mechanisms and compositions of DBC assembly at the mineral-water interface remains limited. In this study, we revealed the "kinetic architecture" of DBC on iron oxyhydroxide at novel insights based on quantitative and qualitative approaches. The results indicated that high molecular weight, highly unsaturated, oxygen-rich (such as carboxyl-rich fraction, phenolics), aliphatics, and long C chains compounds were preferentially adsorbed on the iron oxyhydroxide. 2D-COS analyses directly disclosed the sequential fractionation: aromatic and phenolic groups > aliphatic groups, and few aromatics were continuously adsorbed after the rapid adsorption. Quantitative determinations identified that aromatic and phenolic components were adsorbed rapidly over the first 60 min, while aromatics achieved the dynamic equilibrium until ∼300 min, which was consistent with the 2D-COS observations. Our findings supported the hypothesis that "mineral-OM" and "OM-OM" interactions worked simultaneously, and the adsorption might be co-driven by ligand exchange, hydrophobic interactions, and other mechanisms. This work provided the theoretical basis for organic carbon storage and turnover, and it was valuable for predicting the behaviors and fates of contaminants at the soil-water interface and surface water.

Effect of adsorption on ferrihydrite on the photoreactivity of dissolved black carbon for photodegradation of sulfadiazine.

The selective adsorption of dissolved black carbon (DBC) on inorganic minerals is a widespread geochemical process in the natural environment, which could change the chemical and optical properties of DBC. However, it remains unclear how selective adsorption affects the photoreactivity of DBC for photodegradation of organic pollutants. This paper was the first to investigate the effect of DBC adsorption on ferrihydrite at different Fe/C molar ratios (Fe/C molar ratios of 0, 7.50 and 11.25, and marked as DBC0, DBC7.50 and DBC11.25) on the photoproduction of reactive intermediates generated from DBC and their interaction with sulfadiazine (SD). Results showed that UV absorbance, aromaticity, molecular weight and contents of phenolic antioxidants of DBC were significantly decreased after adsorption on ferrihydrite, and higher decrease was observed at higher Fe/C ratio. Photodegradation kinetics experiments showed that observed photodegradation rate constant of SD (kobs) increased from 3.99 × 10-5 s-1 in DBC0 to 5.69 × 10-5 s-1 in DBC7.50 while decreased to 3.44 × 10-5 s-1 in DBC11.25, in which 3DBC* played an important role and 1O2 played a minor role, while ·OH was not involved in the reaction. Meanwhile, the second-order reaction rate constant between 3DBC* and SD (kSD, 3DBC*) increased from 0.84 × 108 M-1 s-1 for DBC0 to 2.53 × 108 M-1 s-1 for DBC7.50 while decreased to 0.90 × 108 M-1 s-1 for DBC11.25. The above results might be mainly attributed to the fact that the decrease of phenolic antioxidants in DBC weakened the back-reduction of 3DBC* and reactive intermediates of SD as the Fe/C ratio increased, while the decrease of quinones and ketones reduced the photoproduction of 3DBC*. The research revealed adsorption on ferrihydrite affected the photodegradation of SD by changing the reactivity of 3DBC*, which was helpful to understand the dynamic roles of DBC in the photodegradation of organic pollutants.

An Insight into the Exploration of Antibiotic Resistance Genes in Calorie Restricted Diet Fed Mice.

Antibiotic resistance genes (ARGs) threaten the success of modern drugs against multidrug resistant infections. ARGs can be transferred to opportunistic pathogens by horizontal gene transfer (HGT). Many studies have investigated the characteristics of ARGs in various chemical stressors. Studies on the effects of dietary nutrition and dietary patterns on ARGs are rare. The study first demonstrated the effect of calorie restricted (CR) diet on the ARGs and mobile genetic elements (MGEs) in mouse feces and explored their relationship with gut microbiota and their functions. The results showed that the abundance of the total ARGs in mouse feces of the CR group increased, especially tetracycline ARGs (tetW-01). The abundance of the MLSB ARGs (ermB) decreased evidently in mouse feces of the CR group. In addition, the total abundance of MGEs decreased evidently in the CR group, especially tnpA-03. In the meantime, the abundance of Lactobacillus and Bifidobacterium in mouse feces of the CR group increased remarkably. The Spearman correlation analysis between gut microbiota and ARGs showed that several probiotics were significantly positively correlated with ARGs (tetW-01), which might be the main contribution to the increase in ARGs of the CR group.

Maternal vitamin D deficiency aggravates the dysbiosis of gut microbiota by affecting intestinal barrier function and inflammation in obese male offspring mice.

OBJECTIVES: The colonization of gut microbiota during early life may play a critical role in the progression of metabolic syndrome in adulthood. Targeting gut-based genes in the barrier function, inflammation, and lipid transportation are potential therapies for obesity. Therefore, this study focused on whether maternal deficient vitamin D (VD) intake could aggravate the dysbiosis of gut microbiota by affecting the expressions of these genes in the ileum and colon of obese male offspring mice. METHODS: Four-week-old female C57 BL/6 J mice were fed normal (VD-C) or VD-deficient (VD-D) reproductive diets throughout pregnancy and lactation (n = 15/group). Weaning male pups (n = 10/group) were fed either a high-fat (HFD; VD-C-HFD, VD-D-HFD) or normal-fat diet (control) for 16 wk. All biologic samples were obtained after the mice were anesthetized by cervical dislocation. Subsequently, the compositions of the gut microbiota in cecal contents were analyzed using 16 S ribosomal RNA sequencing. Messenger RNA expression in the ileum and colon was determined using real-time reverse transcription-polymerase chain reaction. The distributions of ZO-1 and Claudin-1 were determined using immunohistochemistry testing. RESULTS: Maternal deficient VD intake significantly aggravated the dysbiosis of gut microbiota persisting into adulthood from phylum to genus levels in the cecal contents among obese male offspring mice. This aggravation led to significantly depleted Bacteroidetes and Verrucomicrobia (Akkermansia, Alliprevotella, and Bacteroides), with higher relative abundance of Firmicutes (Lactobacillus, Lachnoclostridium, Romboutsia, and Ruminiclostridium_9) and Firmicutes/Bacteroidetes. The gene expressions of proinflammatory cytokines (Ccl2, Ccl4 and interleukin-1ß) and lipid transportation molecules (Ffar3, Fabp4, and Fabp1) were higher, and the levels of intestinal barrier function (Occludin, ZO-1, and Claudin-1) were lower in the VD-D-HFD group than those in the VD-C-HFD group. Furthermore, there were significant correlations between the dysbiosis of intestinal microbials and expressions of genes related to barrier function, inflammation, and lipid transportation in the ileum and/or colon. CONCLUSIONS: Maternal VD deficiency during pregnancy and lactation could aggravate the dysbiosis of gut microbiota to affect the progression of obesity among male offspring, which might be regulated by genes associated with barrier function, inflammation, and lipid transportation. So early life appropriate VD intake could play a significant role in preventing later obesity.

Dietary Folic Acid Supplementation Inhibits HighFat DietInduced Body Weight Gain through Gut Microbiota-Associated Branched-Chain Amino Acids and Mitochondria in Mice.

The effects of folic acid on body weight gain in obesity and gut microbiota-associated branched-chain amino acids (BCAAs) and mitochondrial function were investigated. Three- to four-wk-old male C57BL/6J conventional (CV) and germ-free (GF) mice were fed a high-fat diet (HD), folic acid-supplemented HD (FSHD) and a normal-fat diet (ND) for 25 wk. In CV mice, the HD-induced increases in body weight and plasma BCAA concentrations, downregulated expression of genes related to BCAA catabolism (Bcat2, Bckdha, or Ppm1k), mitochondrial biogenesis (Pgc-1α, Cox1, Nd1 or Nd6), fusion (Mfn1, Mfn2 or Opa1) and mitophagy (Pink1 or Park2), and upregulated expression of the fission-associated gene Drp1 in epididymal fat were reversely corrected with FSHD feeding. In contrast, the expression of these genes in the liver was the opposite under HD feeding or folic acid supplementation. In GF mice, plasma BCAA concentrations were much less affected by HD feeding and were reduced by FSHD feeding, with almost no alterations in the expression of genes associated with BCAA catabolism and mitochondrial function. Further analysis indicated a correlation between adipose and hepatic Mt C/N and plasma BCAA concentrations, and the latter had a close association with specific gut bacteria. Therefore, dietary folic acid supplementation differentially affected body weight gain, BCAA catabolism, and mitochondrial dynamics and metabolism under HD feeding between CV and GF mice, suggesting that gut bacteria-altered BCAAs and mitochondria might partially share the responsibility for the beneficial effects of dietary folic acid on obesity.