The gut microbiome is altered after bariatric surgery and is associated with weight loss. However, the commensal bacteria involved and the underlying mechanism remain to be determined. We performed shotgun metagenomic sequencing in obese subjects before and longitudinally after sleeve gastrectomy (SG), and found a significant enrichment in microbial species in Clostridia and bile acid metabolizing genes after SG treatment. Bile acid profiling further revealed decreased primary bile acids (PBAs) and increased conjugated secondary bile acids (C-SBAs) after SG. Specifically, glycodeoxycholic acid (GDCA) and taurodeoxycholic acid (TDCA) were increased at different follow-ups after SG, and were associated with the increased abundance of Clostridia and body weight reduction. Fecal microbiome transplantation with post-SG feces increased SBA levels, and alleviated body weight gain in the recipient mice. Furthermore, both Clostridia-enriched spore-forming bacteria and GDCA supplementation increased the expression of genes responsible for lipolysis and fatty acid oxidation in adipose tissue and reduced adiposity via Takeda G-protein-coupled receptor 5 (TGR5) signaling. Our findings reveal post-SG gut microbiome and C-SBAs as contributory to SG-induced weight loss, in part via TGR5 signaling, and suggest SBA-producing gut microbes as a potential therapeutic target for obesity intervention.

Next-generation live biotherapeutics are promising to aid the treatment of obesity and metabolic diseases. Here, we reported a novel anti-obesity probiotic candidate, Roseburia hominis, that was depleted in stool samples of obese subjects compared with lean controls, and its abundance was negatively correlated with body mass index and serum triglycerides. Supplementation of R. hominis prevented body weight gain and disorders of glucose and lipid metabolism, prevented fatty liver, inhibited white adipose tissue expansion and brown adipose tissue whitening in mice fed with high-fat diet, and boosted the abundance of lean-related species. The effects of R. hominis could be partially attributed to the production of nicotinamide riboside and upregulation of the Sirtuin1/mTOR signaling pathway. These results indicated that R. hominis is a promising candidate for the development of next-generation live biotherapeutics for the prevention of obesity and metabolic diseases.

The probiotic impact of microbes on host metabolism and health depends on both host genetics and bacterial genomic variation. Faecalibacterium prausnitzii is the predominant human gut commensal emerging as a next-generation probiotic. Although this bacterium exhibits substantial intraspecies diversity, it is unclear whether genetically distinct F. prausnitzii strains might lead to functional differences in the gut microbiome. Here, we isolated and characterized a novel F. prausnitzii strain (UT1) that belongs to the most prevalent but underappreciated phylogenetic clade in the global human population. Genome analysis showed that this butyrate-producing isolate carries multiple putative mobile genetic elements, a clade-specific defense system, and a range of carbohydrate catabolic enzymes. Multiomic approaches were used to profile the impact of UT1 on the gut microbiome and associated metabolic activity of C57BL/6 mice at homeostasis. Both 16S rRNA and metagenomic sequencing demonstrated that oral administration of UT1 resulted in profound microbial compositional changes including a significant enrichment of Lactobacillus, Bifidobacterium, and Turicibacter. Functional profiling of the fecal metagenomes revealed a markedly higher abundance of carbohydrate-active enzymes (CAZymes) in UT1-gavaged mice. Accordingly, UT1-conditioned microbiota possessed the elevated capability of utilizing starch in vitro and exhibited a lower availability of microbiota-accessible carbohydrates in the gut. Further analysis uncovered a functional network wherein UT1 reduced the abundance of mucin-degrading CAZymes and microbes, which correlated with a concomitant reduction of fecal mucin glycans. Collectively, our results reveal a crucial role of UT1 in facilitating the carbohydrate metabolism of the gut microbiome and expand our understanding of the genetic and phenotypic diversity of F. prausnitzii.

Excess manganese (Mn) and NH4+-N emissions from electrolytic manganese metal industrial tailwater may harm the environment. However, previous studies have not combined Mn-oxidizing microalgae to reclaim Mn with woodchip substrates for nitrogen removal from tailwater. Here, a two-stage bioreactor system was constructed to recover Mn by microalgal-mediated bio-oxidation in an algae reactor (AR) and remove nitrogen by denitrification in a woodchip reactor (WR). The results showed that up to 100 % of Mn2+ in the tailwater was removed after a 3-day incubation period. The maximum amount of biogenerated Mn oxide nanoparticles reached 13.34 mg/L with Mn4+ as the main Mn valence. Mn recovery reached 65.69 % through precipitate collection, and the NH4+-N removal efficiency reached 97 % in the AR. Mn oxidation by algae might promote oxidative removal of NH4+-N. NO3--N and total nitrogen removal efficiencies in the WR reached 82-90 % and 65-87 %, respectively, which was attributed to denitrification. The predominance of the denitrification gene narG in the WR may have driven the efficient nitrate removal. Flavobacterium, Acidovora, Massilia, Arcticibacter, and Acinetobacter were the most abundant genera in the WR and represented dominant denitrifying bacteria in the woodchip microbiome, indicating their important contribution to denitrification. Overall, the combined application of Mn-oxidizing algae and woodchip-denitrifying bioreactors may represent an efficient treatment technology for electrolytic manganese wastewater remediation.

The influence of gut microbiota on Type 2 Diabetes Mellitus (T2DM) is an emerging area of research. This review investigates the relationship between gut microbiota dysbiosis, bacterial translocation, and T2DM. It aims to elucidate how microbial imbalances contribute to the progression of T2DM through bacterial translocation and to evaluate dietary and therapeutic strategies to manage these effects.

Recent studies highlight that dysbiosis in T2DM patients often leads to increased systemic inflammation, impaired glucose metabolism, and disrupted gut barrier integrity. These disruptions promote elevated levels of harmful bacterial components, such as lipopolysaccharides, in the bloodstream. This, in turn, is linked to worsening insulin resistance and metabolic dysfunction. Advances in molecular methods and biomarkers have provided deeper insights into bacterial translocation and its impact on diabetes. Dietary interventions, including nutraceutical agents, high-fiber and low-glycemic index diets, as well as the use of probiotics and prebiotics, have shown promise in restoring gut health and mitigating bacterial translocation.

Maintaining a balanced gut microbiota and intestinal barrier integrity is crucial for managing T2DM. Therapeutic strategies, including dietary modifications and nutraceuticals, have demonstrated potential in reducing bacterial translocation and systemic inflammation. Continued research is needed to refine these approaches and explore novel treatment modalities for improving metabolic health in T2DM patients.

The rapid development of coastal areas has raised concerns about marine environmental pollution. In this study, metagenomics was employed to investigate antibiotic resistance genes (ARGs), mobile genetic elements (MGEs), and bacterial communities in the Yellow Sea and Yangtze River Delta in China. Multidrug resistance genes were the most abundant ARGs in these regions. Transposons and insertion_element_IS91 were the dominant MGEs, closely related to the horizontal gene transfer of ARGs. Temperature, dissolved oxygen, pH, and depth were identified as important environmental factors influencing the distribution of ARGs in seawater. Oil, agriculture, animal husbandry, and wastewater treatment plants are likely the primary sources of ARGs. From the perspective of ARG control, bacterial communities contributed the most to the development of the resistome and may carry ARGs, spreading from the Yangtze River Delta to the Yellow Sea along ocean currents. A comparison with Tara Oceans datasets revealed that the dominant ARG types and bacterial genera in coastal waters were consistent with global characteristics, with variations in ARG subtypes. This study expands knowledge on the distribution patterns of ARGs at an offshore scale and provides a reference for the prevention and control of resistant gene pollution in the Yellow Sea and Yangtze River Delta.

This study investigates the effects Dioscorea opposita polysaccharides (DOP) on insulin resistance, lipid metabolism, oxidative stress, and intestine microbiota in high-fat-diet and streptozotocin induced type 2 diabetes (T2DM) rats. Low dose (DOP-L, 200 mg/kg BW), high dose (DOP-H, 400 mg/kg BW) and D. opposita powder (DO, 400 mg/kg BW) were oral-administrated to T2DM rats. After 6 weeks of treatment, supplementation of DOP-H and DO improved body weight and glucose/lipid metabolism-related indicators, including glucagon-like peptide 1, total cholesterol and high-density lipoprotein cholesterol. DOP-H and DO suppressed liver oxidative stress through increasing the level of superoxide dismutase, catalase, glutathione and reducing malondialdehyde. DOP attenuated the pathological change in liver, such as hepatic steatosis, and thus improved the liver function. Furthermore, the anti-diabetic effects of DOP was correlated with alterations of the gut microbiota, including an increase in Firmicutes and Bacteroidetes and a decrease in Actinobacteria and Proteobacteria, which promoted a healthier gut environment. Further analysis of short-chain fatty acids and metabolites provided evidences of DOP's regulatory effects on cecal contents in T2DM rats. Therefore, DOP-H present decent effects on T2DM, suggesting that DOP can ameliorate the insulin resistance and restore blood lipid level of T2DM rats with high-fat-diet by regulating intestinal microbiota.

The microbially produced amino acid-derived metabolite imidazole propionate (ImP) contributes to the pathogenesis of type 2 diabetes. However, the effects of ImP on endothelial cell (EC) physiology and its role in atherosclerotic coronary artery disease are unknown. Using both human and animal model studies, we investigated the potential contributory role of ImP in the development of atherosclerosis.

Plasma levels of ImP were measured in patients undergoing elective cardiac angiography (n=831) by ultra-high performance liquid chromatography coupled to tandem mass spectrometry. Odds ratios and corresponding 95% CIs for coronary artery disease were calculated based on the ImP quartiles using both univariable and multivariable logistic regression models. The effects of ImP on functional properties of ECs were assessed using human aortic ECs. In a mouse model of carotid artery injury, the impact of ImP on vascular regeneration was examined. Additionally, atheroprone Apoe-/- mice fed a high-fat diet were treated with and without ImP (800 µg), and aortic atherosclerotic lesion area was evaluated after 12 weeks. Next-generation sequencing, Western blot analysis, small interfering RNA-based gene knockdown, and tamoxifen-inducible Cre-loxP experiments were performed to investigate ImP-mediated molecular mechanisms.

Plasma ImP levels in subjects undergoing cardiac evaluation were associated with increased risk of prevalent coronary artery disease. We found that ImP dose dependently impaired migratory and angiogenic properties of human ECs and promoted an increased inflammatory response. Long-term exposure to ImP compromised the repair potential of the endothelium after an arterial insult. In atheroprone Apoe-/- mice, ImP increased atherosclerotic lesion size. Mechanistically, ImP attenuated insulin receptor signaling by suppressing the PI3K (phosphoinositide 3-kinase)/AKT pathway leading to sustained activation of the FOXO1 (forkhead box protein O1) transcription factor. Genetic inactivation of endothelial FOXO1 signaling in ImP-treated mice enhanced the angiogenic activity and preserved the vascular repair capacity of ECs after carotid injury.

Our findings reveal a hitherto unknown role of the microbially produced histidine-derived metabolite ImP in endothelial dysfunction and atherosclerosis, suggesting that ImP metabolism is a potential therapeutic target in atherosclerotic cardiovascular disease.

To investigate the causal relationships between gut microbiota and novel adult-onset type 2 diabetes mellitus(T2DM) subtypes.

We conducted Mendelian randomization (MR) analyses using genome-wide association data from European populations. Initial MR analyses examined associations between gut microbiota and four T2DM subtypes, followed by validation analyses using type 1 diabetes mellitus(T1DM) and T2DM GWAS data. We also performed bidirectional MR analyses and tested for heterogeneity and pleiotropy across all analyses.

Our MR analyses revealed distinctive associations between gut microbiota and T2DM subtypes: six bacterial taxa with severe insulin-deficient diabetes (SIDD), four with severe insulin-resistant diabetes (SIRD), eight with mild obesity-related diabetes (MOD), and eight with mild age-related diabetes (MARD). These associations were distinct from T1DM findings. Six bacterial taxa were validated in T2DM analyses, with four showing directionally consistent effects: Class Clostridia (OR = 0.57, P = 0.045) and Order Clostridiales (OR = 0.57, P = 0.045) were associated with reduced MOD risk, while species Catus (OR = 1.80, P = 0.007) was associated with increased MOD risk, and genus Holdemania (OR = 2.51, P = 0.004) was associated with increased SIRD risk. No significant heterogeneity or pleiotropy was observed across analyses.

Our MR analyses reveal novel causal relationships between gut microbiota and adult-onset T2DM subtypes, though further validation studies are warranted.

Malus hupehensis leaves (MHL), consumed as a daily beverage in Chinese folk tradition and recently recognized as a new food material, are abundant in polyphenols and bioactive compounds that demonstrate hypoglycemic, lipid-lowering, and anti-inflammatory effects. However, the antidiabetic mechanisms have not been fully elucidated. This study aimed to investigate the protective mechanisms of Malus hupehensis leaves' extract (MHLE) against type 2 diabetes mellitus (T2DM). The results showed that MHLE effectively ameliorated glucose and lipid metabolic abnormalities in db/db mice, and attenuated hepatic macrophage activation. Transcriptomic analysis of the liver revealed that MHLE primarily affects genes involved in inflammatory responses and inhibited the TLR4/MAPK pathway to reduce hepatic inflammation. Metagenomic sequencing identified changes in gut microbiota composition and showed that MHLE restored the abundance of Lachnospiraceae bacterium, Oscillospiraceae bacterium, and Clostridia bacterium while reducing the abundance of Escherichia coli, thereby ameliorating gut dysbiosis. The integrated regulation of metabolism, immune response, and the microbial environment by MHLE significantly alleviated symptoms of T2DM. This study offers strong scientific evidence for the potential use of MHL as a functional food.

Arecoline, the main alkaloid in areca nut, has shown potential in modulating metabolism and gut microbiota. This study aimed to evaluate its therapeutic effects on glucose and lipid metabolism, inflammation, liver function, and potential mechanisms in a Type 2 diabetes mellitus (T2DM) mouse model.

T2DM was established in mice with a high-fat, high-sugar diet, and streptozotocin injections. Arecoline significantly reduced fasting blood glucose, enhanced glucose tolerance, and increased insulin sensitivity. Serum lipid profiles showed marked decreases in total cholesterol, triglycerides, and LDL-C levels. Systemic inflammation, as measured by serum levels of IL-1β, IL-6, and MCP-1, decreased significantly. Improvements in liver function were observed, as indicated by reductions in ALT and AST levels. Liver transcriptomic analysis revealed modulation of pathways related to glutathione metabolism, MAPK signaling, and cAMP signaling, which were involved in insulin signaling and oxidative stress response. Additionally, arecoline mitigated gut dysbiosis by restoring microbial diversity, altering gut microbiota composition, and regulating key pathways involved in NAD biosynthesis and fatty acid β-oxidation, which were critical for maintaining energy homeostasis.

Arecoline improves glucose metabolism, lipid profiles, and liver function, while modulating gut microbiota and liver metabolic pathways, showing potential as a therapeutic agent for T2DM.

Type 2 diabetes mellitus (T2DM) is pathologically associated with gut microbiota imbalance, which is implicated in disease progression through metabolic and inflammatory pathways. The therapeutic potential of inulin, a well-characterized prebiotic, has been explored to mitigate T2DM via microbiota modulation. However, the efficacy of this intervention, with its performance dependent on the degree of polymerization (DP), requires further investigation. This study assessed the therapeutic roles of inulin (DP3-60) and fructo-oligosaccharides (FOS, DP3-10) in T2DM management. Dietary administration of these prebiotic compounds demonstrated a significant capacity to alleviate multiple metabolic pathologies, including obesity, insulin resistance, systemic inflammation, oxidative stress, dyslipidemia and hepatic steatosis in high-fat diet (HFD)-fed induced T2DM mice. Significant superior efficacy was observed in FOS for ameliorating glucose metabolic dysregulation, adipocyte hypertrophy, liver weight, and histopathological alterations in colonic tissue, while inulin exhibited greater potency in alleviating oxidative stress. Both inulin and FOS enhanced gut microbiota diversity and richness in T2DM mice, accompanied by a significant reduction in Firmicutes/Bacteroidetes ratio. Notably, the S24-7 family emerged as a crucial microbial taxon modulated by both inulin and FOS. Furthermore, FOS demonstrated superior capacity to restore HFD-induced gut microbiota. Taxonomically significant amplicon sequence variants (ASVs), which were altered by HFD and modulated by inulin and FOS, exhibited distinct taxonomic profiles between the two compounds. This study provides preliminary evidence that the biological effects and beneficial properties of inulin-type fructans exhibit DP-dependent variations, which may enhance their efficient utilization in metabolic disorders.

An increase in branched-chain amino acid (BCAA) levels can result in insulin resistance at different stages of type 2 diabetes (T2D), however, the causes of this increase are unclear. We performed metagenomics and metabolomics profiling in patients with prediabetes (PDM), newly diagnosed diabetes (NDDM), and post-medication type 2 diabetes (P2DM) to investigate whether altered gut microbes and metabolites could explain the specific clinical characteristics of different disease stages of T2D. Here we identify acetolactate synthase (ALS) a BCAA biosynthesis enzyme in Staphylococcus aureus as a cause of T2D insulin resistance. Compared with healthy peoples, patients with PDM, NDDM, and P2DM groups, especially in P2DM group, have increased faecal numbers of S. aureus. We also demonstrated that insulin administration may be a risk factor for S. aureus infection in T2D. The presence of ALS-positive S. aureus correlated with the levels of BCAAs and was associated with an increased fasting blood glucose (FBG) and insulin resistance. Humanized microbiota transplantation experiment indicated that ALS contributes to disordered insulin resistance mediated by S. aureus. We also found that S. aureus phage can reduced the FBG levels and insulin resistance in db/db mice. The ALS-positive S. aureus are associated with insulin resistance in T2D, opening a new therapeutic avenue for the prevention or treatment of diabetes.

Over the last few decades, the prevalence of metabolic diseases such as obesity, diabetes, non-alcoholic fatty liver disease, hypertension, and hyperuricemia has surged, primarily due to high-fat diet (HFD). The pathologies of these metabolic diseases show disease-specific alterations in the composition and function of their gut microbiome. How HFD alters the microbiome and its metabolite to mediate adipose tissue (AT) inflammation and obesity is not well known. Thus, this study aimed to identify the changes in the gut microbiome and metabolomic signatures induced by an HFD to alter obesity. To explore the changes in the gut microbiota and metabolites, 16S rRNA gene amplicon sequencing and metabolomic analyses were performed after HFD and normal diet (ND) feeding. We noticed that, at taxonomic levels, the number of operational taxonomic units (OTUs), along with the Chao and Shannon indexes, significantly shifted in HFD-fed mice compared to those fed a ND. Similarly, at the phylum level, an increase in Firmicutes and a decrease in Bacteroidetes were noticed in HFD-fed mice. At the genus level, an increase in Lactobacillus and Ruminococcus was observed, while Allobaculum, Clostridium, and Akkermansia were markedly reduced in the HFD group. Many bacteria from the Ruminococcus genus impair bile acid metabolism and restrict weight loss. Firmicutes are efficient in breaking down complex carbohydrates into short-chain fatty acids (SCFAs) and other metabolites, whereas Bacteroidetes are involved in a more balanced or efficient energy extraction. Thus, an increase in Firmicutes over Bacteroidetes enhances the absorption of more calories from food, which may contribute to obesity. Taken together, the altered gut microbiota and metabolites trigger AT inflammation, which contributes to metabolic dysregulation and disease progression. Thus, this study highlights the potential of the gut microbiome in the development of therapeutic strategies for obesity and related metabolic disorders.

Firefighters across the world face higher risks of occupational hazards, such as exposure to chemicals, extreme heat, traumatic stressors, and intense physical demands, which can increase their vulnerability to a range of psychological and physiological difficulties. These challenges include the risk of developing chronic stress, depression, and post-traumatic stress disorder (PTSD), potentially leading to detrimental negative coping patterns such as alcohol abuse. The consequent health implications impact both short-term and long-term health and well-being. This study aimed to explore the relationship between mental health status, alcohol consumption patterns, and gut microbiome alterations in firefighters from two different regions-America and Korea. By investigating these relationships, we hope to gain insights into how repeated exposure to severe stressors impacts gut health. Healthy male firefighters (ages 21-50) and controls (matched sex, geography, and age) were recruited via flyers and snowball sampling in the United States and South Korea, resulting in 203 participants (102 firefighters and 101 controls). Firefighters reported significantly higher PTSD symptoms and depression and drank 2.3 times more alcohol than the control group. American firefighters reported more drinking than Koreans. There was a significant correlation between higher alcohol consumption and the likelihood of witnessing deaths by suicide. However, there were no correlations between alcohol consumption and PTSD symptom severity. There were associations between alcohol consumption patterns and aspects of the gut microbiome. This study highlights the mental health challenges faced by firefighters, including elevated rates of PTSD, depression, and alcohol consumption, with specific microbial imbalances linked to PTSD and alcohol use, emphasizing the role of the gut-brain axis.

The composition and functionality of the gut microbiota (GM) changes throughout the life course. As we move into older age, it starts to shift towards a less healthy one, which may lead to an imbalance in the GM community. Strategies that can reverse age-related dysbiosis are an important part of healthy aging. Little is known about the GM composition of older adults with different physical activity (PA) levels and whether it might contribute to healthy ageing. The aim of this study was to compare the GM composition of older adults with different PA levels and assess if it is associated with healthy ageing. 101 participants aged between 65-85 years undertook anthropometric measures, a 6-min walking test, wore an accelerometer for 7 days and provided a faecal sample. Faecal GM composition was analysed using 16S rRNA sequencing. We found that those who fulfilled the WHO/UK PA recommendations had higher relative abundance of several health-related bacteria such as Lactobacillus, F. prausnitzii and Roseburia intestinalis and lower abundance of disease-associated bacteria such as D.piger or Enterobacterales when compared to those who did not reach PA recommendations. These findings suggest that PA might improve the GM composition and has the potential to, at least partially, revert age-associated dysbiosis and promote healthy ageing.

As emerging contaminants, microplastics (MPs) may pose a threat to human health. Their co-exposure with the widespread phycotoxin okadaic acid (OA), a marine toxin known to cause gastrointestinal toxicity, may exacerbate health risk and raise public safety concern. In this study, the toxicity mechanisms of MPs and OA on intestinal microenvironment was explored using human Caco-2 cells as the model, which was combined with an in vitro fecal fermentation experiment. Our results showed that co-exposure to MPs (80 μg/mL) and OA (20 ng/mL) significantly decreased cell viability, increased intracellular reactive oxygen species (ROS) production, elevated lactate dehydrogenase release, impaired ABC transporter activity, promoted OA accumulation, and triggered inflammatory response compared to the control, MPs, and OA groups, indicating that co-exposure directly compromises intestinal epithelial integrity. In vitro fermentation experiments revealed that co-exposure disrupted gut microbial composition, decreasing the relative abundance of some bacteria, such as Parasutterella and Adlercreutzia, while increasing opportunistic pathogens, such as Escherichia-Shigella, increased. These findings provide new insights into the impact and underlying mechanisms of MPs and OA co-exposure on intestinal homeostasis, highlighting the potential health risks associated with MPs.

This study investigates the gut microbiota components associated with metabolic syndrome in patients living with HIV-1 at Bafoussam Regional Hospital, West Cameroon, it focuses on gastrointestinal mucosal barrier disruption and dysbiosis, and their effects on persistent inflammation and metabolic disorders.

A pilot study was conducted involving fourteen patients living with HIV-1. The patients were divided into two groups of seven in each group. One group consisted of patients with metabolic syndrome, and the other group included patients without metabolic syndrome. Gut microbiota was characterized using 16 S rRNA gene-targeted sequencing to analyze microbial diversity and composition. Beta diversity and the relative abundance of bacterial taxa were compared between patients with and without metabolic syndrome.

Patients living with HIV-1 and metabolic syndrome showed significantly altered beta diversity compared to those without metabolic syndrome. A higher relative abundance of Firmicutes and increased proliferation of Proteobacteria were observed in patients with metabolic syndrome. Additionally, a decrease in metabolically beneficial bacteria, such as Bifidobacterium sp., Lactobacillus sp., Akkermansia sp., and Faecalibacterium sp., was noted. Several beneficial bacterial species were associated with participants' metadata, suggesting potential links between gut microbiota and metabolic syndrome.

This preliminary study highlights that gut microbial balance, rather than the presence of specific bacteria, plays a crucial role in managing metabolic health in patients living with HIV-1. The altered gut microbiota in participants with metabolic syndrome emphasizes the need for further research into the optimal gut microbial structure. Understanding the interaction between gut microbiota changes and the chemical environment in these patients could guide targeted interventions to improve metabolic outcomes.

Pancreatic cancer ranks among the most lethal digestive malignancies, exhibiting a steadily increasing incidence and mortality worldwide. Despite significant advances in cancer research, the 5-year survival rate remains below 10%, predominantly due to delayed diagnosis and limited therapeutic options. Concurrently, the gut microbiota-an integral component of host physiology-has emerged as a crucial player in the pathogenesis of pancreatic cancer. Mounting evidence indicates that alterations in gut microbial composition and function may influence tumor initiation, progression, and response to therapy. This review provides an in-depth examination of the intricate interplay between the gut microbiome and pancreatic cancer, highlighting potential diagnostic biomarkers and exploring microbiome-targeted therapeutic strategies to improve patient outcomes.

Gut microbial dysbiosis, or altered gut microbial communities, in Alzheimer's Disease suggests a pathogenic role for gut inflammation and microbial products in shaping a neuroinflammatory environment. Similarly, metabolic diseases, such as obesity and diabetes, are also associated with an increased risk of Alzheimer's Disease. As the metabolic landscape shifts during gut inflammation, and gut inflammation in turn impacts metabolic processes, we explore how these interconnected pathways may contribute to the progression of Alzheimer's Disease. Additionally, we discuss the role of bacterial amyloids produced by gut microbes, which may exacerbate amyloid aggregation in the brain and contribute to neurodegenerative processes. Furthermore, we highlight potential therapeutic strategies aimed at reducing gut inflammation, improving metabolic health, and decreasing amyloid content as a means to mitigate Alzheimer's Disease progression. These approaches, targeting the gut-brain-metabolic axis, could offer promising avenues for delaying or preventing cognitive decline in affected individuals.

Sexual dysfunction, influenced by hormonal imbalances, psychological factors, and chronic diseases, affects a significant portion of the population. Probiotics, known for their beneficial effects on gut microbiota, have emerged as potential therapeutic agents for improving sexual health. This systematic review evaluates the impact of probiotics on sexual function, hormonal regulation, and reproductive outcomes. A comprehensive search identified 3308 studies, with 12 meeting the inclusion criteria-comprising 10 randomized controlled trials (RCTs) and 2 in vivo and in vitro studies. Probiotic interventions were shown to significantly improve sexual function, particularly in women undergoing antidepressant therapy (p < 0.05). Significant improvements in Female Sexual Function Index (FSFI) scores were observed, with combined treatments such as Lactofem with Letrozole and Lactofem with selective serotonin reuptake inhibitors (SSRIs) demonstrating a 10% biochemical and clinical pregnancy rate compared to 0% in the control group (p = 0.05). Probiotic use was also associated with a 66% reduction in menopausal symptoms, increased sperm motility (36.08%), viability (46.79%), and morphology (36.47%). Probiotics also contributed to favorable hormonal changes, including a reduced luteinizing hormone (LH) to follicle-stimulating hormone (FSH) ratio (from 3.0 to 2.5, p < 0.05) and increased testosterone levels. Regarding reproductive outcomes, probiotic use was associated with higher pregnancy rates in women undergoing fertility treatments and improvements in sperm motility, viability, and morphology in men. This review highlights the promising role of probiotics in addressing sexual dysfunction and reproductive health, suggesting their potential as adjunctive treatments for conditions such as depression and infertility. Further research is needed to better understand the underlying mechanisms of these beneficial effects.

Reference genomes of root microbes are essential for metagenomic analyses and mechanistic studies of crop root microbiomes. By combining high-throughput bacterial cultivation with metagenomic sequencing, we constructed comprehensive bacterial and viral genome collections from the roots of wheat, rice, maize, and Medicago. The crop root bacterial genome collection (CRBC) significantly expands the quantity and phylogenetic diversity of publicly available crop root bacterial genomes, with 6,699 bacterial genomes (68.9% from isolates) and 1,817 undefined species, expanding crop root bacterial diversity by 290.6%. The crop root viral genome collection (CRVC) contains 9,736 non-redundant viral genomes, with 1,572 previously unreported genus-level clusters in crop root microbiomes. From these, we identified conserved bacterial functions enriched in root microbiomes across soils and host species and uncovered previously unexplored bacteria-virus connections in crop root ecosystems. Together, the CRBC and CRVC serve as valuable resources for investigating microbial mechanisms and applications, supporting sustainable agriculture.

Recent studies in humans have shown that certain pesticides could affect the composition and functions of the gut microbiota, an essential modulator of vertebrate physiology, leading to potential dysbiosis. However, this relationship remains largely unknown in wild birds despite the implications of pesticides in the current decline of farmland species. The present study sought to fill this gap by providing data on the association between pesticide concentrations in blood and gut microbiota characteristics in relation to individual traits in a farmland raptor, the Montagu's harrier (Circus pygargus). Results showed that females with higher body condition and higher pesticide load exhibited greater gut bacterial richness and diversity, while the relationship was opposite in males with higher body condition. In terms of taxonomic composition, Proteobacteria emerged as the dominant phylum across all nestlings. Differences in the abundance of specific phyla and genera were observed according to pesticide load, with higher levels of Bacteroidota and Leifsonia, but lower levels of Bulkholderia, in nestlings with higher pesticide concentrations in their blood. This study highlights differences in microbiota and contamination by several pesticides according to the phenotypic characteristics of a wild raptor, and shows that farmland birds can represent relevant biosentinels for assessing the health/proper functioning of ecosystems (One Health approach).

The gut microbiome has emerged as a potential influencer of muscle health; however, its role in hospitalized patients remains unclear. This study aimed to investigate the association between gut microbiome diversity and skeletal muscle mass, strength, and quality in hospitalized post-stroke patients.

We conducted a cross-sectional study of post-stroke patients admitted to a rehabilitation facility. Gut microbiome diversity was assessed using 16S ribosomal ribonucleic acid (rRNA) gene sequencing, calculating Operational Taxonomic Unit (OTU) Richness, Faith's Phylogenetic Diversity (PD), and Shannon index. Muscle health was evaluated using skeletal muscle index (SMI) for muscle mass, handgrip strength (HGS) for muscle strength, and bioimpedance analysis-derived phase angle (PhA) for muscle quality. Multiple linear regression analyses were performed, adjusting for potential confounders.

A total of 156 patients (mean age 78.4 years; 55.7 % male) were analyzed. OTU Richness showed significant positive associations with SMI (β = 0.197, p = 0.025), HGS (β = 0.180, p = 0.005), and PhA (β = 0.178, p = 0.022). The Shannon index was also positively associated with SMI (β = 0.120, p = 0.041), HGS (β = 0.140, p = 0.028), and PhA (β = 0.164, p = 0.032). Faith's PD did not demonstrate significant associations with muscle health parameters.

Higher gut microbiome diversity, assessed by OTU Richness and Shannon index, is associated with better muscle mass, strength, and quality in post-stroke patients. These findings suggest a potential role for gut microbiota in muscle health during stroke rehabilitation.

Akkermansia muciniphila is a promising target for managing obesity and type 2 diabetes (T2D), but human studies are limited. We conducted a 12-week randomized, double-blind, placebo-controlled trial involving 58 participants with overweight or obese T2D, who received A. muciniphila (AKK-WST01) or placebo, along with routine lifestyle guidance. Both groups showed decreases in body weight and glycated hemoglobin (HbA1c), without significant between-group differences. In participants with low baseline A. muciniphila, AKK-WST01 supplementation showed high colonization efficiency and significant reductions in body weight, fat mass, and HbA1c, which were not found in the placebo group. However, AKK-WST01 supplementation showed poor colonization and no significant clinical improvements in participants with high baseline A. muciniphila. These findings were verified in germ-free mice receiving feces with low or high A. muciniphila. Our study indicates that metabolic benefits of A. muciniphila supplementation could depend on its baseline intestinal levels, supporting the potential for gut microbiota-guided probiotic supplementation. (ClinicalTrials.gov number, NCT04797442).

Decades of artificial selection have markedly enhanced egg production efficiency, yet the epigenetic underpinnings, notably DNA methylation dynamics in the gut, remain largely unexplored. Here, we investigate how breeds and developmental stages influence DNA methylation profiles in laying hens, and their potential relationship to laying performance and gut health. We compared two highly selected laying hen strains, Lohmann Brown-Classic (LB) and Lohmann Selected Leghorn-Classic (LSL), which exhibited similar egg production but divergent physiological, metabolic, and immunological characteristics. Our sampling encompassed key developmental stages: the pullet stage (10 and 16 wk old), peak production (24 and 30 wk old), and later stage (60 wk old) (n = 99; 10 per group), allowing us to elucidate the temporal dynamics of epigenetic regulation. Our findings highlight a crucial window of epigenetic modulation during the prelaying period, characterized by stage-specific methylation alterations and the involvement of predicted transcription factor motifs within methylated regions. This observation was consistent with the expression patterns of DNA methyltransferases (DNMTs), including DNMT1, DNMT3A, and DNMT3B. In addition, a higher methylation level was observed in specific loci or regions in the LSL compared with the LB strain. Notably, we uncover strain-specific differences in methylation levels, particularly pronounced in genomic regions associated with intestinal integrity, inflammation, and energy homeostasis. Our research contributes to the multidisciplinary framework of epigenetics and egg-laying performance, offering valuable implications for poultry production and welfare.NEW & NOTEWORTHY Our study reveals key methylation changes in the jejunum mucosa of laying hens across developmental stages and between strains, with implications for gut health, immune function, and egg production. These findings highlight a crucial role of epigenetic regulation in optimizing performance.

Dimethicone (GAS), lidocaine (XYL), and protease (PRO) are commonly used as premedications during esophagogastroduodenoscopy (EGD). However, the effects of these drugs on the gastric microbiota remain unexplored. Therefore, we aimed to investigate the effects of these premedications on gastric juice collected from patients undergoing EGD.

Gastric juice was endoscopically aspirated from six patients and divided into six aliquots for in vitro analysis. The samples were mixed with premedications in corresponding treatment sets: GAS, XYL, PRO, MIX (a mixture of GAS, XYL, and PRO), and control (CTL1 and 2; no medication treatment). After extraction of microbial DNA from the treated samples, the 16S rRNA amplicon sequence was analyzed to determine the microbiota profile in terms of (1) the amount of genomic DNA (gDNA), (2) α-diversity indices, Shannon index, number of observed operational taxonomic units (OTUs), and Chao1 index, (3) weighted and unweighted UniFrac distances, and (4) the relative abundance of phyla and genera.

The total amount of extracted gDNA did not significantly differ between the six groups. The α-diversity indices did not significantly differ between treatment groups. Although GAS, PRO, and MIX differed significantly from the technical replicates in the weighted UniFrac distance (p = 0.03 all), no significant difference was observed in the unweighted UniFrac distance. However, significant differences were observed in the relative abundance of several bacterial microbiota at the phylum and genus levels.

Premedications affect the microbiota profile of specific phylum- and genus-level bacterial groups. Trial Registration: University Hospital Medical Information Network Clinical Trials Registry: UMIN-CTR 000040192 and UMIN-CTR 000051289.

Diabetes prevalence continues to increase as a result of people's increasing sugar intake. Diabetes mellitus and its complications (dry skin, constipation, depression, and dental caries), as well as the prohibition of sweets ingestion, seriously affect patients' physical and mental health. Therefore, it is crucial to develop a long-term food for special medical purposes (FSMP) that aids in managing diabetes and its complications. To ensure effective biomedical function and taste, we developed a FSMP beverage formulation containing stevia glycoside, mogroside V, and sodium hyaluronate (SMH-B), each at a concentration of 0.1 mg/mL. Meanwhile, this study verified that SMH-B is an environmentally friendly and biocompatible formulation. Furthermore, both in vivo and in vitro studies have demonstrated that SMH-B significantly lowers blood glucose and lipid levels, enhances skin moisture and elasticity, prevents dental caries, alleviates constipation, reduces oxidative stress, and mitigates depressive symptoms. Notably, the SMH-B compound formula exhibits a more effective adjuvant therapeutic effect compared to single-ingredient formulation composed of stevia glycosides, mogroside V, and sodium hyaluronate. Moreover, SMH-B provides the sweetness desired by diabetic patients without affecting blood glucose levels, while also offering an auxiliary therapeutic role, making it a potential FSMP for diabetes management.

Quinoa β-glucan (QBG) has shown potential benefits in treating type 2 diabetes mellitus (T2DM); however, comprehensive evaluations of its effects remain limited. This study investigates the impact of QBG-derived from hot water extraction (Q-) and microbial fermentation enrichment (Q+)-on serum glucose levels, lipid profiles, appetite-regulating hormones, fecal short-chain fatty acids (SCFAs), and gut microbiota composition and function in streptozotocin/high-fat diet (STZ/HFD)-induced T2DM mice. The results indicate that QBG treatment significantly reduced fasting blood glucose, insulin levels, triglycerides (TG) and total cholesterol (TC), while concurrently increasing high-density lipoprotein cholesterol (HDLC) levels. Additionally, liver and pancreatic function improved, as evidenced by decreased levels of malondialdehyde (MDA), aspartate transaminase (AST), and alanine transaminase (ALT). SCFA levels were significantly higher in QBG-treated groups compared to MC group. QBG treatment also reduced the abundance of Firmicutes and Patescibacteria, along with the Firmicutes/Bacteroidota ratio, while increasing levels of Bacteroidota and Actinobacteria. These findings suggest that QBG can regulate the dysbiosis of SCFAs production in T2DM mice and may indirectly modulate the secretion of appetite-regulating hormones by influencing gut microbiota composition. Furthermore, PICRUSt analysis revealed that QBG treatment, particularly Q + _H, could enhance disrupted metabolism and improve gut microbiota functions, helping restore normal physiological function.

The gut microbiota plays a pivotal role in influencing the metabolism and immune responses of the body. A balanced microbial composition promotes metabolic health through various mechanisms, including the production of beneficial metabolites, which help regulate inflammation and support immune functions. In contrast, imbalance in the gut microbiota, known as dysbiosis, can disrupt metabolic processes and increase the risk of developing diseases, such as obesity, type 2 diabetes, and inflammatory disorders. The composition of the gut microbiota is dynamic and can be influenced by environmental factors such as diet, medication, and the consumption of live bacteria. Since the early 1900s, bacteria isolated from food and have been used as probiotics. However, the human gut also offers an enormous reservoir of bacterial strains, and recent advances in microbiota research have led to the discovery of strains with probiotic potentials. These strains, derived from a broad spectrum of microbial taxa, differ in their ecological properties and how they interact with their hosts. For most probiotics bacterial structural components and metabolites, such as short-chain fatty acids, contribute to the maintenance of metabolic and immunological homeostasis by regulating inflammation and reinforcing gut barrier integrity. Metabolites produced by probiotic strains can also be used for bacterial cross-feeding to promote a balanced microbiota. Despite the challenges related to safety, stability, and strain-specific properties, several newly identified strains offer great potential for personalized probiotic interventions, allowing for targeted health strategies.

Eating disorders (EDs) are a heterogeneous class of increasing mental disorders that are characterized by disturbances in eating behaviors, body weight regulation, and associated psychological dysfunctions. These disorders create physiological imbalances that alter the diversity and composition of the gut microbiota. While evidence suggests that EDs can arise from epigenetic aberrations, alterations in gut microbial communities may also contribute to the development and/or persistence of EDs through epigenetic mechanisms. Understanding the interplay among gut microbial communities, epigenetic processes, and the risk of EDs provides opportunities for designing preventive and/or therapeutic interventions through gut microbiome modulation. This review highlights how microbiome-based therapeutics and specific dietary interventions can contribute to improving various subtypes of EDs by modulating gut microbial communities and mitigating epigenetic aberrations. First, we briefly review the literature on links between epigenetic aberrations and the pathophysiology of EDs. Second, we examine the potential role of the gut microbiome in the pathogenesis of EDs through epigenetic mechanisms. Next, we explore the associations between EDs and other psychiatric disorders, and examine the potential roles of the microbiome in their pathogenesis. Finally, we present evidence supporting the potential of microbiome-based therapeutics and specific dietary interventions to improve EDs through epigenetic modifications.

Electro-assisted technology is promising for enhancing plant activity, optimizing functional microbial communities, and significantly strengthening pollutant removal efficiency. In this study, four reactors were designed as control group (CG), Hydrocotyle vulgaris L. ecological floating bed (PEFB), microbial fuel cell (MFC), and Hydrocotyle vulgaris L. ecological floating bed-microbial fuel cell (PEFB-MFC) to investigate the efficiency and mechanisms for the synchronous removal of conventional and antibiotic contaminants. Results showed that PEFB-MFC hold superior removal performance for sulfamethoxazole (61%), tetracycline (61%), CODCr (65%), NH4+-N (86%), TN (41%), and TP (51%). High-throughput sequencing indicated that Pseudomonadota and Actinomycetota were the predominant phyla in the different reactors. Metagenomic sequencing results showed that pollutant degradation-related metabolic functions, such as those involved in carbohydrate and amino acid metabolism in PEFB-MFC exhibited superior abundance compared to the other reactors. LC-MS analysis revealed sulfamethoxazole degradation occurred through active-site cleavage, and tetracycline underwent demethylation, aldehyde formation, dehydroxylation. This study offers a deeper insight into electro-enhanced PEFB on decontamination performance and functional microbial communities.

There is increasing evidence that gut metabolites have a role in the etiology of obesity. This study aimed to investigate the effects of sodium butyrate (NaB) supplementation on the expression of peroxisome proliferator-activated receptor (PPAR) gamma coactivator-1α (PGC-1α), PPAR-α, and uncoupling protein-1 (UCP-1) genes, as well as on the metabolic parameters and anthropometric indices in persons with obesity.

In this triple-blind placebo-controlled randomized clinical trial, 50 individuals with obesity were randomly assigned to NaB (600 mg/day) + hypo-caloric diet or placebo group + hypo-caloric diet for 8 weeks. The study measured the participants' anthropometric characteristics, food consumption, and feelings of hunger in addition to the serum levels of metabolic indices and the mRNA expression of the PGC-1α, PPAR-α, and UCP-1 genes in peripheral blood mononuclear cells (PBMCs).

PGC-1α and UCP-1 genes expression significantly increased in NaB group compared to the placebo at the endpoint. A significant decrease in weight, BMI, and waist circumference (WC) was observed in NaB group. Among the metabolic factors, NaB significantly decreased fasting blood sugar (FBS) (P = 0.04), low-density lipoprotein cholesterol (LDL-C) (P = 0.038) and increased high-density lipoprotein cholesterol (HDL-C) (P = 0.016). NaB could not significantly change serum GLP-1 level.

This study unveiled NaB supplementation alone cannot have significant beneficial effects on anthropometric, and biochemical factors. NaB could affect anthropometric and metabolic risk variables associated with obesity only when prescribed, along with calorie restriction.

This study was registered in the Iranian Registry of Clinical Trials ( https://en.irct.ir/trial/53968 ) on 31 January 2021 (registry number IRCT20190303042905N2).

Evidence is accumulating that short-chain fatty acids (SCFAs) produced by the gut microbiota play pivotal roles in host metabolism. They contribute to the metabolic regulation and energy homeostasis of the host not only by preserving intestinal health and serving as energy substrates but also by entering the systemic circulation as signaling molecules, affecting the gut-brain axis and neuroendocrine-immune network. This review critically summarizes the current knowledge regarding the effects of SCFAs in the fine-tuning of the pathogenesis of type 2 diabetes mellitus (T2DM) and insulin resistance, with an emphasis on the complex relationships among diet, microbiota-derived metabolites, T2DM inflammation, glucose metabolism, and the underlying mechanisms involved. We hold an optimistic view that elucidating how diet can influence gut bacterial composition and activity, SCFA production, and metabolic functions in the host will advance our understanding of the mutual interactions of the intestinal microbiota with other metabolically active organs, and may pave the way for harnessing these pathways to develop novel personalized therapeutics for glucometabolic disorders.

Radiotherapy is a method of treating cancer through radiation aimed at killing cancer cells or inhibiting their growth. However, radiotherapy has numerous side effects because it kills tumors while causing damage to normal cells or tissues. The literature shows that radiation can cause damage to heart tissue. This study found that engineered yeast that produced butyrate can maintain small intestinal barrier function by recovering GPR109A to reduce intestinal damage caused by abdominal irradiation in mice. We unexpectedly found that engineered yeast could mitigate irradiation-induced heart damage via the gut-heart axis. Mechanistically, engineered yeast enhanced taurine and nicotinamide metabolism by increasing the relative abundance of Akkermansia and Lachnospiraceae_NK4A136; then, yeast modulated cardiac function by activating the Sgcg and Nppa genes to attenuate cardiac damage induced by abdominal irradiation. Finally, we confirmed that engineered yeast mitigated cardiac damage caused by total body irradiation, which protected other vital organs through the intestinal tract. This study has a profound impact on cancer treatment, the emergence of engineered yeast will alleviate radiotherapy side effects and benefit patients.