Dysregulation of gut microbiota homeostasis can lead to various health issues. In this study, we investigated the effects of tangeretin (TAN) on gut microbiota homeostasis in a mouse model (C57BL/6J) of disease, specifically focusing on dextran sulfate sodium (DSS)-induced colitis and antibiotic-associated diarrhea through in vitro fermentation of intestinal bacteria. Our results demonstrated that TAN effectively improved the diversity and structure of the disordered microbiota, increasing the levels of beneficial bacteria such as Lachnospiraceae and Bacteroidaceae, while decreasing harmful bacteria such as Enterococcaceae and Pseudomonadaceae. Additionally, TAN enhanced the production of short-chain fatty acids (SCFAs) in disordered microbial communities. Moreover, the metabolism of TAN by intestinal microorganisms yielded two new metabolites, which exhibited an inverse-conjugate (deconjugate) role, leading to the production of more functional substances with high bioactivity. These findings provide a scientific basis for the potential use of TAN as a prebiotic to regulate intestinal microbiota.

Currently, there are fewer studies on the intestinal microbes of wild zokors, and it is unclear how zokors adapt to special underground environments by regulating their intestinal microbes. Here, we explored the function of intestinal microbes of Eospalax cansus and Eospalax rothschildi based on metagenomics.

Both zokor species have similar intestinal microbial composition, but E. cansus has a higher proportion of bacteria involved in carbohydrate degradation. Functional analysis based on KEGG and CAZy databases indicated that the intestinal microbes of E. cansus harboured stronger carbohydrate degradation ability, mainly in starch and sucrose metabolism, and further in cellulose degradation. Furthermore, the cellulase activity was significantly higher in E. cansus than that in E. rothschildi. Eospalax cansus has a stronger microbial fermentation ability due to an increase in fibre-degrading bacteria like unclassified_f_Lachnospiraceae, Ruminococcus, and Clostridium. In addition, the dominant bacteria isolated from zokor were Bacillus, some of which could degrade both cellulose and hemicellulose.

Metagenomic analysis and bacterial isolation experiments indicate that E. cansus has a stronger microbial cellulose-degrading capacity, possibly as an adaptation to its limited food resources underground. © 2024 Society of Chemical Industry.

To investigate associations between fecal microbiota, short-chain fatty acids (SCFAs), and the efficacy of recombinant human growth hormone (rhGH) treatment in children with growth hormone deficiency (GHD) or idiopathic short stature (ISS).

A 2-phase cohort study was conducted. Phase I included 102 participants (GHD: n = 33, ISS: n = 28, controls: n = 41) for cross-sectional analysis using 16S rRNA sequencing and targeted metabolomics to compare microbial diversity, predicted metabolic pathways, and SCFA levels. Phase II longitudinally monitored 61 rhGH-treated children (GHD = 33, ISS = 28) over 2 years, assessing growth velocity, IGF-1 levels, and fecal microbiota/SCFA dynamics. Statistical analyses included alpha/beta diversity metrics, LEfSe, PERMANOVA, and redundancy analysis (RDA) to link microbial/SCFA profiles with clinical outcomes.

(1). Microbiota Dysbiosis: Untreated GHD/ISS children exhibited reduced beneficial taxa (e.g., Faecalibacterium, Akkermansia) and increased pathobionts (e.g., Streptococcus, Collinsella) compared to controls (PERMANOVA: R 2 = 0.114, P = 0.001). (2). Metabolic Pathways: GHD/ISS groups showed enrichment in xenobiotic degradation (e.g., atrazine) and deficits in nutrient-associated pathways (e.g., carotenoid biosynthesis). (3). rhGH Effects: Treatment increased beneficial taxa (e.g., Bifidobacterium, Faecalibacterium) and modulated amino acid/lipid metabolism pathways (e.g., glycine-serine-threonine metabolism, P = 0.035). (4). SCFAs and Growth Velocity: Higher growth velocity percentiles correlated with elevated acetic acid (GHD-treated: 1952 ± 962.4 vs. untreated: 1290 ± 886.0 μg/g, P = 0.037) and butyric acid levels.

GHD, ISS, and healthy children have different fecal microbiota compositions and SCFA metabolisms. rhGH therapy partially restores microbial balance and alters metabolic pathways, with SCFA levels associated with treatment efficacy. These findings highlight the gut microbiome as a potential modulator of rhGH response and provide insight into microbiota-targeted therapies to improve growth outcomes (e.g., "probiotic interventions").

Due to the continued aging of the global population, cardiovascular diseases (CVDs) remain the main cause of death worldwide, with millions of fatalities from diseases, including stroke and coronary artery disease, reported annually. Thus, novel therapeutic approaches and targets are urgently required for diagnosing and treating CVDs. Recent studies emphasize the vital part of gut microbiota in both CVD prevention and management. Among these, Faecalibacterium prausnitzii (F. prausnitzii) has emerged as a promising probiotic capable of improving intestinal health. Although preliminary investigations demonstrate that F. prausnitzii positively enhances cardiovascular health, research specifically connecting this strain to CVD outcomes remains limited. Based on current research and assessment of possible clinical applications, this paper aimed to investigate the positive effects on cardiovascular health using F. prausnitzii and its metabolites. Targeting gut flora is expected to become a mainstay in CVD treatment as research develops.

Maximizing microbial functions for improving crop performance requires better understanding of the important drivers of plant-associated microbiomes. However, it remains unclear the forces that shapes microbial structure and assembly, and how plant seed-microbiome interactions impact grain quality. In this work, we characterized the seed endophytic microbial communities of malting barley from different geographical locations and investigated associations between microbial (bacterial and fungal) species diversity and malt quality traits. Host genotype, location, and interactions (genotype x location) significantly impacted the seed endophytic microbial communities. Taxonomic composition analysis identified the most abundant genera for bacterial and fungal communities to be Bacillus (belonging to phylum Firmicutes) and Blumeria (belonging to phylum Ascomycota), respectively. We observed that a greater proportion of bacterial amplicon sequence variants (bacterial ASVs) were shared across genotypes and across locations while the greater proportion of the fungal ASVs were unique to each genotype and location. Association analysis showed a significant negative correlation between bacterial alpha diversity indices (Faith PD and Shannon indices) and malt quality traits for barley protein (BP), free amino nitrogen (FAN), diastatic power (DP) and alpha amylase (AA), while fungal alpha diversity (Shannon and Simpson) showed significant negative relationship with β-D-glucan content. In addition, some bacterial and fungal genera were significantly associated with malt extract (ME) -a key trait for maltsters and brewers. We conclude that barley genotype, location, and their interactions shape the seed endophytic microbiome and is key to microbiome manipulation and management during barley production and/or malting.

The gut microbiome and its metabolites may be important role in regulating the pathogenesis of obesity. This study aimed to characterize the gut microbiome and short-chain fatty acid (SCFA) metabolome in obese children. This case-control study recruited children aged 7‒14 years and divided them into a normal group (NG) and an obese group (OG) based on their body mass index. Whole-genome shotgun metagenomic analysis was performed on fecal samples from the OG and NG groups to characterize the signatures and functional potential of the gut microbiota. Serum metabolite profiles were analyzed using high-performance liquid chromatography/mass spectrometry (LC/MS). The Statistical Package for the Social Sciences (SPSS, version 26) and R software were used for data analysis. A total of 99 children were recruited, with 49 in the OG and 50 in the NG. At the phylum level, Proteobacteria were significantly more abundant in children in the OG than those in the NG. At the genus level, Oscillibacter and Alistipes were significantly lower in children in the OG than those in the NG. Caproate levels significantly increased, whereas butyrate and isobutyrate levels decreased in children in the OG than those in the NG. Kyoto encyclopedia of genes and genomes (KEGG) functional analysis revealed 28 enriched KEGG pathways, of which/with the phosphotransferase system (PTS) and enhanced biofilm formation by Escherichia coli were particularly significant in the OG. Spearman's correlation analysis indicated that the genus Oscillibacter and species Clostridium_sp._CAG:302 connect serum metabolites and the gut microbiota in childhood obesity. Childhood obesity is correlated with the symbiotic status of the gut microbiota. The microbiota influences human metabolism via specific pathways, particularly butyrate, caproate, and the genus Oscillibacter, all closely associated with obesity.

Zokor is a group of subterranean rodents that are adapted to underground life and feed on plant roots. Here, we investigated the intestinal microbes of five zokor species (Eospalax cansus, Eospalax rothschildi, Eospalax smithi, Myospalax aspalax, and Myospalax psilurus) using 16S amplicon technology combined with bioinformatics. Microbial composition analysis showed similar intestinal microbes but different proportions among five zokor species, and their dominant bacteria corresponded to those of herbivores. To visualize the relationships among samples, PCoA and PERMANOVA tests showed that the intestinal microbes of zokors are largely clustered by host species, but less so by genetics and geographical location. To find microbes that differ among species, LefSe analysis identified Lactobacillus, Muribaculaceae, Lachnospiraceae_NK4A136_group, unclassified_f_Christensenellaceae, and Desulfovibrio as biomarkers for E. cansus, E. rothschildi, E. smithi, M. aspalax, and M. psilurus, respectively. PICRUSt metagenome predictions revealed enriched microbial genes for carbohydrate and amino acid metabolism in E. cansus and E. smithi, and for cofactor and vitamin metabolism as well as glycan biosynthesis and metabolism in E. rothschildi, M. aspalax, and M. psilurus. Our results demonstrated differences in the microbial composition and functions among five zokor species, potentially related to host genetics, and host ecology including dietary habits and habitat environment. These works would provide new insight into understanding how subterranean zokors adapt to their habitats by regulating intestinal microbes.

Metal exposures are closely related to childhood developmental health. However, their effects on the childhood gut microbiome, which also impacts health, are largely unexplored using microbiome multiomics including the metagenome and metatranscriptome. This study examined the associations of fecal profiles of metal/element exposures with gut microbiome species and active functional pathways in 8- to 12-year-old children (N = 116) participating in the GESTation and Environment (GESTE) cohort study. We analyzed 19 stool metal and element concentrations (B, Na, Mg, Al, K, Ca, V, Cr, Mn, Fe, Co, Ni, Cu, Zn, As, Mo, Cd, Ba, and Pb). Covariate-adjusted linear regression models identified several significant microbiome associations with continuous stool metal/element concentrations. For instance, Zn was positively associated with Turicibacter sanguinis (coef = 1.354, q-value = 0.039) and negatively associated with Eubacterium eligens (coef = -0.794, q-value = 0.044). Higher concentrations of Cd were associated with lower Eubacterium eligens (coef = -0.774, q-value = 0.045). Additionally, a total of 490 significant functional pathways such as biosynthesis and degradation/utilization/assimilation were identified, corresponding to different functions, including amino acid synthesis and carbohydrate degradation. Our results suggest links among metal exposures, pediatric gut microbiome multiomics, and potential health implications. Future work will further explore their relation to childhood health.

Nowadays, obesity has become a major health issue. In addition to negatively affecting body composition and metabolic health, recent evidence shows unfavorable shifts in gut microbiota in individuals with obesity. However, the effects of weight loss on gut microbes and metabolites remain controversial. Therefore, the purpose of this study was to investigate the effects of a 12-week program on gut microbiota and metabolic health in patients with obesity.

We conducted a controlled trial in 23 male and female patients with obesity. Twelve participants completed a 12-week program of caloric restriction combined with strength and HIIT training (INT, pre-BMI 37.33 ± 6.57 kg/m2), and eleven participants were designated as non-intervention controls (pre-BMI 38.65 ± 8.07 kg/m2). Metagenomic sequencing of the V3-V4 region of the 16S rDNA gene from fecal samples allowed for gut microbiota classification. Nuclear magnetic resonance spectroscopy characterized selected serum and fecal metabolite concentrations.

Within INT, we observed a significant improvement in body composition; a significant decrease in liver enzymes (AST, ALT, and GMT); a significant increase in the relative abundance of the commensal bacteria (e.g., Akkermansia muciniphila, Parabacteroides merdae, and Phocaeicola vulgatus); and a significant decrease in the relative abundance of SCFA-producing bacteria (e.g., the genera Butyrivibrio, Coprococcus, and Blautia). In addition, significant correlations were found between gut microbes, body composition, metabolic health biomarkers, and SCFAs. Notably, the Random Forest Machine Learning analysis identified predictors (Butyrivibrio fibrisolvens, Blautia caecimuris, Coprococcus comes, and waist circumference) with a moderate ability to discriminate between INT subjects pre- and post-intervention.

Our results indicate that a 12-week caloric restriction combined with strength and HIIT training positively influences body composition, metabolic health biomarkers, gut microbiota, and microbial metabolites, demonstrating significant correlations among these variables. We observed a significant increase in the relative abundance of bacteria linked to obesity, e.g., Akkermansia muciniphila. Additionally, our study contributes to the ongoing debate about the role of SCFAs in obesity, as we observed a significant decrease in SCFA producers after a 12-week program.

The trial was registered on [05/12/2014] with ClinicalTrials.gov (No: NCT02325804).

Experiences of caregiving-related adversity are common and one of the strongest predictors of internalizing psychopathology (i.e., anxiety and depression). Specifically, individuals who have been exposed to such early adversities have altered affective neurodevelopment, impaired memory systems, increased risk of developing internalizing disorders, greater inflammation, and differences in gastrointestinal (gut) microbiome composition. Crucially, the gut microbiome undergoes a sensitive period of development that precedes neural and immune sensitive periods, thus making it a potentially fruitful target for intervention. Though previous work has assessed neural, immune, and gut microbiome systems in individuals exposed to early adversity, studies have primarily looked at these biological systems independently. The Mind, Brain, and Body study (MBB) implements multimodal and longitudinal design to assess how changes in the gut microbiome following caregiving-related adversity may underlie altered affective neurodevelopment, memory, and immune functioning in youth and contribute to internalizing symptoms. Across three waves, spread approximately 12-18 months apart, youth with and without previous experiences of caregiving-related adversity completed self-report measures of mental and physical health, provided stool, saliva, hair, and blood samples, and completed an MRI scan. Results of this study will expand our knowledge on how the gut microbiome shapes several biological and cognitive systems and motivate future work investigating the gut microbiome as potential target for intervention.

Obesity, a global public health problem, is constantly increasing, so the concerns in preventing and combating it are increasingly focused on the intestinal microbiota. It was found that the microbiota is different in lean people compared to obese individuals, but the exact mechanisms by which energy homeostasis is influenced are still incompletely known. Numerous studies show the involvement of certain bacterial species in promoting obesity and associated diseases such as diabetes, hypertension, cancer, etc. Our aim is to summarize the main findings regarding the influence of several factors such as lifestyle changes, including diet and bariatric surgery, on the diversity of the gut microbiota in obese individuals. The second purpose of this paper is to investigate the potential effect of various microbiota modulation techniques on ameliorating obesity and its comorbidities. A literature search was conducted using the PubMed database, identifying articles published between 2019 and 2024. Most studies identified suggest that obesity is generally associated with alterations of the gut microbiome such as decreased microbial diversity, an increased Firmicutes-to-Bacteroidetes ratio, and increased SCFAs levels. Our findings also indicate that gut microbiota modulation techniques could represent a novel strategy in treating obesity and related metabolic diseases. Although some mechanisms (e.g., inflammation or hormonal regulation) are already considered a powerful connection between gut microbiota and obesity development, further research is needed to enhance the knowledge on this particular topic.

Epigallocatechin gallate (EGCG) has demonstrated potential effects on obesity-induced precocious puberty, but the underlying mechanisms remain unclear. Female mice were randomly assigned into control (CON), EGCG-treated (EGCG), high-fat diet (HFD), and HFD with EGCG treatment (HFDEGCG) groups. Key measurements included body weight, vaginal opening time, and serum sex hormone levels. The gut microbiota was analyzed through 16S rRNA sequencing, fecal metabolites were assessed via metabolomics, and the hypothalamic transcriptome was examined using RNA sequencing. EGCG mitigated weight gain and delayed vaginal opening in mice with obesity-induced precocious puberty. Additionally, it reduced serum estradiol levels and decreased the number of mature ovarian follicles in the HFDEGCG group compared to the HFD group. EGCG treatment partially reversed HFD-induced dysbiosis by increasing the abundance of beneficial bacteria such as Akkermansia. Metabolomic analysis revealed significant alterations in tryptophan metabolism, while transcriptome analysis identified genes involved in metabolic pathways. Correlation analyses underscored the importance of the gut-brain axis in mediating EGCG's effects. Overall, EGCG prevents obesity-induced precocious puberty by modulating the gut microbiota, altering metabolic pathways, and regulating hypothalamic gene expression.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is rapidly increasing in prevalence, impacting over a third of the global population. The advanced form of MASLD, Metabolic dysfunction-associated steatohepatitis (MASH), is on track to become the number one indication for liver transplant. FDA-approved pharmacological agents are limited for MASH, despite over 400 ongoing clinical trials, with only a single drug (resmetirom) currently on the market. This is likely due to the heterogeneous nature of disease pathophysiology, which involves interactions between highly individualized genetic and environmental factors. To apply precision medicine approaches that overcome interpersonal variability, in-depth insights into interactions between genetics, nutrition, and the gut microbiome are needed, given that each have emerged as dynamic contributors to MASLD and MASH pathogenesis. Here, we discuss the associations and molecular underpinnings of several of these factors individually and outline their interactions in the context of both patient-based studies and preclinical animal model systems. Finally, we highlight gaps in knowledge that will require further investigation to aid in successfully implementing precision medicine to prevent and alleviate MASLD and MASH.

Several studies have revealed the positive healthy impacts of branched-chain fatty acids (BCFAs). However, most of these studies evaluated the serum BCFAs in humans, or treatment with exogenous BCFAs in animal or in-vitro models and the health impacts of dietary BCFAs have not yet been studied. Due to positive effects of BCFAs in sport, in the current study, we aimed to investigate the association between dietary BCFAs and metabolic and inflammatory parameters among elite and subelite soccer players.

A cross-sectional study was carried out among 335 elite and subelite soccer players (196 male), aged between 20 and 45 years old. Soccer players were enrolled from 32 teams under the directive of The Chinese Football Association. Demographic, anthropometric, and dietary assessments were performed and laboratory measurement including serum lipids, glycemic markers, and high-sensitivity C-reactive protein was measured.

Those with the highest dietary BCFAs consumption had higher appetite (p = .009). Also, high consumption of dietary BCFAs was associated with lower diastolic blood pressure (odds ratio: 0.958; confidence interval: 0.918-0.999; p = .046) and low high-sensitivity C-reactive protein concentrations in the third tertile of dietary BCFAs (odds ratio: 0.431; confidence interval: 0.300-0.618; p < .001). No other association between biochemical variables and dietary BCFAs was found.

As shown in the current study, higher dietary BCFAs consumption was associated with lower diastolic blood pressure and inflammation. Due to very limited number of studies, further studies are needed to have a better perspective of these associations and their underlying mechanisms.

Short chain fatty acids (SCFA) exist in dietary foods and are produced by the fermentation of gut microbiota, and are considered an important element for regulating host health. Through blood circulation, SCFA produced in the gut and obtained from foods have an impact on the intestinal health as well as vital organs of the host. It has been recognized that the gut is the "vital organ" in the host. As the gut microbial metabolites, SCFA could create an "axis" connecting the gut and to other organs. Therefore, the "gut-organ axes" have become a focus of research in recent years to analyze organism health. In this review, we summarized the sources, absorption properties, and the function of SCFA in both gut and other peripheral tissues (brain, kidney, liver, lung, bone and cardiovascular) in the way of "gut-organ axes". Short chain fatty acids exert both beneficial and pathological role in gut and other organs in various ways, in which the beneficial effects are more pronounced. In addition, the beneficial effects are reflected in both preventive and therapeutic effects. More importantly, the mechanisms behinds the gut and other tissues provided insight into the function of SCFA, assisting in the development of novel preventive and therapeutic strategies for maintaining the host health.

The gastrointestinal tract is where the majority of gut microbiota settles; therefore, the composition of the gut microbiota and the changes in metabolites, as well as their modulatory effects on the immune system, have a very important impact on the development of gastrointestinal diseases. The purpose of this article was to review the role of the gut microbiota in the host environment and immunometabolic system and to summarize the beneficial effects of botanical active ingredients on gastrointestinal cancer, so as to provide prospective insights for the prevention and treatment of gastrointestinal diseases. A literature search was performed on the PubMed database with the keywords "gastrointestinal cancer", "gut microbiota", "immunometabolism", "SCFAs", "bile acids", "polyamines", "tryptophan", "bacteriocins", "immune cells", "energy metabolism", "polyphenols", "polysaccharides", "alkaloids", and "triterpenes". The changes in the composition of the gut microbiota influenced gastrointestinal disorders, whereas their metabolites, such as SCFAs, bacteriocins, and botanical metabolites, could impede gastrointestinal cancers and polyamine-, tryptophan-, and bile acid-induced carcinogenic mechanisms. GPRCs, HDACs, FXRs, and AHRs were important receptor signals for the gut microbial metabolites in influencing the development of gastrointestinal cancer. Botanical active ingredients exerted positive effects on gastrointestinal cancer by influencing the composition of gut microbes and modulating immune metabolism. Gastrointestinal cancer could be ameliorated by altering the gut microbial environment, administering botanical active ingredients for treatment, and stimulating or blocking the immune metabolism signaling molecules. Despite extensive and growing research on the microbiota, it appeared to represent more of an indicator of the gut health status associated with adequate fiber intake than an autonomous causative factor in the prevention of gastrointestinal diseases. This study detailed the pathogenesis of gastrointestinal cancers and the botanical active ingredients used for their treatment in the hope of providing inspiration for research into simpler, safer, and more effective treatment pathways or therapeutic agents in the field.

Dietary fiber (DF) is an important nutrient component in pig's diet that remarkably influences their growth and slaughter performance. The ability of pigs to digest DF depends on the microbial composition of the intestinal tract, particularly in the hindgut. However, studies on how DF alters the growth and slaughter performance of pigs by shaping the gut microbial composition and metabolites are still limited. Therefore, this study aimed to investigate the effects of DF on microbial composition, functions, and metabolites, ultimately altering host growth and slaughter performance using Durco × Bamei crossbred pigs supplemented with 0%, 10%, 17%, and 24% broad bean silage in the basic diet. We found that the final weight, average daily gain, fat, and lean meat weight significantly decreased with increasing DF. Pigs with the lowest slaughter rate and fat weight were observed in the 24% fiber-supplemented group. Gut microbial communities with the highest alpha diversity were formed in the 17% fiber group. The relative abundance of fiber-degrading bacteria, bile acid, and succinate-producing bacteria, including Prevotella sp., Bacteroides sp., Ruminococcus sp., and Parabacteroides sp., and functional pathways, including the butanoate metabolism and the tricarboxylic acid [TCA] cycle, significantly increased in the high-fiber groups. The concentrations of several bile acids significantly decreased in the fiber-supplemented groups, whereas the concentrations of succinate and long-chain fatty acids increased. Our results indicate that a high-fiber diet may alter the growth and slaughter performance of Durco × Bamei crossbred pigs by modulating the composition of Prevotella sp., Bacteroides sp., Ruminococcus sp., Parabacteroides sp., and metabolite pathways of bile acids and succinate.

Childhood obesity is a critical global health concern with rising prevalence and significant long-term health implications. Recent studies have implicated gut microbiota in the development and progression of obesity. This editorial analyzes the research conducted by Li et al, who utilized 16S rRNA gene sequencing to compare the gut microbiome of overweight and healthy-weight children. The study found significant differences in microbial diversity and composition between the two groups, with potential implications for understanding and managing childhood obesity. We analyzed the study's advantages and drawbacks, proposing potential areas for future research to better understand the connection between gut microbiota and obesity.

Introduction: The liver is the only organ capable of full regeneration in mammals. However, the exact mechanism of gut microbiota and metabolites derived from them relating to liver regeneration has not been fully elucidated. Methods: To demonstrate how the gut-liver axis contributes to liver regeneration, using an LC-QTOF/MS-based metabolomics technique, we examine the gut microbiota-derived metabolites in the gut content of C57BL/6J mice at various points after 2/3 partial hepatectomy (PHx). Compound identification, multivariate/univariate data analysis and pathway analysis were performed subsequently. The diversity of the bacterial communities in the gastrointestinal content was measured using 16S rRNA gene sequencing. Then, the integration analysis of gut microbiota and metabolome was performed. Results: After 2/3 PHx, the residual liver proliferated quickly in the first 3 days and had about 90% of its initial weight by the seventh day. The results of PLS-DA showed that a significant metabolic shift occurred at 6 h and 36 h after 2/3 PHx that was reversed at the late phase of liver regeneration. The α and β-diversity of the gut microbiota significantly changed at the early stage of liver regeneration. Specifically, Escherichia Shigella, Lactobacillus, Akkermansia, and Muribaculaceae were the bacteria that changed the most considerably during liver regeneration. Further pathway analysis found the most influenced co-metabolized pathways between the host and gut bacteria including glycolysis, the TCA cycle, arginine metabolism, glutathione metabolism, tryptophan metabolism, and purine and pyrimidine metabolism. Specifically, steroid hormone biosynthesis is the most significant pathway of the host during liver regeneration. Discussion: These findings revealed that during liver regeneration, there was a broad modification of gut microbiota and systemic metabolism and they were strongly correlated. Targeting specific gut bacterial strains, especially increasing the abundance of Akkermansia and decreasing the abundance of Enterobacteriaceae, may be a promising beneficial strategy to modulate systemic metabolism such as amino acid and nucleotide metabolism and promote liver regeneration.

The purpose of this study is to explore the plasma short-chain fatty acid (SCFA) concentrations in 9-12-year-old Japanese children collected in the Hokkaido study, focusing on how factors such as age, sex, and body mass index (BMI) correlate with these levels. The Hokkaido Study on Children's Health is an ongoing longitudinal study since 2002, encompassing 20,926 pregnant women in Hokkaido Prefecture, Japan, between 2003 and 2012. We contacted 1881 children aged 9-12 born between April 2006 and January 2010, and 342 non-fasting plasma samples (boys = 181, girls = 161) were obtained from this cohort, alongside assessments of their height and weight. Plasma SCFA concentrations were determined using N,N-dimethylethylenediamine derivatization method coupled with liquid chromatography-mass spectrometry. Ethyl acetate was used to extract SCFAs from plasma, and the recovery ranged from 83 % to 108 %. Our findings indicate that acetic acid had the highest concentration across all age groups and sexes. The concentrations of butyric acid, valeric acid, and hexanoic acid increased with age, peaking in 12-year-old children. Conversely, the level of 4-hydroxy valeric acid showed a decreasing trend with increasing age groups. This study also explored the correlation between BMI and SCFA concentrations, comparatively higher level of propionic acid was observed in the overweight group. The results obtained in this study enhance our understanding of the role of SCFAs in the growth and development of children and provide a foundation for future nutritional intervention and health promotion strategies.

Deciphering the gut microbiome's link to obesity is crucial. Our study characterized the gut microbial community in Egyptian children and investigated the effect of covariates on the gut microbiome, body mass index (BMI), geographical location, gender, and age. We used 16S rRNA sequencing to characterize the gut microbial communities of 49 children. We then evaluated these communities for diversity, potential biomarkers, and functional capacity. Alpha diversity of the non-obese group was higher than that of the obese group (Chao1, P = 0.006 and observed species, P = 0.003). Beta diversity analysis revealed significant variations in the gut microbiome between the two geographical locations, Cairo and Ismailia (unweighted UniFrac, P = 0.03) and between obesity statuses, obese and non-obese (weighted UniFrac, P = 0.034; unweighted UniFrac, P = 0.015). We observed a significantly higher Firmicutes/Bacteroidetes ratio in obese males than in non-obese males (P = 0.004). Interestingly, this difference was not seen in females (P = 0.77). Multivariable association with linear models (MaAsLin2) identified 8 microbial features associated with obesity, 12 associated with non-obesity, and found 29 and 13 features specific to Cairo and Ismailia patients, respectively. It has also shown one microbial feature associated with patients under five years old. MaAsLin2, however, failed to recognize any association between gender and the gut microbiome. Moreover, it could find the most predominant features in groups 2-9 but not in group 1. Another method used in the analysis is the Linear discriminant analysis Effect Size (LEfSe) approach, which effectively identified 19 biomarkers linked to obesity, 9 linked non-obesity, 20 linked to patients residing in Cairo, 14 linked to patients in Ismailia, one linked to males, and 12 linked to females. LEfSe could not, however, detect any prevalent bacteria among children younger or older than five. Future studies should take advantage of such correlations, specifically BMI, to determine the interventions needed for obesity management.

Childhood obesity with its growing prevalence worldwide presents one of the most important health challenges nowadays. Multiple mechanisms are involved in the development of this condition, as well as in its associations with various cardiometabolic complications, such as insulin resistance, diabetes, metabolic dysfunction-associated steatotic liver disease and cardiovascular diseases. Recent findings suggest that childhood obesity and associated dyslipidemia at least partly originate from epigenetic modifications that take place in the earliest periods of life, namely prenatal and perinatal periods. Hence, alterations of maternal metabolism could be fundamentally responsible for fetal and neonatal metabolic programming and consequently, for metabolic health of offspring in later life. In this paper, we will review recent findings on the associations among intrauterine and early postnatal exposure to undesirable modulators of metabolism, development of childhood obesity and later cardiometabolic complications. Special attention will be given to maternal dyslipidemia as a driven force for undesirable epigenetic modulations in offspring. In addition, newly proposed lipid biomarkers of increased cardiometabolic risk in obese children and adolescents will be analyzed, with respect to their predictive potential and clinical applicability.

Background: The escalating prevalence of hyperuricemia is emerging as a significant public health concern. The association between dietary lignans and hyperuricemia is yet to be fully elucidated. Our study aims to evaluate the relationships between dietary lignan intake and hyperuricemia among middle-aged and elderly Chinese individuals, with an additional focus on investigating the underlying mechanisms. Methods: Dietary lignan intake was measured using a validated Food Frequency Questionnaire in 3801 participants at the baseline. Among them, 2552 participants were included in the longitudinal study with a median follow-up of 10.5 years. The gut microbiota was analyzed by shotgun metagenome sequencing in 1789 participants, and the targeted fecal metabolome was determined in 987 participants using UPLC-MS/MS at the midpoint of follow-up. Results: The multivariable-adjusted HRs (95% CIs) for hyperuricemia incidence in the highest quartile (vs. the lowest quartile) of dietary intake of total lignans, matairesinol, pinoresinol, and secoisolariciresinol were 0.93 (0.78-1.10), 0.77 (0.66-0.90), 0.83 (0.70-0.97), and 0.85 (0.73-1.00), respectively. The gut microbial and fecal metabolic compositions were significantly different across the dietary lignan groups and the hyperuricemia groups. The beneficial associations between dietary lignans and hyperuricemia might be mediated by several gut microbes (e.g., Fusobacterium mortiferum and Blautia sp. CAG-257) and the downstream bile acid products (e.g., NorCA, glycochenodeoxycholic acid, and glycoursodeoxycholic acid). Conclusion: We found that dietary lignans were inversely associated with hyperuricemia incidence, and the gut microbiota-bile acid axis might mediate this association. Our findings provide new perspectives on precise therapeutic targets and underlying mechanisms for conditions associated with elevated uric acid.

Bacteria sense changes in their environment and transduce signals to adjust their cellular functions accordingly. For this purpose, bacteria employ various sensors feeding into multiple signal transduction pathways. Signal recognition by bacterial sensors is studied mainly in a few model organisms, but advances in genome sequencing and analysis offer new ways of exploring the sensory repertoire of many understudied organisms. The human gut is a natural target of this line of study: it is a nutrient-rich and dynamic environment and is home to thousands of bacterial species whose activities impact human health. Many gut commensals are also poorly studied compared to model organisms and are mainly known through their genome sequences. To begin exploring the signals human gut commensals sense and respond to, we have designed a framework that enables the identification of sensory domains, prediction of signals that they recognize, and experimental verification of these predictions. We validate this framework's functionality by systematically identifying amino acid sensors in selected bacterial genomes and metagenomes, characterizing their amino acid binding properties, and demonstrating their signal transduction potential.IMPORTANCESignal transduction is a central process governing how bacteria sense and respond to their environment. The human gut is a complex environment with many living organisms and fluctuating streams of nutrients. One gut inhabitant, Escherichia coli, is a model organism for studying signal transduction. However, E. coli is not representative of most gut microbes, and signaling pathways in the thousands of other organisms comprising the human gut microbiota remain poorly understood. This work provides a foundation for how to explore signals recognized by these organisms.

Cardio-metabolic disease is a significant global health challenge with increasing prevalence. Recent research underscores the disruption of gut microbial balance as a key factor in disease susceptibility. We aimed to characterize the gut microbiota composition and function in cardio-metabolic disease and healthy controls. For this purpose, we collected stool samples of 18 subjects (12 diseased, 6 healthy) and we performed metagenomics analysis and functional prediction using QIIME2 and PICRUSt. Furthermore, we carried out assessments of microbe-gene interactions, gene ontology, and microbe-disease associations. Our findings revealed distinct microbial patterns in the diseased group, particularly evident in lower taxonomic levels with significant variations in 14 microbial features. The diseased cohort exhibited an enrichment of Lachnospiraceae family, correlating with obesity, insulin resistance, and metabolic disturbances. Conversely, reduced levels of Clostridium, Gemmiger, and Ruminococcus genera indicated a potential inflammatory state, linked to compromised butyrate production and gut permeability. Functional analyses highlighted dysregulated pathways in amino acid metabolism and energy equilibrium, with perturbations correlating with elevated branch-chain amino acid levels-a known contributor to insulin resistance and type 2 diabetes. These findings were consistent across biomarker assessments, microbe-gene associations, and gene ontology analyses, emphasizing the intricate interplay between gut microbial dysbiosis and cardio-metabolic disease progression. In conclusion, our study unveils significant shifts in gut microbial composition and function in cardio-metabolic disease, emphasizing the broader implications of microbial dysregulation. Addressing gut microbial balance emerges as a crucial therapeutic target in managing cardio-metabolic disease burden.

It is well documented that propionic acid (PPA) produces behavioral, morphological, molecular and immune responses in rats that are characteristic of autism spectrum disorder in humans. However, whether PPA affects the ultrastructure and synaptic architecture of regions of autistic brain has not been adequately addressed. Earlier we show that single intraperitoneal (IP) injection of PPA (175 mg/kg) produces superficial changes in the spatial memory and learning of adolescent male Wistar rats. However, in neurons, synapses and glial cells of hippocampal CA1 area and medial prefrontal cortex transient (mainly) or enduring alterations were detected. In this study, we used electron microscopic morphometric analysis to test the effect of PPA on different structural parameters of axodendritic synapses of the hippocampus and prefrontal cortex. The animals were treated with a single IP injection of PPA (175 mg/kg). The length and width of synaptic active zone, the area of presynaptic and postsynaptic mitochondria, the distance between presynaptic mitochondria and the synapse active zone, the distance between postsynaptic mitochondria and postsynaptic density and the depth and opening diameter of neuronal porosome complex were evaluated. Our results show that synaptic mitochondria of the hippocampus and prefrontal cortex are the most vulnerable to PPA treatment: in both regions, the area of postsynaptic mitochondria were increased. In general, our results show that even small dose of PPA, which produces only superficial effects on spatial memory and learning is able to alter the synapse architecture in brain regions involved in cognition and autism pathogenesis. Therefore, the microbiome may be involved in the control of neurotransmission in these regions.

Polycystic ovary syndrome (PCOS) is a multifaceted disease with an intricate etiology affecting reproductive-aged women. Despite attempts to unravel the pathophysiology, the molecular mechanism of PCOS remains unknown. There are no effective or suitable therapeutic strategies available to ameliorate PCOS; however, the symptoms can be managed. In recent years, a strong association has been found between the gut microbiome and PCOS, leading to the formulation of novel ideas on the genesis and pathological processes of PCOS. Further, gut microbiome dysbiosis involving microbial metabolites may trigger PCOS symptoms via many mechanistic pathways including those associated with carbohydrates, short-chain fatty acids, lipopolysaccharides, bile acids, and gut-brain axis. We present the mechanistic pathways of PCOS-related microbial metabolites and therapeutic opportunities available to treat PCOS, such as prebiotics, probiotics, and fecal microbiota therapy. In addition, the current review highlights the emerging treatment strategies available to alleviate the symptoms of PCOS.

Rodent models and human clinical studies have shown gut microbiota-derived short-chain fatty acids (SCFAs) play roles in obesity and insulin resistance. These roles have been minimally explored in cats, where in the USA an estimated 60% of cats are overweight or obese. Overweight/obese research cats (n = 7) were transitioned from a maintenance diet to a reduced calorie diet fed ad libitum for 7 days, then calories were restricted to achieve 1-2% weight loss per week for an additional 77 days. Cats then received their original maintenance diet again for 14 days. Significant intentional weight loss was noted after calorie restriction (adjusted p < 0.0001). 16S rRNA gene amplicon sequencing and targeted SCFA metabolomics were performed on fecal samples. Fecal microbial community structure significantly differed between the four study phases (PERMANOVA p = 0.011). Fecal propionic acid was significantly higher during caloric restriction-induced weight loss (adjusted p < 0.05). Repeated measures correlation revealed the relative abundances of Prevotella 9 copri (correlation coefficient = 0.532, 95% CI (0.275, 0.717), p = 0.0002) significantly correlated with propionic acid composition. Like humans, obese cats experienced an altered microbial community structure and function, favoring propionic acid production, during caloric restriction-induced weight loss.

The larynx undergoes significant age and sex-related changes in structure and function across the lifespan. Emerging evidence suggests that laryngeal microbiota influences immunological processes. Thus, there is a critical need to delineate microbial mechanisms that may underlie laryngeal physiological and immunological changes. As a first step, the present study explored potential age and sex-related changes in the laryngeal microbiota across the lifespan in a murine model. We compared laryngeal microbial profiles of mice across the lifespan (adolescents, young adults, older adults and elderly) to determine age and sex-related microbial variation on 16s rRNA gene sequencing. Measures of alpha diversity and beta diversity were obtained, along with differentially abundant taxa across age groups and biological sexes. There was relative stability of the laryngeal microbiota within each age group and no significant bacterial compositional shift in the laryngeal microbiome across the lifespan. There was an abundance of short-chain fatty acid producing bacteria in the adolescent group, unique to the laryngeal microbiota; taxonomic changes in the elderly resembled that of the aged gut microbiome. There were no significant changes in the laryngeal microbiota relating to biological sex. This is the first study to report age and sex-related variation in laryngeal microbiota. This data lays the groundwork for defining how age-related microbial mechanisms may govern laryngeal health and disease. Bacterial compositional changes, as a result of environmental or systemic stimuli, may not only be indicative of laryngeal-specific metabolic and immunoregulatory processes, but may precede structural and functional age-related changes in laryngeal physiology.

Obesity is a persistent metabolic condition resulting from the excessive accumulation or abnormal distribution of body fat. This study aimed to establish an experimental rat model of obesity. The efficacy of treating obesity with Hedan tablets (HDT) was assessed by monitoring changes in weight, blood lipid levels, analyzing inflammatory factors, evaluating organ indices, and observing liver tissue pathology. Furthermore, we utilized 16S ribosomal RNA gene sequencing technology to explore changes in intestinal flora. In addition, GC-MS was used to measure fecal short-chain fatty acid (SCFA) content. The onset of obesity led to a significant decrease in the relative abundance of beneficial bacteria. Conversely, the administration of HDT demonstrated a substantial ability to increase the relative abundance of beneficial bacteria. Obesity resulted in a noteworthy reduction in total SCFAs, a trend significantly reversed in the HDT group. Through correlation analysis, it was determined that HDT mitigated the inflammatory response and improved blood lipid levels by augmenting the abundance of Lactobacillus, Limosilactobacillus, Ruminococcus, and Enterococcus. These particular intestinal flora were identified as regulators of SCFA metabolism, thereby ameliorating metabolic abnormalities associated with obesity. Moreover, HDT intervention elevated the overall fecal concentration of SCFAs, thereby improving metabolic disorders induced by obesity. The anti-obesity effects of HDT are likely attributable to their capacity to influence the composition of intestinal flora and boost SCFA levels in the intestine.

The relationship between gut microbiota and changes in body mass index (BMI) or pediatric overweight in early life remains unclear, and information regarding the preterm population is scarce. This study aimed to investigate how the gut microbiota at 3.5 years of age is associated with (1) later BMI at 5 years, and (2) BMI z-score variations between 2 and 5 years in children from two French nationwide birth cohorts.

Bacterial 16S rRNA gene sequencing was performed to profile the gut microbiota at 3.5 years of age in preterm children (n = 143, EPIPAGE 2 cohort) and late preterm/full-term children (n = 369, ELFE cohort). The predicted abundances of metabolic functions were computed using PICRUSt2. Anthropometric measurements were collected at 2 and 5 years of age during medical examinations or retrieved from children's health records. Statistical analyses included multivariable linear and logistic regressions, random forest variable selection, and MiRKAT.

The Firmicutes to Bacteroidetes (F/B) ratio at 3.5 years was positively associated with the BMI z-score at 5 years. Several genera were positively ([Eubacterium] hallii group, Fusicatenibacter, and [Eubacterium] ventriosum group) or negatively (Eggerthella, Colidextribacter, and Ruminococcaceae CAG-352) associated with the BMI z-scores at 5 years. Some genera were also associated with variations in the BMI z-scores between 2 and 5 years of age. Predicted metabolic functions, including steroid hormone biosynthesis, biotin metabolism, glycosaminoglycan degradation, and amino sugar and nucleotide sugar metabolism, were associated with lower BMI z-scores at 5 years. The unsaturated fatty acids biosynthesis pathway was associated with higher BMI z-scores.

These findings indicate that the gut microbiota at 3.5 years is associated with later BMI during childhood, independent of preterm or term birth, suggesting that changes in the gut microbiota that may predispose to adult obesity begin in early childhood.

In this study, the strain Lactiplantibacillus plantarum DLPT4 was investigated for the immunostimulatory activity in cyclophosphamide (CTX)-induced immunosuppressed BALB/c mice. L. plantarum DLPT4 was administered to BALB/c mice by oral gavage for 30 days, and CTX was injected intraperitoneally from the 25th to the 27th days. Intraperitoneal injection of CTX caused damage to the thymic cortex and intestines, and the immune dysfunction of the BALB/c mice. L. plantarum DLPT4 oral administration exerted immunoregulating effects evidenced by increasing serum immunoglobulin (IgA, IgG, and IgM) levels and reducing the genes expression of pro-inflammatory factors (IL-6, IL-1β, and TNF-α) of the CTX-induced immunosuppressed mice. The results of the metagenome-sequencing analysis showed that oral administration of L. plantarum DLPT4 could regulate the intestinal microbial community of the immunosuppressed mice by changing the ratio of Lactiplantibacillus and Bifidobacterium. Meanwhile, the abundance of carbohydrate enzyme (CAZyme), immune diseases metabolic pathways, and AP-1/MAPK signaling pathways were enriched in the mice administrated with L. plantarum DLPT4. In conclusion, oral administration of L. plantarum DLPT4 ameliorated symptoms of CTX-induced immunosuppressed mice by regulating gut microbiota, influencing the abundance of carbohydrate esterase in the intestinal flora, and enhancing immune metabolic activity. L. plantarum DLPT4 could be a potential probiotic to regulate the immune response.

Generally, fasting and refeeding confer anti- and proinflammatory effects, respectively. In humans, these caloric-load interventions function, in part, via regulation of CD4+ T cell biology. However, mechanisms orchestrating this regulation remain incomplete. We employed integrative bioinformatics of RNA sequencing and high-performance liquid chromatography-mass spectrometry data to measure serum metabolites and gene expression of peripheral blood mononuclear cells isolated from fasting and refeeding in volunteers to identify nutrient-load metabolite-driven immunoregulation. Propionate, a short chain fatty acid (SCFA), and the SCFA-sensing G protein-coupled receptor 43 (ffar2) were coordinately and inversely regulated by fasting and refeeding. Propionate and free fatty acid receptor agonists decreased interferon-γ and interleukin-17 and significantly blunted histone deacetylase activity in CD4+ T cells. Furthermore, propionate blunted nuclear factor κB activity and diminished interleukin-6 release. In parallel, propionate reduced phosphorylation of canonical T helper 1 (TH1) and TH17 regulators, STAT1 and STAT3, respectively. Conversely, knockdown of free fatty acid receptors significantly attenuated the anti-inflammatory role of propionate. Interestingly, propionate recapitulated the blunting of CD4+ TH cell activation in primary cells from obese individuals, extending the role of this metabolite to a disease associated with low-grade inflammation. Together, these data identify a nutrient-load responsive SCFA-G protein-coupled receptor linked pathway to regulate CD4+ TH cell immune responsiveness.

Accumulating evidence suggests that alterations in gut microbiota composition and diversity are associated with liver cirrhosis. But whether gut microbiota promotes or hampers the genesis and development of liver cirrhosis remains vague.

This study aimed to establish a causal relationship between gut microbiota and the development of liver fibrosis and cirrhosis. To achieve this, we employed a 2-sample Mendelian randomization (MR) analysis utilizing genome-wide association study (GWAS) summary statistics. This approach enabled us to assess the potential impact of gut microbiota on liver cirrhosis.

The independent genetic instruments of gut microbiota were obtained from the MiBioGen (up to 18,340 participants), which is a large-scale genome-wide genotype and 16S fecal microbiome dataset. Cirrhosis data were derived from the FinnGen biobank analysis, which included 214,403 individuals of European ancestry (811 patients and 213,592 controls). To assess the causal relationship between gut microbiota and cirrhosis, we applied 4 different methods of MR analysis: the inverse-variance weighted method (IVW), the MR-Egger regression, the weighted median analysis (WME), and the weighted mode. Furthermore, sensitivity analyses were conducted to evaluate heterogeneity and horizontal pleiotropy.

Results of MR analyses provided evidence of a causal association between 4 microbiota features and cirrhosis, including 2 family [Lachnosiraceae: odds ratio (OR): 1.82626178; 95% confidence interval (CI): 1.05208209, 3.17012532; P = 0.0323194; Lactobacillaceae : OR: 0.62897502; 95% CI: 0.42513162, 0.93055788; P = 0.02033345] and 2 genus [Butyricicoccus: OR: 0.41432215; 95% CI: 0.22716865, 0.75566257; P = 0.0040564; Lactobacillus: OR: 0.6663767; 95% CI: 0.45679511, 0.97211616; P = 0.03513627].

Our findings offered compelling evidence of a causal association between gut microbiota and cirrhosis in European population and identified specific bacteria taxa that may regulate the genesis and progression of liver fibrosis and cirrhosis, may offer a new direction for the treatment of cirrhosis.

The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing annually, and emerging evidence suggests that the gut microbiota plays a causative role in the development of NAFLD. However, the role of gut microbiota in the development of NAFLD remains unclear and warrants further investigation. Thus, C57BL/6J mice were fed a high-fat diet (HFD), and we found that the HFD significantly induced obesity and increased the accumulation of intrahepatic lipids, along with alterations in serum biochemical parameters. Moreover, it was observed that the HFD also impaired gut barrier integrity. It was revealed via 16S rRNA gene sequencing that the HFD increased gut microbial diversity, which enriched Colidextribacter, Lachnospiraceae-NK4A136-group, Acetatifactor, and Erysipelatoclostridium. Meanwhile, it reduced the abundance of Faecalibaculum, Muribaculaceae, and Coriobacteriaceae-UCG-002. The predicted metabolic pathways suggest that HFD enhances the chemotaxis and functional activity of gut microbiota pathways associated with flagellar assembly, while also increasing the risk of intestinal pathogen colonization and inflammation. And the phosphotransferase system, streptomycin biosynthesis, and starch/sucrose metabolism exhibited decreases. These findings reveal the composition and predictive functions of the intestinal microbiome in NAFLD, further corroborating the association between gut microbiota and NAFLD while providing novel insights into its potential application in gut microbiome research for NAFLD patients.

The gut microbiota plays a critical role in human growth and development as well as the regulation of human pathophysiological processes. According to research, the gut microbiota controls the host's growth and development in areas such as nutrition, metabolism, endocrine hormones, and immune modulation. The human gut microbiota has an important role in child and adolescent growth, especially when nutritional conditions are poor. In this review, we focus on recent findings about the gut microbiota's influence on child growth, including the relationship between the gut microbiota and linear growth during pregnancy, infancy, childhood, and adolescence. Furthermore, we also review some mechanisms by which intestinal flora influence the host's linear growth. Although the data supports a link between intestinal flora and linear development in children, our review has limitations that prohibit us from fully verifying the causal relationship between gut flora and linear development in children. Improving the gut microbiota, in conjunction with renutrition techniques, has the potential to ameliorate the growth and development impairments currently associated with chronic illness and malnutrition in children.

The problem of rapid decline in egg production performance and poor egg quality is a key obstacle to improving the economic benefits of laying hens. Garcinol is an antioxidant polyphenol plant extract that has multiple physiological functions. Diets with the appropriate amount of garcinol might be able to improve the performance traits and health of late laying hens. Therefore, this study was conducted to evaluate the utilization of garcinol in late laying hens. A total of 400 healthy 59-wk-old Tingfen No. 6 hens were randomly allocated into 4 dietary treatment groups and fed a basal diet supplemented with 0, 100, 300, and 500 mg/kg garcinol for 12 wk, denoted the Con, LG, MG, and HG groups, respectively. The results showed that the addition of garcinol in the diet tended to increase the egg production rate compared with that of the control group (P = 0.080), while the average egg weight was significantly lower (P < 0.05) during the whole period of the experiment. The results showed that MG group hens had higher egg quality and strengthened antioxidant capacity in their serum (P < 0.05). Moreover, the laying hens in the MG group had significantly decreased crypt depth (CD) and increased villus height (VH) in the jejunum and ileum (P < 0.05), as well as an increased ratio of VH to CD (P < 0.05) and increased expression levels of Occludin (P < 0.05) and Claudin-2 (P < 0.05) in the jejunum to improve intestinal barrier function. In addition, dietary supplementation with garcinol influenced the cecal microbiota of laying hens, which was characterized by changes in the microbial community composition, including increased abundances of Firmicutes, Romboutsia, and Ruminococcus torques. In conclusion, dietary 300 mg/kg garcinol supplementation could increase the egg production and egg quality of late laying hens, which may be attributed to the antioxidant effects of garcinol and the improvement of intestinal morphology and epithelial barrier function as well as the regulation of mucosal immune status by altering microbial composition.

Cystic Fibrosis-related gut dysbiosis (CFRGD) has become a recognised complication in children with this condition, and current evidence remains insufficient to guide the selection of probiotic strains for supplementation treatments. The aim of this study was to characterise the effect of three probiotic strains on CFRGD by means of a dynamic in vitro simulation of the colonic fermentation (SHIME®). The configuration of the system included three bioreactors colonised with the faecal inoculum of a child with cystic fibrosis. For 20 days, each bioreactor was supplied daily with either Lacticaseibacillus rhamnosus GG (ATCC 53103 TM), Limosilactobacillus reuteri (DSM 17938) or Lactiplantibacillus plantarum (DSM 22266). The baseline microbiota was characterised by a high abundance of Prevotella, Faecalibacterium and Acidaminococcus genera. After 20 days of supplementation, L. rhamnosus and L. plantarum reduced Prevotella significantly, and the three strains led to increased Faecalibacterium and Bifidobacterium and decreased Acidaminococcus, with some of these changes being maintained 10 days after ceasing supplementation. The metabolic activity remained unaltered in terms of short-chain fatty acids, but branched-chain fatty acids showed a significant decrease, especially with L. plantarum. Additionally, ammonia decreased at 20 days of supplementation, and lactate continuously increased with the three strains. The effects on colonic microbiota of L. rhamnosus, L. reuteri or L. plantarum were established, including increased beneficial bacteria, such as Faecalibacterium, and beneficial metabolites such as lactate; and on the other hand, a reduction in pathogenic genera, including Prevotella or Acidaminococcus and branched-chain fatty acids, overall supported their use as probiotics in the context of CFRGD.

Non-alcoholic fatty liver disease (NAFLD) is a common clinical disease, and its pathogenesis is closely linked to oxidative stress and gut microbiota dysbiosis. Recently accumulating evidence indicates that the thioredoxin and glutaredoxin systems, the two thiol-redox dependent antioxidant systems, are the key players in the NAFLD's development and progression. However, the effects of gut microbiota dysbiosis on the liver thiol-redox systems are not well clarified. This review explores the role and mechanisms of oxidative stress induced by bacteria in NAFLD while emphasizing the crucial interplay between gut microbiota dysbiosis and Trx mediated-redox regulation. The paper explores how dysbiosis affects the production of specific gut microbiota metabolites, such as trimethylamine N-oxide (TMAO), lipopolysaccharides (LPS), short-chain fatty acids (SCFAs), amino acids, bile acid, and alcohol. These metabolites, in turn, significantly impact liver inflammation, lipid metabolism, insulin resistance, and cellular damage through thiol-dependent redox signaling. It suggests that comprehensive approaches targeting both gut microbiota dysbiosis and the thiol-redox antioxidant system are essential for effectively preventing and treating NAFLD. Overall, comprehending the intricate relationship between gut microbiota dysbiosis and thiol-redox systems in NAFLD holds significant promise in enhancing patient outcomes and fostering the development of innovative therapeutic interventions.

Rodent models and human clinical studies have shown gut microbiota-derived short-chain fatty acids (SCFAs) play roles in obesity and insulin resistance. These roles have been minimally explored in cats, where in the USA an estimated 60% of cats are overweight or obese. Overweight/obese research cats (n = 7) were transitioned from a maintenance diet to a reduced calorie diet fed ad libitum for seven days, then calories were restricted to achieve 1-2% weight loss per week for an additional 77 days. Cats then received their original maintenance diet again for 14 days. Significant intentional weight loss was noted after calorie restriction (adjusted p < 0.0001). 16S rRNA gene amplicon sequencing and targeted SCFA metabolomics were performed on fecal samples. Fecal microbial community structure significantly differed between the four study phases (PERMANOVA p = 0.011). Fecal propionic acid was significantly higher during diet-induced weight loss (adjusted p < 0.05). Spearman correlation revealed the relative abundances of Prevotella 9 copri (ρ = 0.6385, p = 0.0006) and Blautia caecimuris (ρ = 0.5269, p = 0.0068) were significantly correlated with propionic acid composition. Like humans, obese cats experienced an altered microbial community structure and function, favoring propionic acid production, during diet-induced weight loss.