Recent studies have focused on the relationship between obesity and gut microbiota. This study aims to identify fecal components and gut bacterial species associated with different BMI categories. In this study, 538 participants aged ≥18 years were categorized into underweight, normal, and obese groups based on BMI (cutoffs: 18.5 and 25.0 kg/m²). We compared 30 fecal components among these groups and calculated correlation coefficients between each component and BMI. Participants were then divided into quartiles based on fecal component levels correlated with BMI, and the prevalence ratio (PR) of obesity was calculated, adjusted for confounding factors. We also analyzed the composition and diversity of gut microbiota and bacterial gene expression among the quartiles for each fecal component. Fecal glycocholic acid (GCA) showed a significant positive correlation with BMI. The PR for obesity in the highest quartile of fecal GCA was 3.30 (95% CI, 1.21-9.54), indicating a significantly higher risk of obesity compared to the lowest quartile. Gut microbiota analysis revealed significant differences in the abundance of Ruminococcaceae Incertae Sedis, Faecalibacterium, and Methanobrevibacter, with Methanobrevibacter being absent in the higher quartiles of fecal GCA. Additionally, gene expression for enzymes involved in the deconjugation of conjugated bile acids, including GCA, was downregulated in the highest quartile. Increased fecal GCA levels are positively correlated with obesity, alongside a depletion of archaea.

Lactucin and lactucopicrin are the characteristic lipid-lowering active components found in Cichorium glandulosum. However, their effects and underlying mechanisms in obesity remain unclear. In the present study, C57BL/6J mice were simultaneously subjected to a high-fat diet (HFD) and treated with drugs to investigate the impacts of lactucin and lactucopicrin on HFD-induced obese mice. The results demonstrated that in HFD obese mice, lactucin and lactucopicrin significantly decreased body weight and the weights of adipose tissues, improved serum metabolic parameters, and increased the content of irisin. Regarding the intermediate metabolites of intestinal flora, which are closely associated with white adipose tissue (WAT) browning, lactucin and lactucopicrin treatment led to a reduction in the levels of 12-α-OH/non-12-α-OH bile acids (BAs) and also tended to enhance the levels of short-chain fatty acids (SCFAs). qRT-PCR results indicated that lactucin and lactucopicrin treatment elevated the expression levels of genes related to beige fat markers, thermogenesis, mitochondrial biogenesis, and lipolysis in WAT, as well as those of thermogenesis and lipolysis genes in brown adipose tissue (BAT). Western blot analysis revealed that lactucin and lactucopicrin up-regulated the expression of uncoupling protein 1 (UCP1), the core protein in thermogenesis, in both WAT and BAT. Moreover, they also up-regulated the expression levels of AMP-activated kinase (AMPK), sirtuin 1 (SIRT1), and PPARγ coactivator 1-alpha (PGC-1α), which are key pathway proteins involved in WAT browning. Furthermore, 16S rRNA sequencing results showed that in HFD obese mice, lactucin and lactucopicrin improved the composition and function of the intestinal microbiota. In conclusion, lactucin and lactucopicrin may promote WAT browning by activating the AMPK/SIRT1/PGC-1α pathway, thereby ameliorating obesity in HFD mice.

We hypothesized that food sensitization in children could be linked to specific gut microbiota. The objective of this study is to assess a group of children with egg white sensitization (ES) from the microbiological and biochemical-metabolic standpoint, applying the microbiota and metabolomics approach to studying the intestinal contents of the feces.

Twenty-eight toddlers with ES (mean age 13.08 months) and 24 healthy controls (mean age 12.85 months) were recruited for feces collection, serum IgE measurement, gut microbiota and metabolomics analysis. Individual microbial diversity and composition were analyzed via targeting the 16S rRNA gene hypervariable V3-V5 regions. The metabolite profiles of human feces were explored by 1 H nuclear magnetic resonance.

Children with ES exhibited relatively high levels of Firmicutes at the phylum level and relatively low levels of Bacteroidetes. Moreover, children with ES exhibited significantly reduced overall gut microbiota diversity and richness compared with healthy children. At the family level, we observed significant increases in the numbers of Clostridiaceae, Lachnospiraceae, Pasteurellaceae and Ruminococcaceae in children with ES. Egg white sensitivity increases orotic acid, nicotinate, methyl succinate, urocanic acid, xanthine, amino acids (tyrosine, lysine, tryptophan, phenylalanine) and short-chain fatty acids ( n -butyrate, valerate) levels according to the results of metabolomics analysis.

In summary, some specific families and genera (dysbiosis) are enriched in the gut microbiota, and increases in the mean concentrations of organic compounds in the fecal metabolite profile are associated with ES in children. These findings may provide evidence of potential strategies to control the development of ES or other atopies by modifying the gut microbiota.

This study elucidated the mechanisms underlying the immunoregulatory and gut-microbiota-modulating effects of Flammulina velutipes residue polysaccharide (FVRP) using cyclophosphamide (CTX)-induced mouse models. FVRP supplementation alleviated CTX-induced intestinal damage and boosted antioxidant enzyme activity and cytokine secretion. Additionally, FVRP enhanced the diversity and total species richness of the gut microbiota, promoting the proliferation of beneficial bacteria (e.g., Prevotellaceae), while reducing the abundance of CTX-derived bacteria (Lachnospiraceae and Rikenellaceae). FVRP facilitates the accumulation of short-chain fatty acids. Untargeted metabolomic analyses of cecal content revealed that FVRP treatment notably restored the levels of 32 endogenous metabolites altered by CTX. Based on a pseudosterility mice model, fecal microbiota transplantation (FMT), and fecal filtrate transplantation (FFT), gut microbiota and associated metabolites were demonstrated to play a crucial role in the immunomodulatory and protective effects of FVRP against intestinal injury. In conclusion, FVRP exhibits significant potential as an immune enhancer and natural therapeutic agent for alleviating intestinal inflammatory conditions.

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.

Purpose: The role of the gut microbiomes has been emphasized in the pathogenesis of obese asthma (OA). However, the molecular mechanism of airway dysfunction underlying OA has not yet been fully elucidated. The effects of microbiomes on arginine metabolism in relation to lung functions and a novel method for delivering arginine to lung tissue based on arginine-loaded red blood cell (RBC)-derived nanovesicles (NVs) (NVArg) will be investigated. Materials and Methods: Inflammatory status, amino acid profiles, and microbial diversity were evaluated in 20 adult patients with OA compared to 30 adult patients with non-OA (NOA) and 10 healthy control (HC) groups. Changes in gut or lung microbial composition that altered arginine metabolism in relation to airway inflammation were investigated in an OA mouse model in vivo. Additionally, this study evaluated the delivery of arginine to lung tissue utilizing NVArg in vivo and in vitro. Results: Significantly increased Bacteroides abundance but decreased serum arginine concentration with lower forced exhaled volume at 1 s (FEV1) (%) was noted in the OA group compared to the NOA and HC groups. In mouse experiments, when OA mice were given living bacteria from normal control (NC) mice, lung arginine concentration and airway resistance were restored. However, the administration of arginine or its metabolite (citrulline) did not increase the arginine levels in the lung tissues. We therefore created NVArg, which successfully delivered arginine into the cytoplasm of the airway epithelial cell line in vitro. Oral administration of NVArg for OA mice significantly induced the AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) pathways in airway epithelial cells, which reduced airway resistance and inflammation. Conclusion: These findings suggest that microbiomes contribute to airway dysfunction by regulating arginine metabolism, whereas NVArg treatment may be a potential option for managing OA.

Diet plays an important role in the composition of gut microbiota. Emerging research suggests that bone homeostasis can also be influenced by the gut microbiota. The aim of this study was to assess possible alterations in gut microbiota in an experimental obesity model induced by a high-fat diet (HFD) and the possible effects on parameters of bone metabolism and remodeling. Male Wistar rats were fed a HFD (60% lipids) or standard (control) diet for 14 weeks. Biochemical and hormonal parameters, bone histomorphometry, bone protein levels, and gut microbiota composition were analyzed. HFD animals exhibited a greater gut microbiota α-diversity represented by the Shannon Index and an increased relative abundance of the Proteobacteria phylum. Histomorphometry detected lower bone formation in the HFD group, accompanied by increased levels of serum and bone leptin and FGF-23 (fibroblast growth factor-23). The Shannon Index was correlated directly with bone FGF-23 (R 0.96, p = 0.04) and inversely with the osteoblastic surface (R -0.95, p = 0.04). The present study disclosed a significant increase in gut microbiota α-diversity and relative abundance of Proteobacteria phylum in obese animals fed a high-fat diet in parallel with increased levels of bone and serum leptin and FGF-23 and lower bone formation. The associations of Shannon Index with bone levels of FGF-23 and reduced osteoblastic surface suggest a link between HFD-induced higher gut microbiota diversity and low bone formation.

Obesity, characterized by excessive adipose tissue accumulation, has become a global health challenge with rapidly increasing prevalence. It contributes significantly to metabolic disorders including insulin resistance (IR). Renshen-zhuye decoction (RZD), a traditional Chinese medicine formula historically used for diabetes, shows potential for improving metabolic parameters, but its effects and mechanisms in obesity and insulin resistance remain unclear.

This study aimed to evaluate the therapeutic benefits of RZD on obesity and insulin resistance, and to elucidate the underlying mechanisms through which it improves glucose and lipid metabolism.

The role of RZD was evaluated in a high-fat diet (HFD) mouse model. The formula was characterized using UPLC-MS. Comprehensive analyses including histopathological staining, immunofluorescence, biochemical assays, 16S rRNA gene sequencing of gut microbiota, and non-targeted metabolomic analysis were performed. To validate the role of gut microbiota, we employed antibiotic treatment (ABX) to deplete intestinal flora and conducted fecal microbiota transplantation (FMT) experiments.

RZD treatment dose-dependently alleviated HFD-induced dyslipidemia and insulin resistance, improving glucose tolerance, insulin sensitivity, and energy expenditure. Gut microbiota analysis revealed that RZD significantly modulated the composition of intestinal flora and their metabolic profiles. Additionally, RZD reduced intestinal and systemic inflammation by enhancing intestinal barrier integrity, particularly through increased expression of tight junction proteins such as Occludin. Importantly, the beneficial effects of RZD on weight management and glucose homeostasis were antagonized by antibiotic intervention, while FMT experiments confirmed that these improvements were mediated through gut microbiota modulation.

This study provides new insights into RZD's modulatory effects on gut microbiota and subsequent improvements in obesity-related metabolic parameters. RZD alleviates HFD-induced obesity and insulin resistance in mice by modulating gut microbiota composition and function, which subsequently improves intestinal barrier integrity, reduces inflammation, and enhances metabolic homeostasis.

Obesity is a major global concern and is generally attributed to a combination of genetic and environmental factors. Several hypotheses have been proposed to explain the evolutionary origins of obesity epidemic, including thrifty and drifty genotypes, and changes in thermogenesis. Here, we put forward the hypothesis of metaflammation, which proposes that due to intense selection pressures exerted by environmental pathogens, specific genes that help develop a robust defense mechanism against infectious diseases have had evolutionary advantages and that this may contribute to obesity in modern times due to connections between the immune and energy storage systems. Indeed, incorporating the genetic variations of gut microbiota into the complex genetic framework of obesity makes it more polygenic than previously believed. Thus, uncovering the evolutionary origins of obesity requires a multifaceted approach that considers the complexity of human history, the unique genetic makeup of different populations, and the influence of gut microbiome on host genetics.

Brassica vegetables contain unique compounds known as glucosinolates (GSLs), which, when hydrolyzed by plant or microbial myrosinase, form bioactive isothiocyanates (ITCs) that offer health benefits to the host. The present study evaluated the impact of cooked broccoli (broccoli myrosinase inactivated) consumption on cecal microbial metabolism of glucoraphanin (GRP) in lean and obese mice and characterized the changes in cecal microbiota following broccoli-containing diets.

Twenty lean and 20 diet-induced obese (DIO) mice were randomized to consume control or cooked broccoli supplemented diets for 7 days. Cooked broccoli consumption increased ex vivo microbial GRP hydrolysis by cecal contents collected from lean and obese mice, led to increased production of sulforaphane (SF), sulforaphane-cysteine (SF-CYS), total ITC, and colonic NAD(P)H: Quinone Oxidoreductase (NQO1) activity. Further investigation revealed increased abundance of health-promoting gut microbiota, including Lachnospiraceae NK4A136 group and Dubosiella newyorkensis, following broccoli-containing diets. The Peptococcaseae family, the Blautia genus, and an amplicon sequence variation (ASV) from the Oscillospiraceae family exhibited negative correlation with total ITC production.

These finding suggest that cooked broccoli consumption enhances microbial GRP hydrolysis to produce more bioactive ITCs and inform future strategies toward altering microbial GSL metabolism to promote gut health in both lean and obese individuals.

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.

Alzheimer's Disease (AD) is a debilitating neurocognitive disorder with an unclear underlying mechanism. Recent studies have implicated gut microbiota dysbiosis with the onset and progression of AD. The connection between gut microbiota and AD can significantly affect the prevention and treatment of AD patients. This systematic review summarizes primary outcomes of human and mouse AD models concerning gut microbiota alterations. A systematic literature search in February through March 2023 was conducted on PubMed, Embase, and Web of Science. We identified 711 as potential manuscripts of which 672 were excluded because of irrelevance to the identified search criteria. Primary outcomes include microbiota compositions of control and AD models in humans and mice. In total, 39 studies were included (19 mouse and 20 human studies), published between 2017 and 2023. We included studies involving well-established mice models of AD (5xFAD, 3xTg-AD, APP/PS1, Tg2576, and APPPS2) which harbor mutations and genes that drive the formation of Aß plaques. All human studies were included on those with AD or mild cognitive impairment. Among alterations in gut microbiota, most studies found a decreased abundance of the phyla Firmicutes and Bifidobacteria, a genus of the phylum Actinomycetota. An increased abundance of the phyla Bacteroidetes and Proteobacteria were identified in animal and human studies. Studies indicated that gut microbiota alter the pathogenesis of AD through its impact on neuroinflammation and permeability of the gastrointestinal tract. The ensuing increase in blood-brain barrier permeability may accelerate Aβ penetrance and formation of neuritic plaques that align with the amyloid hypothesis of AD pathogenesis. Further studies should assess the relationship between gut microbiota and AD progression and therapy preserving beneficial gut microbiota.

Background: Gut microbiomes play a vital role in maintaining whole-body metabolic homeostasis. It has gained significant attention in recent years due to advancements in genome sequencing technologies and a deeper understanding of its relationship with obesity. However, the specific ways in which different microorganisms directly or indirectly influence host obesity, as well as the underlying mechanisms, remain uncertain because of the complexity of gut microbiota composition. Methods: In this review, we summarize the roles of the major gut microbiota phyla such as Bacteroidetes, Firmicutes, Proteobacteria, and Verrucomicrobia in obesity and type 2 diabetes based on studies published in the past five years on PubMed and Google Scholar. The current therapeutic strategies associated with gut microbiota are also explored from clinical trials, and challenges and future directions are discussed. Results and Conclusions: This review will provide a deeper understanding of the functions of major gut microbiota in obesity and type 2 diabetes, which could lead to more individualized and effective treatments for metabolic diseases.

The gut microbiome, comprising bacteria, viruses, fungi, and bacteriophages, is one of the largest microbial ecosystems in the human body and plays a crucial role in various physiological processes. This review explores the interaction between the gut microbiome and enteroendocrine cells (EECs), specialized hormone-secreting cells within the intestinal epithelium. EECs, which constitute less than 1% of intestinal epithelial cells, are key regulators of gut-brain communication, energy metabolism, gut motility, and satiety. Recent evidence shows that gut microbiota directly influence EEC function, maturation, and hormone secretion. For instance, commensal bacteria regulate the production of hormones like glucagon-like peptide 1 and peptide YY by modulating gene expression and vesicle cycling in EE cells. Additionally, metabolites such as short-chain fatty acids, derived from microbial fermentation, play a central role in regulating EEC signaling pathways that affect metabolism, gut motility, and immune responses. Furthermore, the interplay between gut microbiota, EECs, and metabolic diseases, such as obesity and diabetes, is examined, emphasizing the microbiome's dual role in promoting health and contributing to disease states. This intricate relationship between the gut microbiome and EECs offers new insights into potential therapeutic strategies for metabolic and gut disorders.

The intestinal microbiota plays a vital role in animal growth and development. In this study, we explored the impact of oat grain dietary supplementation on growth performance, intestinal microbiota, short-chain fatty acids (SCFAs), and fatty acids (FAs) in Hu sheep. Thirty-two Hu lambs were randomly assigned to a control group (RC) or an oat grain-supplemented group (RO). After 90 days on their respective diets, rumen digesta were collected from six randomly selected Hu lambs per group to assess microbial diversity, SCFAs, and FAs. The RO diet significantly enhanced growth in Hu sheep (p < 0.01) and increased α-diversity, as indicated by Chao1 and Shannon indices. Core phyla in both groups were Firmicutes and Bacteroidota, with predominant genera including Prevotella, Rikenellaceae_RC9_gut_group, and F082. Oat grain supplementation led to significant shifts in microbial composition, increasing the abundance of Acidobacteriota, Proteobacteria, Chloroflexi, Actinobacteriota, and Subgroup_2, while decreasing Bacteroidota and Oscillospiraceae (p < 0.05). The RO group also exhibited lower levels of isobutyric and citraconic acids but higher levels of azelaic acid (p < 0.05). These results indicate that oat grain supplementation enhances beneficial rumen microbes and optimizes FAs and SCFAs composition, thereby promoting weight gain in Hu sheep.

The role of the gut archaeal microbiome (archaeome) in health and disease remains poorly understood. Methanogenic archaea have been linked to multiple sclerosis (MS), but prior studies were limited by small cohorts and inconsistent methodologies. To address this, we re-evaluated the association between methanogenic archaea and MS using metagenomic data from the International Multiple Sclerosis Microbiome Study. We analyzed gut microbiome profiles from 115 MS patients and 115 healthy household controls across Buenos Aires (27.8%), Edinburgh (33.9%), New York (10.4%), and San Francisco (27.8%). Metagenomic sequences were taxonomically classified using kraken2/bracken and a curated profiling database to detect archaea, specifically Methanobrevibacter species. Most MS patients were female (80/115), aged 25-72 years (median: 44.5), and 70% were undergoing treatment, including dimethyl fumarate (n = 21), fingolimod (n = 20), glatiramer acetate (n = 14), interferon (n = 18), natalizumab (n = 6), or ocrelizumab/rituximab (n = 1). We found no significant differences in overall archaeome profiles between MS patients and controls. However, treated MS patients exhibited higher abundances of Methanobrevibacter smithii and M. sp900766745 compared to untreated patients. Notably, M. sp900766745 abundance correlated with lower disease severity scores in treated patients. Our results suggest that gut methanogens are not directly associated with MS onset or progression but may reflect microbiome health during treatment. These findings highlight potential roles for M. smithii and M. sp900766745 in modulating treatment outcomes, warranting further investigation into their relevance to gut microbiome function and MS management.IMPORTANCEMultiple sclerosis (MS) is a chronic neuroinflammatory disease affecting the central nervous system, with approximately 2.8 million people diagnosed worldwide, mainly young adults aged 20-30 years. While recent studies have focused on bacterial changes in the MS microbiome, the role of gut archaea has been less explored. Previous research suggested a potential link between methanogenic archaea and MS disease status, but these findings remained inconclusive. Our study addresses this gap by investigating the gut archaeal composition in MS patients and examining how it changes in response to treatment. By focusing on methanogens, we aim to uncover novel insights into their role in MS, potentially revealing new biomarkers or therapeutic targets. This research is crucial for enhancing our understanding of the gut microbiome's impact on MS and improving patient management.

Obesity is a growing health concern worldwide, including United Arab Emirates. Bariatric surgery is an effective treatment option, with to date unclear weight loss mechanisms. In this prospective study, we explored post-bariatric surgery changes in energy homeostasis, gut peptides, hormones, and gut microbiota.

We recruited 19 Emirati adults who were planning to undergo sleeve gastrectomy (SG). We assessed the energy requirements using 24-hour diet recalls, indirect calorimetry for resting energy expenditure (REE), and a questionnaire for appetite. Anthropometrics included body mass index (BMI), waist circumference, waist-to-height ratio, fat mass, fat-free mass, and percentage of body fat. Gut peptides, including peptide YY (PYY), glucagon-like peptide-1/2 (GLP-1/2), ghrelin (GHR), cholecystokinin (CCK), insulin, and leptin, were quantified using ELISA. Gut microbiota composition at phylum and genus levels, including the Firmicutes/Bacteroidetes (F/B) ratio and alpha (α) and beta (β) diversity, was determined by sequencing amplicons of the V3-V4 region of the 16S rRNA at baseline and three months post-surgery. Comparisons used paired sample T-test, Wilcoxon, and McNemar test. QIIME 2 was used to identify taxa and their relative abundance; subsequent analyses were done in R for (α) and (β) diversity (package qiime2R) and Wilcoxon signed-rank test in R for differences in microbiota at phylum and genus levels. We conducted Spearman correlation analyses between genera and energy homeostasis, appetite, anthropometrics, hormones, and gut peptides.

At three months post-SG, energy intake, appetite, all anthropometric indices, insulin, leptin, and GLP-1 significantly decreased; PYY and GHR significantly increased, and REE was stable. β-diversity of the gut microbiota and its composition at phylum and genus levels significantly changed post-surgery, yet F/B remained constant. Energy intake, BMI, and appetite negatively correlated with several taxa that significantly increased post-SG.

Gut peptides, hormones, and microbiota change partly account for bariatric surgery's weight-loss benefits. Understanding these alterations can inform personalized interventions targeting obesity.

Domestic ducks are economically important agricultural animals, and their body size is a crucial economic trait. The intestinal flora plays a pivotal role in influencing body metabolism, growth, and development. Currently, no literature is available on the potential effect of the intestinal flora of domestic ducks on body size. This study used 16S rRNA sequencing technology to investigate the fecal microbiota of 229 individuals reared under identical feeding conditions. The findings revealed that partridge ducks with large body sizes (LBS) exhibited a higher level of intestinal microbial diversity than ducks with small body sizes (SBS). Notably, the gut microbiota composition of SBS displayed significantly elevated proportions of Streptococcus, Rothia, and Psychrobacter compared to their counterparts with LBS. Conversely, Lactobacillus was significantly more abundant in LBS. Jeotgalibaca and Psychrobacter were identified as key biomarkers of SBS, whereas Lactobacillus and Bacteroides were predominant biomarkers of LBS. Functional predictions based on intestinal microbiota indicated discernible differences among different body types, particularly evident in non- partridge ducks. The present study investigated the correlation between the intestinal microbiota and body size of domestic ducks, aiming to provide practical insights for the production management of domestic duck farming.

Understanding the link between prepregnancy nutritional status and gut microbiota during pregnancy may lead to novel maternal and child health interventions. We explored the association of prepregnancy body mass index (BMI) status with gut microbiota diversity and abundance during pregnancy.

A cross-sectional study was conducted on 90 pregnant women from primary health centers in Jakarta, Indonesia. Trained staff interviewed women on sociodemographic characteristics and nutrient intake, gathered data on prepregnancy BMI from antenatal records, and obtained fecal samples. Samples were analyzed for microbiota diversity indices [Shannon, Faith phylogenetic diversity (Faith PD), and Chao1] and abundance using 16S ribosome ribonucleic acid sequencing. Multivariate logistic regression was performed although adjusting for carbohydrate and protein intake, ethnicity, and education to determine the relationship between prepregnancy BMI and the alpha diversity index and the presence of the phylum Firmicutes and genera Prevotella and Blautia.

Pregnant women who were overweight or obese (BMI ≥23.0 kg/m2) before pregnancy had significantly lower odds of having gut microbiota diversity above the median of Shannon index [adjusted odds ratio (aOR): 0.4, 95% confidence interval (CI): 0.1, 0.9, P = 0.042], Faith PD (aOR: 0.2, 95% CI: 0.1, 0.8, P = 0.015), and Chao1 (aOR: 0.3, 95% CI: 0.1, 0.7, P = 0.006) compared with those who were neither overweight nor obese. Prepregnant women with overweight or obesity also had significantly lower odds of having levels above the median of the phylum Firmicutes (aOR: 0.38, 95% CI: 0.15, 0.98, P = 0.045) and genus Blautia (aOR: 0.32, 95% CI: 0.12, 0.85, P = 0.022) compared with women without overweight and obesity.

Prepregnancy overweight or obese status was associated with lower gut microbiota diversity and lower abundance of Firmicutes and Blautia among pregnant women in an urban community. These findings suggest that prepregnancy interventions to control BMI may improve gut flora and potentially benefit pregnant women.

Multiple sclerosis (MS) is defined as an inflammatory disorder that chronically affects the central nervous system of young people mostly and is distributed globally. It is associated with degeneration and demyelination of the myelin sheath around the nerves, resulting in multiple neurological disability symptoms ranging from mild to severe cases that end with paralysis sometimes. MS is one of the rising diseases globally that is unfortunately associated with reduced quality of life and adding national economic burdens. The definite MS mechanism is not clearly defined; however, all the previous researches confirm the role of the immune system as the master contributor in the pathogenesis. Innate and adaptive immune cells are activated peripherally then attracted toward the central nervous system (CNS) due to the breakdown of the blood-brain barrier. Recently, the gut-brain axis was shown to depend on gut metabolites that are produced by different microorganisms in the colon. The difference in microbiota composition between individuals is responsible for diversity in secreted metabolites that affect immune responses locally in the gut or systemically when reach blood circulation to the brain. It may enhance or suppress immune responses in the central nervous system (CNS) (repeated short forms); consequently, it may exacerbate or ameliorate MS symptoms. Recent data showed that some metabolites can be used as adjuvant therapy in MS and other inflammatory diseases. This review sheds light on the nature of MS and the possible interaction between gut microbiota and immune system regulation through the gut-brain axis, hence contributing to MS pathogenesis.

The gut microbiota plays a crucial role in the communication between the gut, liver, and brain through the production of short chain fatty acids (SCFAs). SCFAs serve as key mediators in the Gut-Liver-Brain Axis, influencing various physiological processes and contributing to overall health. SCFAs are produced by bacterial fermentation of dietary fiber in the gut, and they exert systemic effects by signaling through various pathways. In the Gut-Liver axis, SCFAs regulate liver metabolism through peroxisome proliferator-activated receptor-γ (PPAR-γ), AMP-activated protein kinase (AMPK) and other pathways, promotes fat oxidation, modulate inflammation through mTOR pathway, and impact metabolic health. In the Gut-Brain axis, SCFAs influence brain function, behavior, and may have implications for neurological disorders, in which G-protein coupled receptors (GPCRs) play an essential role, along with other pathways such as hypothalamic-pituitary-adrenal (HPA) pathway. Understanding the mechanisms by which SCFAs mediate communication between the gut, liver, and brain is crucial for elucidating the complex interplay of the Gut-Liver-Brain Axis. This review aims to provide insight into the role of gut microbiota-derived SCFAs as mediators of the Gut-Liver-Brain Axis and their potential therapeutic implications. Further research in this area will be instrumental in developing novel strategies to target the Gut-Liver-Brain Axis for the prevention and treatment of various health conditions.

Background: Short-chain fatty acids (SCFAs), which are produced by the microbial fermentation of undigested carbohydrates, play an important role in the metabolism and physiology of the host. SCFAs are involved in the regulation of maternal metabolism during pregnancy and influence weight gain, glucose metabolism, and metabolic hormones. Methods: In 2017, women who were treated for gestational diabetes mellitus (GDM) at the University Medical Centre Ljubljana were invited to participate in a longitudinal study. A total of 45 women were included in this study and comprehensively phenotyped. During the second and third trimester of pregnancy, the women with GDM provided fecal samples for SCFA analysis. The samples were analyzed by high-performance liquid chromatography for the simultaneous determination of acetate, propionate, and butyrate. Results: SCFA concentrations in feces differed between overweight/obese and normal-weight women with GDM. Acetate and propionate concentrations were significantly higher in pregnant women who were overweight or obese before pregnancy compared to normal-weight women but butyrate concentrations were not. Butyrate was elevated in the third trimester in the group with excessive gestational weight gain. Conclusions: The relationship between SCFAs and obesity is complex, and the association between SCFAs and GDM remains to be clarified. Regardless of the conflicting publications on the role of SCFAs, our study showed that higher acetate and propionate levels were associated with the weight categories of overweight or obesity before pregnancy and higher butyrate levels were associated with excessive gestational weight gain.

The present study investigated the impact of butyrate glycerides (BG) on lipid metabolism, intestinal morphology, and microbiota of laying hens. Four hundred eighty 54-week-old Hy-line Brown laying hens were randomly selected and divided into five groups. The control group (ND) was fed a basal diet. Meanwhile, the remaining groups were given a basal supplemented with 0.5, 1, 2, and 4 g/kg of the product containing BG and were designated as BG-0.5, BG-1, BG-2, and BG-4 groups, respectively. The findings showed that: (1) BG supplementation significantly decreased (P < 0.001) the blood Glu levels (BG-0.5, BG-1, BG-2, and BG-4) and increased (P < 0.001) the serum HDL-C levels (BG-2, and BG-4). (2) The BG-2 and BG-4 groups showed an increase (P < 0.01) in abdominal lipid HSL activity. (3) The levels of hepatic TC and TG in all BG groups were significantly decreased (P < 0.05). (4) The addition of BG resulted in a significant reduction in the mRNA expression of the liver X receptor alpha (LXRα) (P < 0.05). (5) All BG groups presented a substantial reduction in duodenal crypt depth and a notable increase in the ratio of villus height to crypt depth (V/C) (P < 0.01). Additionally, all BG groups exhibited a significant increase in villus height in the ileum (P < 0.001). (6) Both the BG-1 and BG-4 groups exhibited a significant reduction in the amounts of n-butyric and n-glutaric acids in the cecum contents (P < 0.05). (7) The inclusion of BG did not substantially impact the diversity of cecal microbiota in laying hens. However, it dramatically boosted the proportion of the beneficial bacterium Alistipes (P < 0.05) and reduced the abundance of the harmful bacterium Verrucomicrobiota (P < 0.05). Overall, incorporating BG with glycerol monobutyrate as the diet's primary active component reduces fat accumulation in laying hens' blood and liver. It potentially regulates lipid metabolism via the PPARγ-LXRα-SREBP1c pathway. Additionally, BG has the potential to enhance the structure of the small intestine's mucous membrane and increase the presence of beneficial bacteria. Under the experimental conditions, late-laying hens supplemented with 4 g/kg BG performed best overall.

Microorganisms in the gut play a pivotal role in human health, influencing various pathophysiological processes. Certain microorganisms are particularly essential for maintaining intestinal homeostasis, reducing inflammation, supporting nervous system function, and regulating metabolic processes. Short-chain fatty acids (SCFAs) are a subset of fatty acids produced by the gut microbiota (GM) during the fermentation of indigestible polysaccharides. The interaction between GM and SCFAs is inherently bidirectional: the GM not only shapes SCFAs composition and metabolism but SCFAs also modulate microbiota's diversity, stability, growth, proliferation, and metabolism. Recent research has shown that GM and SCFAs communicate through various pathways, mainly involving mechanisms related to inflammation and immune responses, intestinal barrier function, the gut-brain axis, and metabolic regulation. An imbalance in GM and SCFA homeostasis can lead to the development of several chronic diseases, including inflammatory bowel disease, colorectal cancer, systemic lupus erythematosus, Alzheimer's disease, and type 2 diabetes mellitus. This review explores the synergistic interactions between GM and SCFAs, and how these interactions directly or indirectly influence the onset and progression of various diseases through the regulation of the mechanisms mentioned above.

This study aimed to investigate the changes in fecal short-chain fatty acids (SCFAs) content in UCP1 knock-in pigs (KI pigs) and their effect on adipogenesis. Fecal samples from five 6-month-old wild-type (WT) and KI pigs were collected for targeted metabolomics and 16s rRNA sequencing analyses to identify differences in SCFAs and gut microbiota that may contribute to regulating fat deposition in pigs. The metabolome of pig fecal samples targeted for an analysis of SCFAs identified seven SCFAs, with caproic acid (except isovaleric acid) being the significantly different one. The results of the fecal 16s rRNA analysis demonstrated a notable reduction in the abundance of Streptococcus spp. in the KI pigs in comparison to the WT pigs, with a statistically significant difference. Correlation analyses demonstrated a statistically significant positive correlation between the abundance of Streptococcus spp. and SCFAs, as well as pig body weight and fatness. It was postulated that the reduction in SCFAs in the intestinal tracts of KI pigs may be associated with a reduction in Streptococcus spp. abundance. Compared to WT pigs, the concentration of fecal SCFAs in KI pigs was significantly reduced, which may be related to the decreased abundance of Streptococcus. The in vitro experiments showed that caproic acid could significantly enhance the differentiation efficiency of porcine SVF cells into mature adipocytes by activating the FFAR4 gene.

Non-starch polysaccharides have been demonstrated to have significant benefits in treating some chronic metabolic diseases such as hyperglycemia. However, the preventive effect of non-starch polysaccharides from Castanea mollissima Bl. (CMNSP) on type 2 diabetes mellitus (T2DM) remain underexplored. The objective of this study was to investigate the effect of CMNSP on glucose and lipid metabolism, intestinal barrier, gut microbiota and their metabolites in high fat diet/streptozotocin-induced T2DM mice. The results revealed that CMNSP significantly mitigated hyperglycemia, insulin resistance, hyperlipidemia, and prevented pancreatic atrophy, hepatic steatosis and enhanced the expression at mRNA level and corresponding protein of PI3K/AKT/Glut2 signaling pathway in liver. Moreover, CMNSP enhanced the level of SCFAs and restored intestinal barrier damage and gut microbiota disturbance in diabetic mice. Further fecal metabolomics analysis identified that CMNSP primarily influenced the metabolic pathways such as Primary bile acid biosynthesis and Taurine and hypotaurine metabolism, and were significantly correlated with changes in dominant bacterial genera including Bacteroides and Lactobacillus.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a significant global health issue, affecting over 30% of the population worldwide due to the rising prevalence of metabolic risk factors such as obesity and type 2 diabetes mellitus. This spectrum of liver disease ranges from isolated steatosis to more severe forms such as steatohepatitis, fibrosis, and cirrhosis. Recent studies highlight the role of gut microbiota in MASLD pathogenesis, showing that dysbiosis significantly impacts metabolic health and the progression of liver disease. This review critically evaluates current microbiome-centered therapies in MASLD management, including prebiotics, probiotics, synbiotics, fecal microbiota transplantation, and emerging therapies such as engineered bacteria and bacteriophage therapy. We explore the scientific rationale, clinical evidence, and potential mechanisms by which these interventions influence MASLD. The gut-liver axis is crucial in MASLD, with notable changes in microbiome composition linked to disease progression. For instance, specific microbial profiles and reduced alpha diversity are associated with MASLD severity. Therapeutic strategies targeting the microbiome could modulate disease progression by improving gut permeability, reducing endotoxin-producing bacteria, and altering bile acid metabolism. Although promising, these therapies require further research to fully understand their mechanisms and optimize their efficacy. This review integrates findings from clinical trials and experimental studies, providing a comprehensive overview of microbiome-centered therapies' potential in managing MASLD. Future research should focus on personalized strategies, utilizing microbiome features, blood metabolites, and customized dietary interventions to enhance the effectiveness of these therapies.

Inflammatory bowel disease (IBD) represents a cluster of chronic idiopathic inflammatory disorders situated at the nexus of intricate interplays. The primary aim of the present investigation is to perform an umbrella review of metaanalyses, systematically offering a comprehensive overview of the evidence concerning risk factors for IBD.

To achieve this, we searched reputable databases, including PubMed, Embase, Web of Science, and the Cochrane Database of Systematic Reviews, from inception through April 2023. Two authors independently assessed the methodological quality of each metaanalysis using the AMSTAR tool and adhered to evidence classification criteria.

In total, we extracted 191 unique risk factors in meta-analyses, including 92 significantly associated risk factors. The top ten risk factors were human cytomegalovirus (HCMV) infection, IBD family history, periodontal disease, poliomyelitis, campylobacter species infection, hidradenitis suppurativa, psoriasis, use of proton pump inhibitors, chronic obstructive pulmonary disease, and western dietary pattern.

In conclusion, this umbrella review extracted 62 risk factors and 30 protective factors, most of which were related to underlying diseases, personal lifestyle and environmental factors. The findings in this paper help to develop better prevention and treatment measures to reduce the incidence of IBD, delay its progression, and reduce the burden of IBD-related disease worldwide.

https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42023417175.

Obesity is prevalent in type 1 diabetes (T1D) and is problematic with higher risk for diabetes complications. It is unknown to what extent gut microbiome changes are associated with obesity and T1D.

This work aimed to describe the gut microbiome and microbial metabolite changes associated with obesity in T1D. We hypothesized statistically significant gut microbial and metabolite differences in lean T1D youth (body mass index [BMI]: 5%-<85%) vs those with obesity (BMI: ≥95%).

We analyzed stool samples for gut microbial (using metagenomic shotgun sequencing) and short-chain fatty acid (SCFA) differences in lean (n = 27) and obese (n = 21) T1D youth in a pilot study. The mean ± SD age was 15.3 ± 2.2 years, glycated hemoglobin A1c 7.8 ± 1.3%, diabetes duration 5.1 ± 4.4 years, 42.0% female, and 94.0% were White.

Bacterial community composition showed between sample diversity differences (β-diversity) by BMI group (P = .013). There was a higher ratio of Prevotella to Bacteroides in the obese group (P = .0058). There was a differential distribution of significantly abundant taxa in either the lean or obese groups, including increased relative abundance of Prevotella copri, among other taxa in the obese group. Functional profiling showed an upregulation of branched-chain amino acid (BCAA) biosynthesis in the obese group and upregulation of BCAA degradation, tyrosine metabolism, and secondary bile acid biosynthesis in the lean group. Stool SCFAs were higher in the obese vs the lean group (P < .05 for all).

Our findings identify a gut microbiome and microbial metabolite signature associated with obesity in T1D. These findings could help identify gut microbiome-targeted therapies to manage obesity in T1D.

Probiotics, as common regulators of the gut microbiota, have been used in research to alleviate clinical symptoms of atopic dermatitis (AD).

Our research team has previously identified a potential relieving effect of Clostridium butyricum on the treatment of AD, but the specific mechanism of how Clostridium butyricum alleviates AD has not yet been confirmed.

In this study, we explored the relieving effect of Clostridium butyricum on AD through in vivo and in vitro experiments. AD mice induced by 2,4-dinitrofluorobenzene (DNFB) were orally administered with 1 × 108 CFU of Clostridium butyricum for three consecutive weeks.

Oral administration of Clostridium butyricum reduced ear swelling, alleviated back skin lesions, decreased mast cell and inflammatory cell infiltration, and regulated the levels of inflammation-related cytokines. Clostridium butyricum activated the intestinal immune system through the TLR4/MyD88/NF-κB signaling pathway, suppressed the expression of inflammatory factors IL-10 and IL-13, and protected the damaged intestinal mucosa.

Clostridium butyricum administration improved the diversity and abundance of the gut microbiota, enhanced the functionality of the immune system, and protected the epidermal barrier.

Wounds in patients with diabetes present significant physical and economic challenges due to impaired healing and prolonged inflammation, exacerbated by complex interactions between microbes. Especially, the development and healing of diabetic foot ulcers (DFUs) remain an urgent clinical problem. The human gut harbors a vast microbial ecosystem comprising intestinal flora and their metabolic products. Recent advancements in research have illuminated the concept of the "gut-skin axis," revealing intricate relationships between gut microbiota, microbiota-derived metabolites, and various skin diseases, including DFUs. This review aims to unravel the formation and healing process of DFUs in the context of the gut-skin axis. We reviewed the current research progress worldwide regarding to the gut-skin axis, compared and discussed significant changes in the microbiota colonizing the skin and gut in patients with DFUs. The roles of microbiota-derived metabolites such as lipopolysaccharides, short-chain fatty acids, and trimethylamine-N-oxide in the development of DFUs are highlighted. We also reviewed treatment strategies currently employed in clinical practice and identified potential therapeutic targets such as probiotics for treating DFUs. The need for more comprehensive experimental designs to elucidate the intricate relationship between gut microbiota and its metabolites in the context of DFUs are therefore highlighted.

The relationship between the gut microbiota (GM) and the health of human beings has been a topic of growing interest in the last few years. Legumes are a rich source of indigestible carbohydrates, including resistant starch (RS), which are substrates of the GM. The aim of this study was to evaluate the effect of the indigestible fraction of legumes on the fecal microbiota of normal-weight (NW) and obese (O) donors. Accordingly, a preclinical in vitro fermentation model was developed (Goñi and Martín-Carrón, Nutr Res 18:1077-1089, 1998). Short-chain fatty acid (SCFAs) production was measured via gas chromatography. In addition, the fecal microbiota was characterized via 16 S rRNA sequence analysis. The results revealed that the ratio of the relative abundance of Firmicutes to Bacteroidetes was lower in O individuals than in NW individuals. Bacteroides was the predominant genus in the fecal inoculum of the O group. Total SCFAs production was significantly greater in the chickpea (C) group than in the lentil (L) and white bean (WB) groups among the samples from the NW group. In contrast, WB presented the highest production of SCFAs in the samples from the O group. These results suggest that fermentation products (SCFAs) are determined by the components of the legumes, including RS, and the type of microbiota donor (NW or O individuals).

Golden Retrievers have a high risk of obesity, which is prevalent in dogs and is associated with inflammation and cancer, impairing the health and life expectancy of companion animals. Microbial and metabolite biomarkers have been proposed for identifying the presence of obesity in humans and rodents. However, the effects of obesity on the microbiome and metabolome of Golden Retrievers remains unknown. Therefore, this study was designed to evaluate the signatures of serum biochemistry indexes, gut microbiota and plasma metabolites in non-obese and obese Golden Retrievers, aiming to recognize potential biomarkers of canine obesity.

A total of 8 non-obese (Ctrl group) and 8 obese (Obe group) Golden Retrievers were included in the present study to collect blood and feces samples for measurements. The fecal microbiome and plasma metabolome were determined using 16S rRNA amplicon sequencing and liquid chromatography-mass spectrometry, respectively.

Results showed that the alanine aminotransferase activity and total bilirubin concentration, which have been measured using serum biochemistry analysis, were higher in the Obe group than in the Ctrl group (p < 0.05). Moreover, there was a significant difference in gut microbiota composition between the two groups (p < 0.05). The phyla Proteobacteria, Fusobacteriota, and Bacteroidota as well as genera Fusobacterium, Prevotella, Faecalibacterium, Escherichia-Shigell, and Alloprevotella were more abundant, while phylum Firmicutes and genera Peptoclostridium, Blautia, Turicibacter, Allobaculum, and Erysipelatoclostridium were less abundant in the Obe group compared to the Ctrl group (p < 0.05). Plasma concentrations of citrulline and 11-dehydrocorticosterone were significantly higher in the Obe group than those in the Ctrl group (p < 0.05). Close correlations between serum biochemistry parameters, gut microbiome, and plasma metabolites were observed in the current study.

The obesity-induced shifts in serum biochemistry indexes, gut microbiota, and plasma metabolites profiles suggest that obese Golden Retrievers exhibit a different microbiome and metabolome than non-obese ones, and the certain metabolites like citrulline and 11-dehydrocorticosterone could be considered as potential biomarkers to recognize obese Golden Retrievers.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent chronic liver condition marked by excessive lipid accumulation in hepatic tissue. This disorder can lead to a range of pathological outcomes, including metabolic dysfunction-associated steatohepatitis (MASH) and cirrhosis. Despite extensive research, the molecular mechanisms driving MASLD initiation and progression remain incompletely understood. Oxidative stress and lipid peroxidation are pivotal in the "multiple parallel hit model", contributing to hepatic cell death and tissue damage. Gut microbiota plays a substantial role in modulating hepatic oxidative stress through multiple pathways: impairing the intestinal barrier, which results in bacterial translocation and chronic hepatic inflammation; modifying bile acid structure, which impacts signaling cascades involved in lipidic metabolism; influencing hepatocytes' ferroptosis, a form of programmed cell death; regulating trimethylamine N-oxide (TMAO) metabolism; and activating platelet function, both recently identified as pathogenetic factors in MASH progression. Moreover, various exogenous factors impact gut microbiota and its involvement in MASLD-related oxidative stress, such as air pollution, physical activity, cigarette smoke, alcohol, and dietary patterns. This manuscript aims to provide a state-of-the-art overview focused on the intricate interplay between gut microbiota, lipid peroxidation, and MASLD pathogenesis, offering insights into potential strategies to prevent disease progression and its associated complications.

Gynostemma pentaphyllum is a herbaceous vine of Cucurbitaceae family, and its principal pharmacological components, gypenosides (GPs), have been proved to be effective in various liver diseases. However, the mechanisms of GPs on liver injury are still to be studied for further. This investigation utilized the CCl4-induced liver injury rat model (LI) to comprehensively explore the mechanism of action of GPs in the treatment of chemical liver injury by comparing the metabolomic changes in four groups rats. In this study, the therapeutic efficacy of GPs in a liver injury rat model induced by weekly gavage of CCl4 was evaluated by inflammatory factors, oxidative damage indexes, and histopathological sections. Then, GC-MS technology was used to identify the metabolic profile of GPs in treating liver injury. Finally, the content variation of metabolites (BAs and SCFAs) was measured to elucidate the mechanism of GPs in the treatment of CCl4-induced liver injury. After 8 weeks of administration, GPs effectively reduced the degree of LI and appeared a substantial tendency of reversing in the levels of MDA, GSH, CYP7E1, CYP7A1 and CYP27A1. Untargeted metabolomics suggested that GPs may play a role in BAs and SCFAs metabolism. Targeted metabolomics and ELISA confirmed the key role of GPs in increasing SCFAs levels and regulating BAs metabolism. Overall, this study indicated that GPs can alleviate CCl4-induced liver injury. And GPs may exert beneficial effects on LI by affecting their metabolites (SCFAs and BAs).

The effects of three dietary oils (rapeseed oil, camellia oil, linseed oil) with different fatty acid compositions on the growth performance, digestion and gut microbiota of SD rats after 8 weeks of feeding were studied. The serum metabolic index and liver histomorphology of rats were measured using an automatic biochemical analyzer and light microscope. Furthermore, 16S rDNA amplicon sequencing technology was used to analyze the gut microbiota. It was found that these differences in fatty acid composition had no significant effect on body fat and liver tissue. However, after digestion, the rapeseed oil group showed lowest triglyceride content (1.22 ± 0.15) and a lower LDL/HDL ratio (0.41 ± 0.02). For gut microbiota distribution, the linseed oil group showed a higher Firmicutes/Bacteroides ratio (6.11 ± 0.54) and a high proportion of Lactobacillus. These data indicate that both the unsaturated fatty acid content and n-3 unsaturated fatty acids collectively had an effect on digestion metabolism, and the influence order may be n-3 unsaturated fatty acids > unsaturated fatty acid content.

Associated to various illnesses, Western Diet (WD) is acknowledged to have deleterious effects on human gut microbiota, decreasing bacterial diversity, lowering gut bacteria associated to health (such as Akkermansia muciniphila), while increasing those linked to diseases (e.g., Proteobacteria). In this study, we evaluated the potential of two new prebiotics to counteract the negative effect of WD on gut microbiota, namely raffinose family oligosaccharides (RFO) from chickpeas and laminarin (LAM) from algae, when compared to the well-known inulin (INU). The effects of prebiotics on gut microbiota composition and metabolic activities were investigated in the Mucosal-Artificial Colon, set-up to reproduce WD condition, as compared to healthy control (n = 3). None of the prebiotics was able to efficiently offset the shift in microbiota induced by WD. Nevertheless, when compared to non-supplemented WD, all prebiotics showed significant impacts on microbiota composition, that were both prebiotic and donor-dependant. RFO was the only prebiotic to enhance α-diversity, while it led to an increase in Blautia and Butyricicoccaceae, associated with higher amounts of gas and butyrate. LAM and INU did not strongly impact microbial metabolic activities but were associated with a rise in Prevotella_9/Agathobacter and Faecalibacterium, respectively. To conclude, this study showed that all tested prebiotics had different impacts on human gut microbiota structure and activities, which was further donor-dependent. M-ARCOL appears as a suitable in vitro tool to better understand the mechanisms of action of prebiotic compounds in relation to gut microbes and define responders and non-responders to prebiotic supplementation, opening the possibility of customized nutritional strategies.

The aim of this study is to examine the physiological effects of emodin on intestinal microorganisms and the liver in the BALb/c mice.

Following an 8-week administration of emodin at doses of 25, 50, and 100 mg/kg/day,pathological analyses revealed that emodin significantly reduced the colon length, induced colonic crypt inflammation,diminished the colonic mucus layer,and decreased the fluorescence intensity of colonic tight junction proteins ZO-1 and Occludin. Concurrently, 16S rDNA gene sequencing corroborated that emodin altered the diversity and composition of the intestinal microbiota by increasing the Firmicutes to Bacteroides ratio. Simultaneously, the non-targeted metabolomics analyses exhibited significant alternations in both short chain fatty acids and free fatty acids between the emodin-treated and the normal groups, indicating emodin-induced disturbance in intestinal metabolic disorder. Furthermore, emodin exhibited a significant elevation in LPS levels in colon, serum and liver as well an marked increase in the levels of TC, TG, AST, and ALT in serum. Additionally, histological examination employing by HE and oil-red O staining furtherly verified that the administration of varying doses emodin induced hepatic inflammation and lipid accumulation. Whereas qRT-PCR and Western blot analyses demonstrated that the administering of varying doses of emodin upregulated the mRNA levels of TNF-α, IL-1β, IL-6, and IL-18 as well as the expression of TLR4, Myd88, and P-65. Following the combined administration of probiotics, the high-dose emodin did not significantly influence ALT and AST levels in mice. However, the faeces of the high-dose emodin transplanted in mice and induced a significant increase in AST levels and in the relative abundance of Firmicutes and Proteobacteria.

These findings further corroborate that emodin induces liver injury via the intestinal dysfunction. These findings suggested that emodin may disrupt intestinal microbiota and resulted in significant alternations in endogenous metabolites in mice, thereby facilitating the entry of LPS and FFAs into the liver, potentially leading to hepatic injury.

Gut microbiome dysbiosis is involved in non-alcoholic fatty liver disease (NAFLD) development. Hepatic transmembrane 4 L six family member 5 (TM4SF5) overexpression promotes NAFLD. However, how gut microbiota are associated with TM4SF5-mediated NAFLD remains unexplored. We analyzed the gut microbiome using feces from hepatocyte-specific TM4SF5-overexpressing transgenic (Alb-TGTm4sf5-Flag, TG) or Tm4sf5-/- knock-out (KO) mice fed a normal chow diet (NCD), high-fat diet (HFD) for 2 weeks (HFD2W), or methionine-choline-deficient diet (MCD) for 4 weeks to investigate associations among Tm4sf5 expression, diet, and the gut microbiome. TG-NCD mice showed a higher Firmicutes-to-Bacteroidetes (F/B) ratio, with less enrichment of Akkermansia muciniphila and Lactobacillus reuteri. NASH-related microbiomes in feces were more abundant in TG-HFD2w mice than in KO-HFD2w mice. Further, TG-MCD showed a higher F/B ratio than TG-NCD or KO mice, with decreases or increases in microbiomes beneficial or detrimental to the liver, respectively. Such effects in TG-MCD animals were correlated with functional pathways producing short-chain fatty acids (SCFAs). Furthermore, potential functional pathways of the gut microbiome were metabolically parallel to NAFLD features in TG-MCD mice. These results suggest that hepatocyte Tm4sf5 supports gut microbiome dysbiosis and metabolic activity, leading to SCFA production and hepatic inflammation during NAFLD development.

Saccharomyces cerevisiae accumulates glycogen, a hyperbranched glucose polymer with multiple bio-functionalities. In this study, mutants of S. cerevisiae that accumulate excessive amounts of glycogen were developed through UV mutagenesis. From over 30,000 mutants, the mutant strain CEY1, which exhibited the highest glycogen production, was selected using iodine vapor screening. The glycogen structures of wild type (WT) and CEY1 were analyzed and found to be relatively similar in molecular weight, hydrodynamic diameter, and side-chain distribution. The glycogen from CEY1 contained long branches (DP >12) 23.6 % greater than those in Escherichia coli TBP38. In addition, WT and CEY1 glycogen showed 32 %-34 % digestibility, which is significantly lower than E. coli glycogen. The glycogen content in dried CEY1 cells was increased to 21.7 % during laboratory-scale fed-batch fermentation. Glycogen with a homogeneous structure was accumulated to 17.5 % (w/w dried cell), and the total glucan content was increased by 33.2 % during large-scale fed-batch fermentation. In a mouse model, a diet containing 30 % CEY1 increased the production of butyrate and populations of beneficial bacteria, including Bacteroides and Parabacteroides. Therefore, glycogen from CEY1 exhibits a distinct structure from other polysaccharides, with notably slow and low digestibility, thereby indicating its potential application as a dietary supplement.