Search Results (1,098)

Background/Objectives: Stunting and weight faltering (WF) remain pressing public health challenges in low- and middle-income countries, with long-term consequences for child growth, development, and survival. While the role of gut health in early growth is increasingly recognized, evidence on how the gut microbiome and metabolome respond to nutritional interventions in WF infants is scarce. This study explored gut microbiome and metabolome changes in Indonesian infants aged 6–12 months who overcame WF following a one-month intervention. Methods: Infants were assigned to either a Nutritional Advice (NA) group or a Nutritional Advice plus Oral Nutritional Supplements (NAONS) group. Stool samples were collected before and after the intervention for microbiome (16S rRNA sequencing) and metabolome (LC-MS) analysis. Results: Significant shifts in gut microbial composition (beta diversity) and species richness (Chao1 index) were observed in both groups, suggesting enhanced microbial diversity and gut resilience. Within-group analysis revealed increases in beneficial genera such as Faecalibacterium and Peptostreptococcus, and a reduction in pro-inflammatory Fusobacterium in the NA group. The NAONS group showed a notable decrease in Proteus, a potentially pathogenic genus. Between-group comparisons indicated higher abundances of Lactococcus and Leuconostoc in the NAONS group, likely reflecting the influence of milk protein-rich supplements on microbial colonization, favoring lactic acid bacteria over SCFA-producing taxa, leading to better gut health. Metabolome analysis revealed significant changes in the NA group, increases in metabolites like Threonine, Tryptophan, and Xylose pointed to improved energy metabolism and gut health, while a decrease in Oxalic Acid suggested better metabolic efficiency. In contrast, the NAONS group, while benefiting from rapid weight gain, displayed a distinct metabolic profile influenced by high milk protein intake. No significant correlations were found between microbiome and metabolome changes, highlighting the complexity of gut-host interactions, suggesting that the interventions led to independent shifts in the aforementioned profiles. Conclusions: Overall, the findings suggest that nutritional interventions may enhance gut health and support recovery from weight faltering, providing insights into strategies that may contribute to restoring healthy growth trajectories and preventing stunting by modulating gut health. Full article

Background/Objectives: Colorectal cancer (CRC) accounts for nearly 10% of global cancer cases and is the second leading cause of cancer-related mortality. While age and genetics are non-modifiable risk factors, nutrition and its impact on gut microbiota are emerging as key determinants in CRC prevention and management. We aimed to systematically evaluate recent evidence on the role of diet and microbiota-targeted interventions—including probiotics, prebiotics, synbiotics, and postbiotics—in modulating CRC risk and therapeutic outcomes. Methods: A structured literature search was performed in PubMed, ResearchGate, Scopus, and ScienceDirect up to July of 2025. Reference lists of relevant reviews and clinical trials were also screened. A total of 36 studies were selected according to PRISMA guidelines. Data were extracted on dietary exposures, microbiota modulation, metabolite profiles, and CRC-related outcomes. Evidence quality was assessed using appropriate appraisal tools for observational and interventional designs. Results: Western-type diets were consistently associated with microbiota dysbiosis, the enrichment of pro-inflammatory and genotoxic taxa, and elevated CRC risk. Diets rich in fiber and polyphenols enhanced commensals producing short-chain fatty acids (e.g., butyrate), with anti-inflammatory and antineoplastic effects. Probiotics, prebiotics, and postbiotics demonstrated potential to restore microbial balance, improve epithelial integrity, and enhance tolerance to conventional therapies. Conclusions: Current evidence supports a complex interplay between nutrition, the gut microbiota, and CRC, with strong translational potential. Microbiota-modulating nutritional strategies, particularly fiber-rich diets and synbiotics, show the most consistent microbiota-related benefits in CRC prevention and represent promising adjuncts to standard therapies. However, much of the available research is still based on preclinical models. Therefore, there is a pressing need for well-designed clinical studies in human populations to validate these findings and inform evidence-based guidelines. Full article

The gut microbiome is essential for nutrient absorption, immune function, and overall metabolic health. A balanced microbial community allows for the breakdown of carbohydrates, proteins, fats, vitamins, and minerals into maximally absorbed nutrients and provides protection against inflammation. Dysbiosis, or microbial imbalance, disrupts these processes and leads to malabsorption, barrier dysfunction, and toxic metabolite production. These imbalances contribute to a wide variety of diseases, from obesity, diabetes, and cardiovascular disease to anemia, osteoporosis, and nervous system dysfunctions. Advances in sequencing, metabolomics, and functional assays have facilitated an enhanced understanding of the ecological and biochemical complexity of gut microbes. AI-based models are also providing new insights into personalized diet and therapeutic approaches. Through the redefinition of malnutrition and chronic disease within microbial ecology, science proves the potential for engineered probiotics, precision prebiotics, and gut-targeted therapies. These innovations hold the potential to improve global health and propel precision medicine in nutrition. Full article

Background/Objectives: Long-term hospitalization in cardiac patients is associated with significant metabolic and microbial alterations that may influence disease progression and prognosis. Although lipid imbalances, metabolomic shifts, and gut microbiome dysbiosis have each been linked individually to cardiovascular outcomes, their integrated evaluation in long-term-hospitalized patients remains underexplored. Methods: We conducted a retrospective observational study including 51 cardiac patients hospitalized for more than 25 days, compared with a control group of 41 patients hospitalized for short and intermediate durations (3–24 days). Clinical and demographic data were collected, alongside lipid profiling, metabolomic assessment through liquid chromatography–mass spectrometry (LC-MS), and gut microbiome analysis using GI360™ sequencing. Ethical approval was obtained, and all data were anonymized. Lipid-related findings are exploratory due to the small number of complete measurements. Results: Preliminary lipid trends were characterized by higher levels of LDL, triglycerides, and Lp(a), and lower HDL, in the long-term group. Metabolomic analyses revealed decreased energy-related metabolites (ATP, phosphocreatine ratio), altered amino acid patterns, and increased ketone utilization. Gut microbiome evaluation demonstrated a significant increase in dysbiosis index, with reduced diversity and dominance of potentially pathogenic taxa. These findings were correlated with clinical severity scores. Cross-domain relationships are exploratory and based on associative profiling rather than deep integrative modelling. Conclusions: Long-term hospitalization in cardiac patients is associated with distinct lipid, metabolomic, and gut microbiome profiles that may serve as predictive biomarkers of adverse outcomes. Future studies should validate these findings in larger cohorts and explore their integration into personalized management strategies. Full article

Immune checkpoint inhibitors (ICIs) have transformed cancer therapy, yet their benefits remain limited to a subset of patients, underscoring the need for more reliable biomarkers and novel therapeutic strategies. The gut microbiome has emerged as a critical modulator of systemic immunity and a promising determinant of ICI response. Evidence links specific microbial features, taxa, and bioactive metabolites to enhanced antitumor immunity, whereas disruptions, such as antibiotic exposure, are associated with poorer outcomes. Advances in sequencing and multi-omics technologies have provided more profound insights into microbiome-immune crosstalk, though methodological heterogeneity continues to challenge reproducibility. Translational studies demonstrate that microbiome-based intervention, including fecal microbiota transplantation (FMT), biotics supplementation, and engineered microbial strains, can enhance ICI efficacy or mitigate immune-related toxicities. Despite encouraging early clinical signals, broader implementation requires methodological rigor, standardized protocols, and innovative trial designs that account for host and environmental factors. For clinicians, the most immediate strategies involve prudent antibiotic stewardship and patient enrollment in microbiome-focused clinical trials. Overall, the gut microbiome is a promising biomarker and a therapeutic target, representing a new frontier for personalizing immunotherapy and improving patient outcomes in oncology. Full article

Autism spectrum disorder is markedly heterogeneous and frequently accompanied by gastrointestinal symptoms that often correlate with behavioral phenotypes. Emerging evidence suggests that the microbiota–gut–brain axis may contribute to these associations through multiple bidirectional communication routes—including neural, immune, and endocrine pathways, as well as microbial metabolites such as short-chain fatty acids and tryptophan–kynurenine intermediates. This narrative review synthesizes clinical, mechanistic, and interventional evidence published between January 2010 and July 2025, clarifies the extent to which current data support association versus causation, evaluates key confounding factors, summarizes evidence for interventions such as probiotics, prebiotics, and fecal microbiota transplantation, and outlines future directions for precision research and targeted interventions based on functional pathways and stratified subgroups. Full article

The rapidly advancing field of gut microbiota research has revealed its pivotal role in human health, with growing evidence implicating microbial dysbiosis in the development of metabolic diseases, particularly type 2 diabetes mellitus (T2DM). This narrative review synthesizes recent findings on the complex, bidirectional relationship between the gut microbiota–metabolic axis and T2DM, drawing upon data from human and experimental studies published in the past decade. Patients with T2DM consistently demonstrate marked gut dysbiosis, characterized by reduced microbial diversity and depletion of beneficial butyrate-producing taxa such as Faecalibacterium prausnitzii and Roseburia intestinalis. In contrast, increases in pro-inflammatory bacteria including Escherichia-Shigella and Lactobacillus are commonly observed. Such compositional changes are linked to metabolic dysfunction through altered microbial metabolites, including elevated trimethylamine N-oxide (TMAO), which has been associated with insulin resistance and increased diabetes risk. Moreover, gut microbiota imbalances correlate with systemic inflammation, as indicated by higher levels of cytokines such as IFN-γ and IL-6. These findings underscore the gut microbiota’s central role in energy metabolism and inflammation in T2DM. Understanding these mechanisms could inform novel therapeutic and preventive strategies—such as microbiota-targeted dietary, probiotic, or pharmacologic interventions—to improve metabolic outcomes and enhance clinical management of diabetes. Full article

Background: Blue light-induced retinal photodamage represents a growing public health concern globally. Lactic acid bacteria and their bioactive metabolites represent a promising therapeutic strategy for mitigating such damage. Methods: This study evaluated the protective efficacy of Limosilactobacillus fermentum IOB802 and Lactobacillus plantarum subsp. plantarum IOB602 against blue light-induced retinal injury using both in vitro and in vivo models. Results: In ARPE-19 cells exposed to blue light, treatment with postbiotics from IOB802 and IOB602 significantly restored cell viability (p < 0.05), enhanced antioxidant enzyme activities (GSH-Px, SOD, and CAT, p < 0.05), and reduced inflammatory cytokine levels (IL-6, IL-1β, TNF-α, and VEGF, p < 0.05). Subsequent validation in a murine blue light-induced retinal damage model demonstrated that IOB802 notably preserved retinal architecture, upregulated antioxidant defenses, and promoted the expression of tight junction proteins. Mechanistically, IOB802 suppressed inflammation by inhibiting the phosphorylation of the IκBα/NF-κB pathway. Through 16S rDNA sequencing and short-chain fatty acid (SCFA) profiling, IOB802 was further shown to restore gut microbial diversity, increase beneficial bacteria, including Lachnospiraceae, Rikenellaceae, and Bacteroidaceae (p < 0.05), and elevate concentrations of key SCFAs (butyrate, acetate, and propionate; p < 0.05), underscoring the role of the gut–retina axis in mediating retinal protection. Conclusions: In summary, IOB802 and its postbiotics alleviate blue light-induced retinopathy through antioxidative, anti-inflammatory, and microbiota-modulating mechanisms, offering novel insights into microbiome-based interventions for retinal diseases. Full article

Background: Previous studies have indicated that the gut microbiome and plasma metabolites play key roles in autism spectrum disorder (ASD), but their causal relationships remain unclear. Linkage disequilibrium score regression (LDSC) and Mendelian randomization (MR) are powerful tools for assessing genetic causality. This study uses LDSC and MR to investigate the genetic links between the gut microbiome and ASD and explore the mediating role of plasma metabolites. Methods: To explore the genetic relationships between the gut microbiome, plasma metabolites, and ASD, we obtained summary statistics from large-scale genome-wide association studies (GWAS). Gut microbiome data came from a MiBioGen consortium meta-analysis (N = 18,340), ASD data from the Danish Psychiatric Central Research Register (DPCRR) (N = 18,382), and plasma metabolite data from the Canadian Longitudinal Study of Aging (CLSA) (N = 8299). We applied LDSC and bidirectional MR to analyze the genetic associations between the gut microbiome and ASD and plasma metabolites and ASD. Mediation MR was used to assess the mediating role of plasma metabolites in the gut microbiome-ASD relationship. Results: LDSC analysis revealed significant genetic correlations between the gut microbiota Lachnospiraceae NK4A136 group and Sellimonas with ASD. Moreover, bidirectional MR demonstrated causal effects of five gut microbial genera on ASD risk, as indicated by inverse variance weighted (IVW) methods. Similarly, we identified 49 plasma metabolites that exhibited genetic correlations with ASD, and 58 metabolites had causal effects on ASD in MR analysis. Mediation analysis revealed that specific bacteria, Ruminiclostridium5, reduce the occurrence of ASD through metabolites Delta-CEHC and Docosadioate (C22-DC). Furthermore, Ruminococcaceae UCG005 and Sutterella modulate ASD by inhibiting Serotonin and N-acetyl-L-glutamine, respectively. Conclusions: This study provides evidence of a causal relationship between the gut microbiome and ASD, with plasma metabolites acting as a potential mediator. Our findings offer new insights into the causal mechanisms linking the gut microbiome and ASD and provide a theoretical foundation for microbiome-based therapeutic strategies. Full article

The interaction between the gut microbiota and the host immune system is pivotal in maintaining health or driving disease pathogenesis. The gut microbiota directly or indirectly modulates immune cells activation and inflammatory cytokines secretion through microbial metabolites, including short-chain fatty acids (SCFAs), tryptophan metabolites, bile acids, and polyamines. Conversely, the immune system regulates microbial community composition by maintaining the integrity of the epithelial barrier. In addition, antibiotics and probiotics can further regulate the inflammatory response by altering gut microbiota structure and microbial metabolites levels. This review systematically examines the bidirectional regulatory mechanisms among the gut microbiota, microbial metabolites, and inflammatory cytokines, and explores the impact of antibiotics and probiotics on this interaction network. These insights provide new targets for immune-related diseases. Full article

The gut microbiota plays a vital role in regulating the host’s physiological functions, including metabolism and immunity. The microbial composition and metabolism are modulated by multiple factors; host sex is an important yet under-explored determinant. To investigate the sex-dependent differences in the gut microbiota within the small and large intestine, sixteen somatic mature Jiangshan black pigs (eight males and eight females) were analyzed. The ileal and colonic microbial community and metabolites were profiled using 16S rRNA gene high-throughput sequencing and gas chromatography. Distinct sex-related discrepancies were observed in both the microbial composition and metabolism of the ileum and colon. In the ileum, compared with the male group, the female group exhibited higher abundances of Unclassified Chloroplast and Pseudomonas but a lower abundance of Romboutsia (adjusted p < 0.05). Functional prediction indicated enrichment in amino acid metabolism pathway in females, with more copy numbers of genes encoding key enzymes for propionate (mmdA) generation and elevated valerate levels (p < 0.05). In the colon, compared with the male group, the female group showed higher abundances of Streptococcus, Phascolarctobacterium, and Prevotella spp. and lower abundances of Eubacterium coprostano-ligenes group, Blautia, Christensenellaceae R-7 group, and Ruminococcus (adjusted p < 0.05). Additionally, the female group had more copies of genes mmdA and LcdA (associated with lactate production), along with higher concentrations of propionate and lactate (p < 0.05). Correlation analysis between microbial metabolites and sex-biased bacteria further revealed that the SCFA concentration positively correlated with Prevotella spp. and negatively correlated with Romboutsia, Christensenellaceae R-7 group, and Blautia. Collectively, these findings highlight the pronounced sex-dependent discrepancies in the microbial composition and metabolism within the small and large intestines of Jiangshan black pigs, providing new insights for precisely modulating the microbiota community and metabolism in pigs according to sex. Full article

Chronic kidney disease (CKD) affects over 850 million individuals globally and has no cure. The treatment of CKD centers on lifestyle interventions, including dietary changes, that slow disease progression. As emerging evidence suggests that fruit and vegetable-derived (poly)phenols may slow CKD, the goal of this narrative review is to synthesize current knowledge on the role of dietary (poly)phenols in CKD. To identify relevant articles, we searched databases including PubMed, Google Scholar, and Web of Science to identify relevant articles, using keywords including (poly)phenols, CKD, gut microbiome, and cardiovascular disease, among others. The relevant articles were synthesized into a summary of the evidence for (poly)phenols as a therapeutic strategy in CKD, though the paucity and heterogeneity of available research in this area precludes the identification of specific doses or types of (poly)phenols needed to slow CKD progression. The review is supplemented through our discussion of the gut microbiota and microbially derived metabolites as key targets in mediating the progression of CKD itself as well as subsequent cardiovascular outcomes. Finally, we discuss the integration of (poly)phenol-rich dietary patterns into CKD nutrition guidelines, highlighting future research directions to elucidate the potential therapeutic role of (poly)phenols in CKD. Full article

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by T-cell-mediated destruction of pancreatic beta cells, resulting in insulin deficiency. Both genetic predisposition and environmental factors contribute to T1D development, with growing evidence implicating the gut microbiome as a critical environmental modulator in disease pathogenesis. Gut microbial composition and derived metabolites influence immune homeostasis and autoimmunity. This review summarizes recent advances elucidating immune dysregulations in T1D and novel therapeutic strategies to preserve beta cell function. We discuss approaches such as immune cell engineering, including CAR-Treg therapy, and targeted modulation of immune signaling pathways like JAK-STAT. Furthermore, we explore the role of the gut microbiota and its metabolites in modulating host immunity and describe emerging microbiome-targeting interventions, including fecal microbiota transplantation and metabolite supplementation. These interventions show promise in modulating disease progression in preclinical and early clinical studies. An integrated understanding of immune and microbiome-related mechanisms is critical for developing next-generation therapies. Further research and clinical trials are needed to optimize these approaches and translate them into durable, personalized treatments for individuals with T1D. Full article

Atopic dermatitis (AD) is a multifactorial skin disorder characterized by immune and barrier dysfunction. The gut–skin axis is a bidirectional pathway through which gut and skin influence each other via microbial metabolites. Bioactive metabolites produced by microbial transformation of phytochemicals show potential for AD prevention. This study developed a computational systems biology pipeline that prioritized gut-derived metabolites from Philippine medicinal plants by integrating metabolite prediction, pharmacokinetics, network analysis, and molecular simulations. From 2231 predicted metabolites, 31 satisfied pharmacological criteria and were mapped to 199 AD-associated targets, with ALB, CASP3, and PPARG identified as hub genes. Two metabolites, THPOC and PM38, exhibited complementary target affinities and strong binding stability. THPOC stabilized ALB and CASP3, supporting barrier integrity and apoptosis regulation, while PM38 strongly engaged PPARG, modulating lipid metabolism and anti-inflammatory transcription. They exhibited comparable or superior docking scores, stable MD interactions, and favorable binding free energies, compared to abrocitinib, an approved AD treatment. DFT analysis confirmed electronic stability and donor–acceptor properties linked to target selectivity. These findings highlight THPOC and PM38 as promising immunometabolic modulators acting on key AD-related pathways. Collectively, this study introduces a reproducible systems-based computational discovery framework, offering a novel preventive strategy for AD. Full article

Xanthohumol (XN), a polyphenol from hops (Humulus lupulus), exhibits antioxidant, anti-inflammatory, antihyperlipidemic, and chemo-preventive activity. Preclinical evidence suggests gut microbiota are critical to mediating some of these bioactivities. Nevertheless, its precise impact on human gut microbiota, particularly at supplemental doses, remains poorly characterized. We evaluated 200 mg/day XN for 3 weeks on human gut microbiota in a eubiotic and dysbiotic model using the Simulator of the Human Intestinal Microbial Ecosystem (SHIME^®). Functional assessments of microbiota included quantification of XN metabolites, short-chain fatty acids (SCFAs), and untargeted metabolomics of the digestive metabolome. Bacterial composition was assessed by 16S rRNA gene sequencing. XN reduced alpha-diversity and short-chain fatty acid production in both models, as well as altered taxa abundance variably between models. XN disrupted bile acid metabolism through inhibition of microbial bile salt hydrolase (BSH). The modulation of bile acid metabolism has important implications for host-level bioactivity of XN. Full article