Search Results (570)

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by impaired social interaction, communication deficits, and repetitive behaviors. Recent research highlights the role of the gut microbiota in ASD pathophysiology, particularly through the microbiota–gut–brain axis. The microbiota may influence neurodevelopment via multiple signaling pathways, including the GABAergic and serotonergic systems, as well as the mTOR signaling pathway. This analytical review examines current evidence on microbiota alterations in ASD and evaluates microbiota-targeted strategies for diagnosis and treatment, focusing on fecal microbiota transplantation (FMT), probiotics, and diet-based therapeutic approaches. The review also provides a critical appraisal of the microbiota–gut–brain axis in the context of autism spectrum disorder. Full article

This study investigated the effects of dietary standardized ileal digestible (SID) lysine levels and amylose to amylopectin ratios on the intestinal health of broilers fed an 18.5% crude protein diet from 22 to 42 days of age. A total of 540 healthy male Ross 308 broilers were randomly assigned to nine treatments in a 3 × 3 factorial design consisting of three SID lysine levels (1.00%, 1.20%, and 1.40%) and three AM/AP ratios (0.19, 0.29, and 0.41), with six replicates of 10 birds each. Ileal morphology, intestinal barrier function and inflammation-related gene expression, and the composition of cecal microbiota were evaluated. Significant interactions between lysine level and AM/AP ratio were observed for Occludin, ZO-1, Claudin-1, and TNF-α expression, with the highest expression in the 1.40% lysine + 0.41 AM/AP group and the lowest in the 1.00% lysine + 0.19 AM/AP group. The VH/CD ratio showed a significant interaction, with the highest value in the 1.20% lysine + 0.19 AM/AP group and the lowest in the 1.40% lysine + 0.41 AM/AP group. IL-18 and IL-10 were primarily affected by the main effects of lysine and AM/AP ratio. The expression levels of both IL-10 and IL-18 increased with increasing lysine level and increasing starch AM/AP ratio. Dietary SID lysine level and AM/AP ratio interactively regulate the expression of barrier-related genes, inflammatory status, intestinal morphology, and cecal microbiota, potentially contributing to enhanced intestinal health in broilers. However, because microbial metabolites were not measured, the functional significance of the observed microbiota alterations remains speculative. In broilers fed an 18.5% CP diet, a combination of 1.20% SID lysine with an AM/AP ratio of 0.19 was identified as the optimal strategy for maintaining intestinal morphology from 22 to 42 days of age. Full article

Colorectal cancer (CRC) remains a leading cause of cancer-related morbidity and mortality, with substantial heterogeneity that is not fully explained by genetic alterations alone. Emerging evidence positions metabolic reprogramming as a central driver of tumor behavior, integrating glycolysis, mitochondrial function, lipid and amino acid metabolism, and autophagy into coordinated networks that extend beyond cancer cells to the tumor microenvironment. Tumor–immune metabolic competition and metabolite-mediated signaling shape immune responses, often promoting immunosuppression and resistance to immunotherapy, particularly in microsatellite-stable (MSS) CRC. Systemic factors, including obesity, insulin resistance, and the diet–microbiota axis, further modulate tumor metabolism and immune function, reinforcing disease progression. Metabolic biomarkers reflecting these multi-level interactions, spanning tumor-intrinsic pathways, immune contexture, and host metabolism, offer promising opportunities for improved patient stratification and therapeutic targeting, although clinical validation remains limited. Current treatments, including chemotherapy, targeted agents, and immune checkpoint inhibitors, are effective in selected subgroups but are constrained by resistance mechanisms. In this review, we propose an integrative immunometabolic framework in which tumor, immune, and systemic metabolic processes co-evolve, defining CRC progression and treatment response. Targeting this interconnected network through combinatorial and metabolism-oriented strategies may enable precision therapies, particularly for immunotherapy-resistant MSS CRC. Full article

Hepatocellular carcinoma (HCC) is the most frequent type of primary liver cancer and one of the leading causes of cancer-related mortality globally, with its incidence increasingly driven not only by viral hepatitis and alcohol-related etiologies but also by metabolic dysfunction-associated steatotic liver disease. Dietary intake can modify gut microbial activity and the production of microbial metabolites, which in turn may regulate hepatic immune signaling and metabolic pathways along the gut–liver axis. Microbiota-derived metabolites have emerged as important immunometabolic mediators linking dietary factors to hepatic immune responses and metabolic reprogramming. These metabolites, which have been shown to influence hepatic immune cell function and inflammatory signaling, include short-chain fatty acids, secondary bile acids, and tryptophan-derived indoles. Changes in the production and composition of these metabolites have been associated with immune dysregulation, chronic inflammation, and metabolic reprogramming that promote hepatocellular carcinoma development. This review highlights how diet–microbiota interactions reshape hepatic immunometabolism and discusses their potential translational relevance for prevention and therapeutic strategies in hepatocellular carcinoma. Full article

Growing evidence indicates that the gut microbiota is not a static ecosystem but a rhythmic metabolic organ whose oscillatory activity is tightly coordinated with host circadian biology. Disruption of this temporal alignment, through irregular diet, sleep disturbance, shift work, or social jet lag, may profoundly alter microbial composition and the production of neuroactive metabolites. These alterations have emerged as potential contributors to the pathophysiology of mood disorders. This review introduces the concept of chrono-metabolic psychiatry, a framework integrating circadian rhythms, gut microbiota dynamics, and host metabolic signaling in the development and course of depressive and bipolar disorders. In this framework, the term “chrono-metabolic” refers to the integration of biological timing, host metabolic regulation, and microbiota-derived metabolic signaling. Chrono-metabolic psychiatry therefore shifts the focus from static dysbiosis or neurotransmitter imbalance alone to the time-dependent interactions among circadian misalignment, microbial rhythmicity, immune regulation, metabolite production, and affective instability. Diurnal fluctuations in short-chain fatty acids, tryptophan–kynurenine metabolites, bile acids, and microbial-derived neurotransmitters interact with clock gene regulation, hypothalamic–pituitary–adrenal axis activity, neuroinflammation, and synaptic plasticity. Chrono-disruption may represent a transdiagnostic vulnerability factor and may confirm the bidirectional relationship between mood instability and microbiota rhythmicity. Emerging therapeutic implications, including chrono-nutrition, time-restricted feeding, targeted probiotic administration (“chronobiotics”), and the microbiota-modulating effects of psychotropic medications are discussed. By shifting from a compositional to a temporal–metabolic perspective, this model highlights the importance of microbial oscillations rather than static dysbiosis alone. Integrating circadian biology into microbiota research may enable metabolomic stratification and pave the way for precision psychiatry approaches grounded in host–microbe metabolic crosstalk. Future longitudinal and time-resolved multi-omics studies are needed to validate this framework and to translate it into clinically actionable interventions. Full article

Leishmaniases are vector-borne diseases transmitted by phlebotomine sand flies. While bacterial associations in sand fly microbiota are well studied, fungal communities remain poorly characterized, despite their potential role in insect biology and parasite transmission. This study aimed to isolate and characterize yeast-like and filamentous fungi from different developmental stages of Lutzomyia longipalpis, the main vector of visceral leishmaniasis in the Americas, to expand knowledge on fungal microbiota and its possible relevance to vector–parasite interactions. Sand fly eggs, larvae, pupae, and adults were sampled from a laboratory colony. Fungi were isolated from insect tissues and diets using culture-based methods. Morphological identification was complemented by partial sequencing of the ITS1-5.8S-ITS2 rDNA region to identify the species. Four fungi were consistently recovered: Candida guilliermondii, Cutaneotrichosporon dermatis, Penicillium sp., and Aspergillus sp. Their presence varied across developmental stages. Presence in the gut was observed for Cu. dermatis, Penicillium sp. and Aspergillus sp. in larvae and C. guilliermondii in adult females. Evidence suggested their presence in different stages from larvae to pupae, and sex-specific differences in adults, with fungi detected only in females. This work documented the mycobiota that may be associated with L. longipalpis, including the first report of Cutaneotrichosporon in sand flies. These findings highlight fungi that may be potential modulators of sand fly biology and Leishmania development, warranting further investigation into their ecological and epidemiological roles. Full article

Modern dairy production has greatly increased milk yield, but high productivity is often accompanied by greater metabolic pressure, particularly during the transition period. Ketosis, fatty liver, and subacute ruminal acidosis are major disorders that limit health, efficiency, and sustainability in high-yielding dairy ruminants. This review examines the rumen microbiota as a central biological interface linking diet, ruminal fermentation, epithelial function, hepatic metabolism, and inflammation. Under homeostatic conditions, the rumen microbiota supports lactation by converting dietary fibre, starch, and nitrogen into volatile fatty acids, microbial protein, and other metabolites required for gluconeogenesis, milk component synthesis, and epithelial maintenance. However, under excessive nutritional or physiological stress, especially high-concentrate feeding and periparturient negative energy balance, this system may shift toward dysbiosis, acid accumulation, lipopolysaccharide release, epithelial barrier impairment, and activation of gut–liver inflammatory pathways. These changes can contribute to the occurrence and interaction of subacute ruminal acidosis, ketosis, and fatty liver. We further summarize key factors affecting rumen microbial stability, including diet structure, host variation, physiological stage, environmental stress, feeding management, and ruminal epithelial volatile fatty acid absorption. Finally, microbiome-oriented strategies, such as gradual dietary transition, nutritional preconditioning, probiotics, postbiotics, functional metabolites, host metabolic support, and epithelial-targeted interventions, are discussed. Maintaining rumen microbial homeostasis should be regarded as a core principle for balancing high milk yield with long-term metabolic health. Future research should move beyond descriptive profiling toward causal validation of host–microbe interactions and the development of microbiome-based early-warning and individualized nutritional management systems. Full article

Dietary zeaxanthin exhibits low intestinal absorption efficiency, and circulating levels are reduced in individuals with type 2 diabetes, suggesting potential metabolic relevance. However, its role during early-stage diabetes remains incompletely understood. This study examined whether dietary zeaxanthin modulates early metabolic and inflammatory responses and influences host–microbiome interactions during early T2DM progression. Four-week-old male db/db mice and wild-type C57BL/6J mice were fed an AIN-93M diet with or without 0.02% (w/w) zeaxanthin for 4 weeks. Zeaxanthin attenuated body weight gain, adiposity, hyperinsulinemia, and circulating keratinocyte-derived chemokine levels in diabetic mice. These effects were accompanied by reduced ileal membrane localization of Niemann-Pick C1-like protein 1 and decreased hepatic expression of CD36, nuclear factor kappa B p65, and phosphoenolpyruvate carboxykinase 1, without significant improvement in fasting blood glucose or hepatic triglyceride accumulation. Cecal microbiota analysis showed reduced microbial richness in diabetic mice that was not restored by zeaxanthin; however, zeaxanthin induced selective compositional shifts, including enrichment of fermentation-associated taxa (e.g., Ruminococcaceae) and normalization of Clostridium XIVb. Predicted microbial pathways related to fermentation, amino acid biosynthesis, and cofactor metabolism were also altered. Collectively, dietary zeaxanthin modulated early metabolic and inflammatory adaptation and was associated with alterations in intestinal lipid handling, inflammatory signaling, and gut microbiome composition during early T2DM progression. Full article

Background: The dietary index for gut microbiota (DI-GM) holds promise for improving metabolic status, yet its mechanistic insight into metabolic syndrome (MetS) is unclear. Methods: In this cross-sectional study, we analyzed data from 20,800 participants in the NHANES (2005–2018). The DI-GM was developed based on dietary patterns, and MetS was defined according to the NCEP-ATP III criteria. Global DI-GM scores came from the Global Dietary Database (164 nations), with MetS burden estimation employing Global Burden of Disease data. We explored mediation by phenotypic age, insulin resistance (HOMA-IR), and inflammation. Secondary analyses involved subgroup stratification, restricted cubic splines (RCS), sensitivity testing, propensity score matching, and multiple imputations. Results: Globally, higher national DI-GM correlated inversely with metabolic risk factor frequency and major MetS sequelae. NHANES analysis found each one-unit DI-GM rise was associated with an 11% lower MetS likelihood (adjusted OR = 0.89, 95%CI: 0.87–0.91). RCS indicated a non-linear exposure–response curve, with prevalence reduction stabilizing above DI-GM = 4.972. Stratification showed significant effect modification by race/ethnicity, education, and income (p-interaction < 0.05). Mediation analysis identified significant roles for phenotypic aging (24.77%) and HOMA-IR (47.98%), but not inflammation (0.54%). Conclusions: A DI-GM-aligned diet correlated with lower MetS prevalence, with insulin sensitivity and phenotypic aging accounting for part of this association. Microbiota-targeted nutrition guidelines for MetS should prioritize metabolic health over anti-inflammation. Full article

Background: Overweight and obesity are chronic diseases that result from complex interactions including genetics, environment, eating behaviors, and limited access to a healthy diet. Amaranth protein (AmProt) has several health benefits, but no studies have examined its effects on the modulation of children’s gut microbiota. The work aimed to analyze serum levels and changes in gut microbiota in children aged 8–10 years with different body mass index (BMI) values after supplementation with AmProt. Methods: Participating children were allocated into three groups according to their BMI: normal weight (NW), overweight (OW), and with obesity (OB). Children received AmProt for 90 days. Levels of fasting blood glucose, cholesterol, triglycerides, and insulin were analyzed before and after diet supplementation. HOMA-IR and adinopectin/leptin ratio were evaluated. Feces were collected and metagenome analysis was carried out. Results: No changes in glucose levels were observed across groups and treatments; however, cholesterol and triglycerides levels tended to decrease. The HOMA-IR value increased in relation to BMI and no changes were observed after treatment. Firmicutes were highly abundant in all groups. The lower abundance of Ruminococcus was observed in the OW and OB groups. In the OW group, Blautia, Butyricicoccus, and Roseburia were also observed in increased abundance. In all groups, AmProt consumption tended to increase the abundance of Coproccus, Prevotella, and Collinsella. Conclusions: Supplementation of the children’s diet with AmProt showed an improvement in serum cholesterol and triglyceride levels, which could be related to changes in the microbiota related to lipid metabolism. Full article

Type 2 diabetes mellitus is a relevant cardio–renal–metabolic disorder in which chronic low-grade inflammation and oxidative stress have a crucial function in linking insulin resistance, endothelial dysfunction, β-cell impairment, and progressive organ injury. In this context, nutrition has emerged as a key modifiable determinant of metabolic homeostasis, capable of influencing inflammatory signalling, redox balance, mitochondrial function, and gut microbiota–host interactions. The objective of this review is to critically summarise the mechanistic connections among inflammation, oxidative stress, and diabetes progression, and to investigate how dietary factors and patterns, as well as nutrition-responsive biomarkers, influence these pathways and their cardiorenal consequences. We discuss the effects of macronutrient quality, dietary fibre, fatty acids, polyphenols, and specific micronutrients, including vitamin C, vitamin E, selenium, zinc, and magnesium, as well as the role of Mediterranean, DASH, and plant-based diets in improving glycaemic control, endothelial function, and cardio-renal risk profiles. We also summarise established and emerging biomarkers of inflammation and oxidative stress that may improve risk stratification and the evaluation of nutrition-based interventions. Overall, current evidence supports a shift from a purely glucose-centred approach toward an integrated model in which dietary modulation of inflammatory and oxidative pathways helps reduce cardiovascular and renal risk. However, heterogeneity of interventions, variability in biomarker assessment, and interindividual differences in dietary response represent major limitations. Future research should focus on biomarker-informed, precision-oriented nutritional approaches integrated within contemporary cardio–renal–metabolic care. Full article

Host–microbiota interactions during the neonatal window of opportunity have gained significant interest as factors influencing long-term health. Factors such as nutrient availability may shape the microbial community, and iron is no exception to this rule. Although the use of iron supplementation is widespread during infancy, this micronutrient is known to have profound effects on gut microbiota. This study aimed to determine how early-life iron supplementation shapes gut microbiota composition and whether it influences recovery from gut dysbiosis later in life. Three-week-old female C57BL/6 mice were fed an iron-excess diet for five weeks during the critical period of microbiota establishment. After a two-week washout period to normalize luminal iron content, dysbiosis was induced using either dextran sulfate sodium-induced acute colitis or antibiotic treatment. Mice were then allowed an 8-week recovery period. Gut microbiota composition was longitudinally analyzed by 16S rRNA gene sequencing of fecal samples. Early-life iron supplementation induced durable alterations in gut microbiota composition, with differences persisting even after luminal iron normalization (β-diversity, PERMANOVA p < 0.01). At the endpoint, mice exposed to an iron-sufficient diet remained significantly more distant from their baseline compared to the excess iron group in both the dextran sulfate sodium (33% greater distance) and antibiotic (41% greater distance) models (both p < 0.05). Notably, this pattern was not observed when supplementation occurred in adulthood. In the dextran sulfate sodium model, mice that received an iron-sufficient diet during early life showed an expansion of the probiotic Ligilactobacillus murinus, which positively correlated with fecal succinate levels. Conversely, in the antibiotic-induced model, early-life exposure to an iron-sufficient diet was associated with a more pronounced dysbiosis characterized by a nearly two-fold-greater loss in α-diversity compared to 500 ppm mice (∆Shannon: 1.98 ± 0.22 vs. 1.02 ± 0.25, p < 0.01). These findings suggest that early-life iron supplementation influences long-term host–microbiota interactions and recovery from gut dysbiosis. Full article

Seasonal variation can strongly restructure the gut microbiota of herbivores, but under captive conditions it remains unclear whether these shifts outweigh host-species effects when diet is standardized. Here, we profiled the gut microbiota of captive mouflon, argali, and blue sheep in summer and winter using 16S rRNA amplicon sequencing, ASV-based compositional beta-diversity analysis, ANCOM-BC2, and PICRUSt2 functional prediction. Across hosts, Chao1 richness decreased in winter, whereas Shannon diversity remained comparatively stable, indicating that seasonal change affected richness more strongly than evenness. CLR-based ordination further showed that the three species were relatively close in summer but became more clearly separated in winter, especially mouflon and blue sheep, consistent with pronounced seasonal restructuring under a common diet. At the phylum level, summer communities were broadly similar and dominated by Firmicutes_A and Bacteroidota, whereas winter brought stronger taxonomic shifts in mouflon and blue sheep, including marked increases in Proteobacteria and Firmicutes_D. Argali showed a narrower and taxonomically different seasonal response. Genus-level analyses similarly indicated that winter restructuring was host-dependent rather than uniform, with winter-associated enrichment of several Bacillales/Planococcaceae-related lineages and Proteobacteria-associated taxa, particularly in mouflon and blue sheep. Predicted functional profiles inferred by PICRUSt2 also shifted between summer and winter within each host species, suggesting that seasonal restructuring extended beyond taxonomy, although these results should be interpreted as inferred functional potential rather than direct metabolic activity. Overall, our findings support seasonality as the primary axis of gut microbiota variation in captivity, while the host species modulates the magnitude and taxonomic features of these seasonal changes. These results highlight the need to consider seasonal effects in captive management and provide a basis for future multi-omics validation of host-microbiome interactions in wild ungulates. Full article

Chronic kidney disease (CKD) is associated with a markedly increased risk of cardiovascular (CV) morbidity and mortality that cannot be fully explained by traditional risk factors. Emerging evidence highlights the central role of the gut–kidney–heart axis, whereby gut microbiota dysbiosis promotes the generation and systemic accumulation of uremic toxins, including indoxyl sulfate (IS), p-cresyl sulfate (PCS), and trimethylamine N-oxide (TMAO). These metabolites contribute to endothelial dysfunction, oxidative stress, inflammation, and vascular remodeling, thereby accelerating CV disease progression in CKD. Dietary patterns represent a key modifiable factor influencing gut microbiota composition and metabolic activity. The Mediterranean diet, characterized by high intake of plant-based foods, dietary fiber, and polyphenols, and low consumption of red and processed meats, has emerged as a promising microbiota-targeted strategy. It promotes saccharolytic fermentation, enhances short-chain fatty acid production, and reduces proteolytic pathways responsible for uremic toxin generation. Accumulating evidence from observational studies, meta-analyses, and dietary intervention trials suggests that adherence to Mediterranean and plant-based dietary patterns is associated with reduced uremic toxin burden, improved renal outcomes, and lower CV risk in CKD populations. However, direct interventional evidence linking Mediterranean diet adherence to changes in specific uremic toxin levels remains limited. This narrative review summarizes current evidence on diet–microbiota interactions in CKD and highlights the Mediterranean diet as a biologically plausible strategy for targeting the gut–kidney–heart axis. Future well-designed randomized controlled trials (RCTs) are needed to confirm causal relationships and support clinical implementation. Full article

Background/Objectives: Diet is a primary and modifiable determinant of gut microbiota composition, diversity, and metabolic activity, thereby shaping microbial-derived metabolites, immune and inflammatory signalling, neuroendocrine regulation, and neural communication with the central nervous system. Western dietary patterns, characterised by high intake of ultra-processed foods, saturated fats, and low dietary fibre, are consistently associated with gut dysbiosis, impaired intestinal barrier function, chronic low-grade inflammation, and increased risk of depression, anxiety, cognitive impairment, and neurodegenerative disorders. Methods: This narrative review synthesises evidence from human observational studies, randomised controlled trials, animal models, and mechanistic investigations examining interactions among diet, gut microbiota, and mental health or neurobiological outcomes. Literature searches were conducted in PubMed, Scopus, and Web of Science for articles published up to December 2025. Results: The study highlights the therapeutic potential and limitations of dietary interventions, prebiotics, probiotics, and psychobiotics, and critically evaluates them. Also facilitates an improved understanding of diet–microbiome–brain interactions, which may help the development of personalised, nutrition-based strategies integrated into mental health prevention and clinical care. Conclusions: These findings support diet-based, microbiome-informed strategies as scalable adjuncts in mental health prevention and care. Full article