Search Results (1,873)

Pinctada martensii is a marine resource with potential for bioactive peptide development, but its anti-photoaging properties remain underexplored. In this study, Pinctada martensii meat hydrolysates (PME) were prepared by enzymatic hydrolysis, and their anti-photoaging effects were evaluated in an in vivo ultraviolet-B (UVB)-irradiated nude mouse model. The results showed that PME markedly ameliorated UVB-induced skin damage. UVB increased epidermal thickness from 21.60 μm in the Control to 47.50 μm in the Model, and PME reduced epidermal thickness to 22.46 μm. Dermal collagen content decreased from 64.58% in the Control to 26.22% in the Model and was restored to 52.75% by PME. UVB upregulated matrix metalloproteinases-1 (MMP-1), MMP-3 and MMP-9 by approximately 2.20-, 1.93- and 3.09-fold relative to the Control, and PME suppressed these matrix metalloproteinases (MMPs) by approximately 61%, 65% and 52%, respectively. Extracellular signal-regulated kinase (ERK) expression increased to 1.41-fold in the Model and was reduced to about 1.05-fold after PME treatment, suggesting inhibition of collagen degradation-related pathways. Untargeted serum metabolomics identified 205 differential metabolites between the Model and the Control, and PME shifted metabolite profiles toward those of the Control. Total short-chain fatty acids (SCFAs) decreased from 868.69 μmol/g in the Control to 301.34 μmol/g in the Model and increased to approximately 562 μmol/g after PME treatment, accompanied by modulation of the gut microbiota including recovery of Lachnospiraceae members, indicating involvement of the gut–skin axis. These findings support the potential of Pinctada martensii meat as a source for developing novel functional foods targeting skin photoaging. Full article

Background: Pediatric Short bowel syndrome (SBS) is the leading cause of intestinal failure and is characterized by persistent dysbiosis that negatively impacts intestinal adaptation and growth. Although microbiota modulation via pre-, pro-, and synbiotics represents a promising strategy, current evidence remains fragmented. This narrative review aims to critically assess the efficacy and safety of such interventions in the management of pediatric SBS. Methods: A structured literature search was conducted on PubMed up to November 2025. Fourteen relevant studies were included, comprising clinical trials, preclinical animal models, and significant case reports regarding the use of biotics in SBS. Results: The analysis reveals a microbiological dichotomy based on nutritional status: parenteral nutrition (PN)-dependent patients exhibit an excess of Proteobacteria associated with infectious risk, whereas weaned patients present a metabolic risk of D-lactic acidosis due to carbohydrate fermentation. Regarding efficacy, long-term synbiotic treatments (>12 months) demonstrated significant improvements in growth and nutritional status, likely mediated by increased production of short-chain fatty acids (SCFAs) and mucosal adaptation, unlike short-term probiotic cycles. However, serious adverse events (Lactobacillus sepsis and D-lactic acidosis) were reported, predominantly in patients with central venous catheters or malabsorption. Conclusions: Biotics offer therapeutic potential for intestinal failure, but their use cannot be empirical. The safety profile should be carefully selected, especially in central venous catheter (CVC) carriers. Future strategies must evolve towards precision medicine, prioritizing non-D-lactate-producing strains and personalized protocols based on the patient’s nutritional phase. Full article

The gut microbiota’s (GM) regulation of inflammation and oxidative stress is supported by existing evidence, and its dysregulation relates to brain disease. Indeed, probiotics and prebiotics have been shown to improve cognitive function. This is associated with a stronger gut and blood–brain barrier and less gut inflammation. Oligofructose-enriched inulin alters the GM, reduces body fat, and lowers interleukin-6 (IL-6) in obese patients. Moreover, by increasing glutathione (GSH), the ketogenic diet (KD) prevents seizures and also benefits the intestinal short-chain fatty acid (SCFA) profile. Given the evidence on managing epileptic conditions, the aim of this review is to assess how changing the gut microbiota (GM) can be a therapeutic method for preventing neurodegenerative dysfunctions associated with epileptic seizure onset and progression, with a focus on innovative supplement strategies, including endogenous and exogenous antioxidants, nutrition, and new phyto-therapies. Indeed, though drugs are the main treatment for epilepsy, the KD and other supplements are increasingly being considered. These compounds affect neuronal excitability, neurotransmitter release, and neuroinflammation, thus providing an anticonvulsant effect. Specifically, the KD prevents seizures by increasing GSH levels, which represents a crucial endogenous antioxidant that plays a key role in counteracting neuroinflammation and gut microbiota dysfunction. Furthermore, due to their antioxidant and anti-inflammatory properties, plant extract derivatives may be new agents that could reduce neuroinflammation in seizures, affecting the gut–brain axis (GBA) through the intestinal microbiota. In conclusion, data suggest that further clinical studies are needed to explore how the GM impacts epilepsy, and how specific nutraceuticals might offer probiotic benefits. Thus, a combined effect of nutraceuticals and functional food might be appealing, potentially resulting in a more beneficial therapeutic outcome. Full article

Ulcerative colitis (UC) is a chronic inflammatory bowel disease with a rising global incidence in recent years. Dengzhan shengmai (DZSM), a plant-based formulation clinically used in the management of cerebrovascular diseases, possesses documented anti-inflammatory and antioxidant properties; however, its effects on UC are unclear. In this study, we investigated the therapeutic potential and underlying mechanism of DZSM in a dextran sulfate sodium (DSS)-induced murine colitis model. Our results showed that DZSM significantly alleviated UC-related parameters. Mechanistically, DZSM remodeled gut microbiota dysbiosis, specifically enriching the abundance of short-chain fatty acid (SCFA)-producing bacteria and elevating colonic levels of SCFAs. Notably, butyrate upregulated the expression of the sodium-dependent vitamin C transporter 1 (SVCT1) in colonic epithelial cells, thereby enhancing cellular vitamin C (VitC) uptake. The accumulated VitC synergized with butyrate to exert potent antioxidant and anti-inflammatory effects, further reinforcing epithelial barrier function. Importantly, fecal microbiota transplantation (FMT) confirmed that the protective effects of DZSM on UC were achieved by modulating gut microbiota, at least partially. Collectively, our findings demonstrate for the first time that DZSM alleviates DSS-induced colitis in mice through a novel butyrate-SVCT1-VitC axis driven by gut microbiota remodeling, providing new mechanistic insights into the microbiota-dependent efficacy of plant-based medicine. Full article

The gut microbiota plays a critical role in hindgut health and nutrient utilization in monogastric animals. Alfalfa fiber meal (AFM) was rich in essential vitamins and minerals as a valuable nutritional supplement. In this study, an in vitro fermentation model was established using fecal microbiota from pregnant sows as the inoculum to evaluate the effects of different supplementation levels of alfalfa fiber powder (AFM) on fermentation metabolites and microbial community composition, with particular attention to interactions between the microbiota and metabolites. Fecal inocula from healthy sows were fermented with AFM at three inclusion levels: low (LAFM: 50 mg), medium (MAFM: 100 mg), and high (HAFM: 200 mg). Fermentation samples were collected at 8, 12, 24, and 36 h for analysis of gas production and short-chain fatty acid (SCFAs) concentrations. Microbial community composition was characterized at 36 h, followed by correlation analysis between dominant genera and fermentation parameters. The results showed that total gas and hydrogen production increased significantly with both AFM level and time, while hydrogen sulfide decreased across all treatments. Methane production rose in the early stages and remained elevated only in the high-AFM group. AFM supplementation promoted the production of total and individual short-chain fatty acids in a dose- and time-dependent manner. Microbial analysis revealed reduced Fusobacterium and increased Lactobacillus, Bacteroides, and Collinsella, with high AFM further enriching Prevotella and Megasphaera. Positive correlations were observed between SCFA production and Collinsella, Prevotella, and Olsenella, whereas hydrogen sulfide correlated negatively with Prevotella and Sharpea. AFM effectively improved gut microbial composition and fermentation efficiency, with 100 mg identified as a more balanced level of fermentation additive supplementation for pregnant sows under in vitro conditions. Full article

Background and Objectives: Cardiometabolic disease, a term encompassing metabolic syndrome (MS) and cardiovascular disease (CVD), represents a major and growing global health burden driven by interconnected metabolic and cardiovascular dysfunction. Emerging evidence suggests that the gut microbiota plays a central role in modulating metabolic, inflammatory, and cardiovascular (CV) pathways, giving rise to the concept of the heart–gut axis. However, human evidence integrating microbiome-mediated mechanisms across the cardiometabolic spectrum remains incompletely synthesized. This focused systematic review aimed to synthesize the current human evidence on microbiome-mediated mechanisms linking metabolic syndrome (MS) and related metabolic phenotypes with cardiovascular risk (CVR) and subclinical cardiovascular (CV) outcomes within the conceptual framework of the heart–gut axis. Materials and Methods: A systematic literature search was conducted in PubMed, Scopus, Web of Science, and the Cochrane Library in accordance with PRISMA 2020 guidelines. Human observational and interventional studies evaluating gut microbiota composition, function, or microbiota-derived metabolites in relation to cardiometabolic, and CV outcomes were included. Risk of bias was assessed using the Cochrane RoB 2 and ROBINS-I tools, and findings were synthesized narratively. Results: Ten human studies published between 2016 and 2025 met the inclusion criteria. Across these studies, gut dysbiosis was consistently associated with adverse cardiometabolic risk profiles and subclinical CV outcomes, including insulin resistance, systemic inflammation, subclinical atherosclerosis, and CV prognosis in high-risk populations. Microbiota-derived metabolites, particularly trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), as well as emerging metabolites such as phenylacetylglutamine (PAGln) and imidazole propionate (ImP), were identified as key mediators linking metabolic syndrome and related metabolic disturbances with CVR and subclinical cardiovascular disease (CVD). Markers of intestinal barrier dysfunction and endotoxemia further supported the role of chronic low-grade inflammation within the heart–gut axis. Conclusions: Current human evidence supports the heart–gut axis as a biologically plausible and clinically relevant contributor to cardiometabolic disease. Gut microbiota-derived metabolites, intestinal barrier dysfunction, and systemic inflammation represent interconnected pathways linking MS with CVR. Advancing our understanding of these mechanisms may inform the development of microbiome-targeted strategies to complement established approaches for cardiometabolic and CV prevention. Full article

Background: Perimenopause is characterized by pronounced fluctuations in ovarian steroids, which are associated with an increase vulnerability to anxiety symptoms. Growing evidence indicates that declining estrogen levels influence gut microbiota composition and microbial metabolic activity, thereby modulating neuroimmune and neuroendocrine pathways involved in emotional regulation. This review explores gut microbiota alterations occurring during the menopausal transition and critically evaluates dietary strategies targeting microbiota–gut–brain mechanisms potentially relevant to perimenopausal anxiety. Methods: A structured literature search was conducted in PubMed, Scopus, and Web of Science to identify clinical, translational, and preclinical studies addressing: (i) gut microbiota changes across perimenopause and menopause; (ii) microbiota–gut–brain pathways implicated in anxiety; and (iii) dietary patterns, nutrients, probiotics, and prebiotics with documented microbiota-modulating effects. The available evidence was synthesized narratively, with particular attention to biological plausibility and clinical relevance. Results: The perimenopause transition is associated with reduced microbial diversity, depletion of Lactobacillus, Bifidobacterium, and short-chain fatty acid (SCFA)-producing taxa, and enrichment of pro-inflammatory microbial signatures. These alterations are linked to increased intestinal permeability, altered tryptophan-kynurenine metabolism, immune activation, and dysregulated hypothalamic–pituitary–adrenal axis activity. Dietary interventions, including Mediterranean-style diets, fiber- and polyphenol-rich foods, fermented products, and selected probiotic and prebiotic formulations, have been shown to modulate gut microbial composition, enhance SCFA production, and attenuate inflammatory and neuroendocrine stress pathways. Preliminary evidence suggests potential anxiolytic benefits; however, randomized controlled trials specifically targeting perimenopausal populations remain limited. Conclusions: Gut microbiota dysbiosis may contribute to anxiety vulnerability in perimenopausal women through interconnected immune, metabolic, and neuroendocrine mechanisms. Dietary modulation of the intestinal microbiota represents a biologically plausible and low-risk complementary approach to support emotional well-being during this transitional period. Well-designed, perimenopause-specific clinical trials are needed to confirm efficacy and inform microbiome-based nutritional strategies. Full article

Background: Emerging evidence links the gut microbiome to chronic pain processing. Inulin, a prebiotic fibre, modulates the gut microbiome, while physiotherapy-supported exercise (PSE) improves pain and function. We evaluated the effects of inulin supplementation with and without PSE on knee osteoarthritis (OA) pain. Methods: In a 2 × 2 factorial RCT, 117 community-dwelling adults with knee OA received 6 weeks of: (A) 20 g/day inulin, (B) digital PSE (Joint Academy™), (C) inulin +PSE, or (D) 10 g/day maltodextrin. Primary outcome: pain (Numerical Rating Scale). Secondary: 30 s sit-to-stand (30-CST), timed up and go (TUG), grip strength, and quantitative sensory testing. Serum short-chain fatty acids (SCFAs) and glucagon-like peptide-1 (GLP-1) were measured. The study was not powered to detect synergistic interaction. Results: A total of 117 participants (58.1% female; mean ± SD age = 67.5 ± 9.4 years; BMI = 29.5 ± 5.3 kg/m²; NRS = 3.96 ± 2.67) completed the trial. Pain improved with inulin (baseline-adjusted between-group mean difference (Δ) = −1.11 [95%CI −2.18, −0.04], p = 0.045) and PSE (Δ = −1.55 [95%CI −2.52, −0.58], p = 0.002) compared to placebo, with no synergistic effect. PSE improved TUG (p = 0.02) and 30-CST (p = 0.0004), while inulin improved grip strength (p = 0.002), pressure pain thresholds (p = 0.009) and temporal summation (p = 0.025) compared to placebo and had significantly lower dropout rates (3.6%) compared with PSE (21% p < 0.01). Only inulin increased SCFA butyrate (p = 0.0248) and GLP-1 (p = 0.0109), and higher GLP-1 was associated with improved grip strength, suggesting a gut–muscle link. Conclusions: Inulin and PSE each produced meaningful pain reductions. Only inulin improved pain sensitivity and grip strength, the latter paralleled by increased GLP-1, and had much higher rates of retention compared to PSE. Full article

Adolescence represents a critical window of metabolic plasticity, during which profound hormonal, neurobiological, and physiological remodelling increases susceptibility to nutritional exposures. In parallel with the rising prevalence of obesity, insulin resistance, metabolic syndrome, and non-alcoholic fatty liver disease among young people, there is growing interest in the potential for functional food components to modulate epigenetic pathways that govern metabolic programming. This narrative review synthesises current evidence (2015–2025) from PubMed, Scopus, Web of Science, and Embase to elucidate how diet-derived bioactive compounds influence epigenetic regulation relevant to adipogenesis, appetite control, insulin signalling, and lipid homeostasis during adolescence. Particular emphasis is placed on molecular mechanisms, including DNA methylation changes in genes regulating adipocyte differentiation, hypothalamic neuropeptide expression, and pancreatic β-cell function; histone modifications, such as acetylation and methylation events that remodel chromatin accessibility in metabolic tissues; and modulation of microRNA networks implicated in lipid metabolism, inflammatory signalling, and insulin secretion. Furthermore, the review examines the interplay between diet, the gut microbiota, and the epigenome, highlighting the role of microbially derived short-chain fatty acids (SCFAs) as endogenous histone deacetylase inhibitors and mediators of epigenetic remodelling in adipose tissue. By linking these mechanisms to specific functional food components, including polyphenols, long-chain omega-3 fatty acids, fermentable dietary fibre, and other bioactive molecules, we demonstrate how nutritional signals can counteract maladaptive metabolic trajectories and potentially reduce the intergenerational transmission of metabolic risk. A deeper understanding of these epigenetic effects provides the foundation for developing personalised nutrition strategies aimed at preventing metabolic disorders from emerging during adolescence and beyond. Full article

Type 2 diabetes (T2D) represents a major public health challenge, being associated with significant metabolic and cardiovascular complications. Evidence-based nutritional interventions are essential for the prevention and management of the disease. Dietary fibers, particularly soluble fibers such as psyllium, β-glucan, inulin, and fermentable fiber blends, have demonstrated beneficial effects on glycemia, glycated hemoglobin (HbA1c), lipid profile, body weight, and medication requirements. This narrative review synthesizes the results of recent clinical trials and meta-analyses, highlighting the underlying physiological mechanisms, including colonic fermentation and short-chain fatty acid (SCFA) production, as well as the impact on gut microbiota composition. The findings support the integration of soluble fibers into a personalized dietary plan as part of a multidimensional strategy for T2D management. Further long-term randomized studies are warranted to standardize doses and assess the metabolic and microbiota-mediated effects of dietary fibers. Full article

Introduction: Intensive chemotherapy protocols and hematopoietic stem cell transplantation (HSCT) in children with cancer frequently lead to severe complications, such as mucositis and immune dysfunction. A growing body of evidence indicates that these complications are closely associated with the patient’s nutritional status and the composition of the gut microbiome, which becomes profoundly destabilized as a result of cytotoxic therapy and antibiotic use. Background: The aim of this review is to critically evaluate the current state of knowledge on the interplay between gut dysbiosis, metabolomic profiles—with particular emphasis on short-chain fatty acids (SCFAs)—and treatment-related toxicity in pediatric patients, as well as to delineate pathways toward personalized nutritional therapy. Methods: A narrative review was conducted, including clinical and preclinical studies published between January 2015 and October 2025. PubMed/MEDLINE, Embase, Cochrane Library, and other databases were searched, focusing on changes in microbiome composition, correlations between gut-derived metabolites and the severity of complications (sepsis, graft-versus-host disease [GvHD], mucositis), and the effects of targeted nutritional interventions (probiotics, prebiotics, postbiotics, and fecal microbiota transplantation [FMT]) on microbiome modulation during anticancer therapy. Results: The analysis demonstrates that pediatric oncologic treatment leads to a marked reduction in microbial diversity, including the loss of protective Clostridiales taxa (e.g., Faecalibacterium), accompanied by an overgrowth of Proteobacteria pathobionts. Metabolomic profiling indicates that low SCFA levels (e.g., butyrate < 20–50 µmol/g) are a strong predictor of severe mucositis, prolonged neutropenia, and an increased risk of sepsis. Interventions aimed at restoring eubiosis and enhancing SCFA production show potential in strengthening the intestinal barrier, modulating immune responses, and enabling maintenance of the planned relative dose intensity (RDI) of chemotherapy by reducing treatment-related toxicity. Conclusions: Gut microbiome profiling and fecal metabolomics represent promising prognostic tools in pediatric oncology. There is an urgent need for further research employing “omics”-based approaches to develop precise, individually tailored nutritional protocols. Such strategies, including postbiotics and FMT, may minimize treatment-related adverse effects and improve long-term clinical outcomes in pediatric patients. Full article

Background/Objectives: Accumulating evidence and clinical observations suggest that the gut microbiome plays a crucial role in functional dyspepsia (FD). However, the precise characterization of this relationship is unclear. This systematic review and meta-analysis aimed to elucidate the potential role of the gut microbiome in FD based on evidence from published clinical studies. Methods: A comprehensive search of three databases (PubMed, Google Scholar, and Web of Science) was conducted, and 17 relevant clinical studies, including 8 observational studies and 9 interventional studies, published up to September 2025, were identified. Data on the gut microbiome and FD were extracted and subjected to meta-analysis. Results: Meta-analysis revealed no significant differences in gut microbiota α- or β-diversity between patients with FD and healthy controls (Shannon index: standardized mean difference [SMD] = −0.12, 95% confidence interval [CI] −0.90 to 0.67, I² = 88%). In contrast, effective interventions induced notable shifts in the microbial community structure (pooled SMD = 0.27, 95% CI −0.28 to −0.83, I² = 58%). These shifts were accompanied by increased short-chain fatty acid (SCFA) production and intestinal tight-junction protein levels, which coincided with improved FD symptoms. Conclusions: Although no significant differences in the gut microbiota were detected between patients with FD and healthy controls, interventions in patients with FD induced marked changes in the microbial community. Modulation of gut microbiota-related metabolites, such as SCFAs, may represent a promising therapeutic strategy for the management of FD. Full article

Background/Objectives: Animal studies have shown that food additives may adversely affect the gut microbiome. However, the effect of food additives on the microbiome in adults with Crohn’s disease (CD) remains less explored. This study investigated the impact of food additives on gut microbiome and fibre fermentation capacity in adults with CD and healthy controls (HCs) using in vitro faecal fermentations. Methods: Faeces from 6 HCs and 6 patients with CD in clinical remission (Harvey Bradshaw Index < 5) were used for in vitro fermentation of a fibre mix with one of 12 food additives (calcium propionate, carboxymethylcellulose, carrageenan kappa, cinnamaldehyde, maltodextrin, polysorbate-80, potassium sorbate, sodium benzoate, sodium sulphite, titanium dioxide, turmeric, and xanthan gum). Short-chain fatty acids (SCFAs) were measured using gas chromatography, the microbiome was profiled with 16S rRNA amplicon sequencing and total bacterial load was measured with qPCR. Results: Maltodextrin increased acetate production in both groups. In HCs, turmeric increased acetate and butyrate production, sodium sulphite reduced acetate production, and maltodextrin reduced butyrate production. Microbiome Shannon α-diversity increased with titanium dioxide (both groups), and with carrageenan kappa only in patients with CD. In both groups, the addition of maltodextrin and polysorbate-80 induced significant shifts in microbiome structure (β-diversity). Significant shifts were seen with maltodextrin (HC: R² = 6.8%, p = 0.001; CD: R² = 5.1%, p = 0.004) and sodium sulphite (HC: R² = 6.9%, p = 0.001). Maltodextrin significantly decreased the estimated absolute abundance of Escherichia–Shigella in patients CD; sodium benzoate, potassium sorbate, and calcium propionate did so in HCs. Faecalibacterium decreased in the presence of polysorbate-80 in the HC and CD groups, as well as in the presence of maltodextrin in the CD group. Total bacterial load decreased with polysorbate-80, potassium sorbate, maltodextrin and calcium propionate in both groups. Xanthan gum decreased total bacterial load in HCs. Conclusion: Certain food additives significantly affected fibre fermentation capacity and microbiome structure, with only modest differences observed according to participants’ health status. Full article

Background: Gut microbiota alterations are increasingly recognized as key contributors to the development and clinical course of inflammatory bowel disease (IBD), particularly in pediatric patients, in whom microbial maturation and immune regulation are still evolving. Objective: This study aimed to assess intestinal microbiota composition and dysbiosis severity in pediatric IBD, with comparative analyses according to disease phenotype (Crohn’s disease versus ulcerative colitis) and therapeutic strategy (biologic versus non-biologic treatment). Methods: A prospective cohort of 60 pediatric patients diagnosed with IBD based on Porto criteria was evaluated. Fecal samples were obtained at baseline and after three months of combined standard IBD treatment and adjunct microbiota-targeted therapy, and were analyzed using an AI-assisted microbiota profiling platform. A semi-quantitative dysbiosis score was calculated based on the relative abundance of proinflammatory taxa and depletion of short-chain fatty acid (SCFA)-producing bacteria. Microbial parameters were correlated with clinical and therapeutic variables, including the Organism of Interest metric and the Gut Microbiota Index (GMI). Results: Dysbiosis severity was significantly higher in patients with Crohn’s disease compared with ulcerative colitis (9.65 ± 1.44 vs. 8.42 ± 1.88, p = 0.037). Patients receiving biologic therapy showed a trend toward lower dysbiosis scores and improved microbial indices, although statistical significance was not reached. Severe dysbiosis was identified in 46.7% of the cohort. Strong positive correlations were observed between the dysbiosis score, Organism of Interest metric and GMI (r = 0.68–0.72, p < 0.01). Conclusions: Pediatric IBD is associated with a reproducible dysbiotic profile, more pronounced in Crohn’s disease and partially modulated by biologic therapy. The observed correlations between microbiota-derived indices support their potential utility as complementary markers of intestinal microbial imbalance and disease activity. Full article

Diarrhea in kids is a significant health and economic concern for small-scale ruminant farms. This study aims to investigate the properties of Lactobacillus amylovorus as a treatment for kids with diarrhea and its effect on the composition of the gut microbiota. A total of 20 neonatal goats (approximately 2 months old) were divided into three groups: healthy control (HC, n = 4), diarrhea (D, n = 8), and diarrhea treated with probiotic (DT, n = 8). We tracked gut microbial profiles, fecal consistency, short-chain fatty acids (SCFAs), and clinical symptoms. Probiotic-treated kids recovered fully from diarrhea within two weeks, while their untreated counterparts showed signs of clinical deterioration and gradual emaciation. Kids with diarrhea had lower microbial richness, according to alpha diversity analysis, and this was only partially restored after probiotic treatment. The kids with diarrhea had the lowest Shannon, ACE, Simpson, Dominance, Pielou-e, and Chao1 indices compared to the HC group, while the administration of Lactobacillus amylovorus significantly (p < 0.05) restored their normal enrichment in the DT group compared to the D group. The healthy group had a higher abundance of Verrucomicrobiota, while Firmicutes and Bacteroidota predominated in all groups. Bacteroides and Akkermansia predominated in the healthy and treated groups. At the genus level, analysis showed elevated levels of Escherichia-Shigella and UCG-005 in kids with diarrhea. In addition, the concentration of each SCFA in the D group was significantly (p < 0.05) lower than in the HC group. This study provides novel evidence that Lactobacillus amylovorus administration not only alleviates diarrhea but also uniquely restores the production of key SCFAs—including butyrate, acetate, and propionate—in neonatal goats, a finding not previously reported in this species. The concurrent recovery of microbial diversity and SCFA profiles highlights the dual mechanistic potential of Lactobacillus amylovorus as a gut microbiota modulator and metabolic therapeutic in young ruminants. These results lend credence to its potential as a probiotic treatment for small ruminant enteric diseases. Full article