Search Results (1,081)

Butyrate supplementation has gained considerable attention for its potential benefits in livestock, particularly concerning intestinal health and growth performance. This review synthesizes recent research on the diverse roles of butyrate, across various livestock species. As a short-chain fatty acid, butyrate is known for enhancing intestinal development, improving immune function, and modulating microbial diversity. Studies indicate that butyrate supports gut barrier integrity, reduces inflammation, and optimizes feed efficiency, especially during the critical weaning and post-weaning periods in calves, piglets, and lambs. Supplementation with butyrate in livestock has been shown to increase average daily gain (ADG), improve gut microbiota balance, promote growth, enhance gut health, boost antioxidant capacity, and reduce diarrhea. Additionally, butyrate plays a role in the epigenetic regulation of gene expression through histone acetylation, influencing tissue development and immune modulation. Its anti-inflammatory and antioxidant effects have been demonstrated across various species, positioning butyrate as a potential therapeutic agent in animal nutrition. This review suggests that optimizing butyrate supplementation strategies to meet the specific needs of each species may yield additional benefits, establishing butyrate as an important dietary additive for enhancing growth performance and health in livestock. Full article

It is critical to sustain the diversity of the microbiota to maintain host homeostasis and health. Growing evidence indicates that changes in gut microbial biodiversity may be associated with the development of several pathologies, including type 2 diabetes mellitus (T2DM). Metformin is still the first-line drug for treatment of T2DM unless there are contra-indications. The drug primarily inhibits hepatic gluconeogenesis and increases the sensitivity of target cells (hepatocytes, adipocytes and myocytes) to insulin; however, increasing evidence suggests that it may also influence the gut. As T2DM patients exhibit gut dysbiosis, the intestinal microbiome has gained interest as a key target for metabolic diseases. Interestingly, changes in the gut microbiome were also observed in T2DM patients treated with metformin compared to those who were not. Therefore, the aim of this review is to present the current state of knowledge regarding the association of the gut microbiome with the antihyperglycemic effect of metformin. Numerous studies indicate that the reduction in glucose concentration observed in T2DM patients treated with metformin is due in part to changes in the biodiversity of the gut microbiota. These changes contribute to improved intestinal barrier integrity, increased production of short-chain fatty acids (SCFAs), regulation of bile acid metabolism, and enhanced glucose absorption. Therefore, in addition to the well-recognized reduction of gluconeogenesis, metformin also appears to exert its glucose-lowering effect by influencing gut microbiome biodiversity. However, we are only beginning to understand how metformin acts on specific microorganisms in the intestine, and further research is needed to understand its role in regulating glucose metabolism, including the impact of this remarkable drug on specific microorganisms in the gut. Full article

Weaning in piglets presents significant physiological and immunological challenges, including gut dysbiosis and increased susceptibility to post-weaning diarrhoea (PWD). Abrupt dietary, environmental, and social changes during this period disrupt the intestinal barrier and microbiota, often necessitating antimicrobial use. Sustainable dietary strategies are critical to addressing these issues while reducing reliance on antimicrobials. Reducing dietary crude protein mitigates the availability of undigested proteins for pathogenic bacteria, lowering harmful by-products like ammonia and branched-chain fatty acids, which exacerbate dysbiosis. Organic acid supplementation improves gastric acidification, nutrient absorption, and microbial balance, while also serving as an energy-efficient alternative to traditional grain preservation methods. Increasing intestinal butyrate, a key short-chain fatty acid with anti-inflammatory and gut-protective properties, is particularly promising. Butyrate strengthens intestinal barrier integrity by upregulating tight junction proteins, reduces inflammation by modulating cytokine responses, and promotes anaerobic microbial stability. Exogenous butyrate supplementation via salts provides immediate benefits, while endogenous stimulation through prebiotics (e.g., resistant starch) and probiotics promotes sustained butyrate production. These interventions selectively enhance butyrate-producing bacteria such as Roseburia and Faecalibacterium prausnitzii, further stabilising the gut microbiota. Integrating these strategies can enhance gut integrity, microbial resilience, and immune responses in weaned piglets. Their combination offers a sustainable, antimicrobial-free approach to improving health and productivity in modern pig production systems. Full article

Introduction Emerging evidence suggests an association between obesity and Functional Gastrointestinal Disorders (FGIDs). Childhood obesity and FGIDs share many common features, such as high prevalence in the pediatric population, risk factors related to diet and lifestyle, gut microbiota impairments, and psychological distress. This narrative review aims to summarize the main evidence regarding FGIDs in childhood obesity, with a specific focus on the role of diet and its impact on the microbiota. Additionally, the review highlights potential common-ground solutions for preventing and managing both obesity and FGIDs. Methods A comprehensive PubMed search was conducted. Keywords used included terms related to children and adolescents, obesity, functional gastrointestinal disorders, and microbiota. Results The review emphasizes the importance of holistic, multidisciplinary approaches to managing symptoms. In addition to nutrition education, physical activity, and medical care, complementary strategies such as psychological interventions and personalized dietary modifications (e.g., low-FODMAP and fiber-enriched diets) are critical. Given the interplay between gut microbiota alterations, obesity, and FGIDs, microbiota modulation through probiotics, prebiotics, and integrative support shows significant promise. However, the variability in current evidence underlines the need for robust longitudinal studies to develop standardized protocols and maximize treatment efficacy. Conclusions Bridging gaps in knowledge and practice with an integrated, evidence-based framework could improve patient outcomes and deepen understanding of the complex relationship between metabolic and gastrointestinal health in children and adolescents. Full article

Metabolic alterations, including hypermetabolism, lipid imbalances, and glucose dysregulation, are pivotal contributors to the onset and progression of Amyotrophic Lateral Sclerosis (ALS). These changes exacerbate systemic energy deficits, heighten oxidative stress, and fuel neuroinflammation. Simultaneously, gastrointestinal dysfunction and gut microbiota (GM) dysbiosis intensify disease pathology by driving immune dysregulation, compromising the intestinal barrier, and altering gut–brain axis (GBA) signaling, and lastly advancing neurodegeneration. Therapeutic and preventive strategies focused on nutrition offer promising opportunities to address these interconnected pathophysiological mechanisms. Diets enriched with antioxidants, omega-3 fatty acids, and anti-inflammatory compounds—such as the Mediterranean diet—have shown potential in reducing oxidative stress and systemic inflammation. Additionally, microbiota-targeted approaches, including probiotics, prebiotics, postbiotics, and fecal microbiota transplantation, are emerging as innovative tools to restore microbial balance, strengthen gut integrity, and optimize GBA function. This review highlights the critical need for personalized strategies integrating immunonutrition and microbiota modulation to slow ALS progression, improve quality of life, and develop preventive measures for neurodegenerative and neuroinflammatory diseases. Future research should prioritize comprehensive dietary and microbiota-based interventions to uncover their therapeutic potential and establish evidence-based guidelines for managing ALS and related disorders. Full article

The gut–brain axis (GBA) is a complex communication network connecting the gastrointestinal tract (GIT) and the central nervous system (CNS) through neuronal, endocrine, metabolic, and immune pathways. Omega-3 (n-3) fatty acids, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are crucial food components that may modulate the function of this axis through molecular mechanisms. Derived mainly from marine sources, these long-chain polyunsaturated fatty acids are integral to cell membrane structure, enhancing fluidity and influencing neurotransmitter function and signal transduction. Additionally, n-3 fatty acids modulate inflammation by altering eicosanoid production, reducing proinflammatory cytokines, and promoting anti-inflammatory mediators. These actions help preserve the integrity of cellular barriers like the intestinal and blood–brain barriers. In the CNS, EPA and DHA support neurogenesis, synaptic plasticity, and neurotransmission, improving cognitive functions. They also regulate the hypothalamic–pituitary–adrenal (HPA) axis by reducing excessive cortisol production, associated with stress responses and mental health disorders. Furthermore, n-3 fatty acids influence the composition and function of the gut microbiota, promoting beneficial bacterial populations abundance that contribute to gut health and improve systemic immunity. Their multifaceted roles within the GBA underscore their significance in maintaining homeostasis and supporting mental well-being. Full article

Asthma is a chronic inflammatory respiratory disease that affects millions globally and poses a serious public health challenge. Current therapeutic strategies, including corticosteroids, are constrained by variable patient responses and adverse effects. In this study, a polyphenolic extract derived from the Tibetan medicinal plant Spenceria ramalana Trimen (SRT) was employed and shown to improve experimentally (ovalbumin + cigarette smoke, OVA + CS) induced asthma in rats. Initially, the potential therapeutic mechanism of the polyphenolic components in SRT on OVA + CS-induced asthma was predicated by network pharmacology analysis. Subsequently, in vivo experiments identified that SRT polyphenols exhibit significant anti-asthmatic activities, primarily mediated by lowering inflammatory cell counts such as the WBC (white blood cell), eosinophils, and neutrophils, decreasing the expression of inflammatory cytokines (IL-4, IL-5, IL-13, and TNF-α), alleviating lung histological damage (reduced inflammation, collagen deposition, and mucus secretion), and enhancing the epithelial barrier integrity (upregulation of ZO-1, occludin, and claudin-1). Additionally, SRT polyphenols downregulated the PI3K/Akt (Phosphoinositide 3-kinase/protein kinase B) signaling pathway, improved gut microbiota disruption, and regulated fecal metabolites (glucose-6-glutamate, PS (16:0/0:0), 8-aminocaprylic acid, galactonic acid, Ascr#10, 2,3,4,5,6,7-hexahydroxyheptanoic acid, phosphodimethylethanolamine, muramic acid, 9-oxohexadeca-10e-enoic acid, and sedoheptulose) in asthmatic rats. In conclusion, SRT polyphenols exerted multifaceted protective effects against OVA + CS-induced asthma in rats, highlighting their potential value in preventing asthma via the PI3K/Akt signaling pathway. Full article

This comprehensive review explores the biological functions of Perilla frutescens seed proteins and peptides, highlighting their significant potential for health and therapeutic applications. This review delves into the mechanisms through which perilla peptides combat oxidative stress and protect cells from oxidative damage, encompassing free radical scavenging, metal chelating, in vivo antioxidant, and cytoprotective activities. Perilla peptides exhibit robust anti-aging properties by activating the Nrf2 pathway, enhancing cellular antioxidant capacity, and supporting skin health through the promotion of keratinocyte growth, maintenance of collagen integrity, and reduction in senescent cells. Additionally, they demonstrate antidiabetic activity by inhibiting α-amylase and α-glucosidase. The cardioprotective effects of perilla peptides are underscored by ACE-inhibitory activities and combat oxidative stress through enhanced antioxidant defenses. Further, perilla peptides contribute to improved gut health by enhancing beneficial gut flora and reinforcing intestinal barriers. In liver, kidney, and testicular health, they reduce oxidative stress and apoptotic damage while normalizing electrolyte levels and protecting against cyclophosphamide-induced reproductive and endocrine disruptions by restoring hormone synthesis. Promising anticancer potential is also demonstrated by perilla peptides through the inhibition of key cancer cell lines, alongside their anti-inflammatory and immunomodulating activities. Their anti-fatigue effects enhance exercise performance and muscle function, while perilla seed peptide nanoparticles show potential for targeted drug delivery. The diverse applications of perilla peptides support their potential as functional food additives and therapeutic agents. Full article

Neuroinflammation is a complex and dynamic response of the central nervous system (CNS) to injury, infection, and disease. While acute neuroinflammation plays a protective role by facilitating pathogen clearance and tissue repair, chronic and dysregulated inflammation contributes significantly to the progression of neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and Multiple Sclerosis. This review explores the cellular and molecular mechanisms underlying neuroinflammation, focusing on the roles of microglia, astrocytes, and peripheral immune cells. Key signaling pathways, including NF-κB, JAK-STAT, and the NLRP3 inflammasome, are discussed alongside emerging regulators such as non-coding RNAs, epigenetic modifications, and the gut–brain axis. The therapeutic landscape is evolving, with traditional anti-inflammatory drugs like NSAIDs and corticosteroids offering limited efficacy in chronic conditions. Immunomodulators, gene and RNA-based therapeutics, and stem cell methods have all shown promise for more specific and effective interventions. Additionally, the modulation of metabolic states and gut microbiota has emerged as a novel strategy to regulate neuroinflammation. Despite significant progress, challenges remain in translating these findings into clinically viable therapies. Future studies should concentrate on integrated, interdisciplinary methods to reduce chronic neuroinflammation and slowing the progression of neurodegenerative disorders, providing opportunities for revolutionary advances in CNS therapies. Full article

It is known that probiotics have direct and indirect effects on many systems in the body, especially the gastrointestinal system. Interest in using probiotic strain-derived cell components and metabolites has also increased as a result of the significant benefits of probiotics. Although many terminologies and definitions are used for these components and metabolites, the International Scientific Association of Probiotics and Prebiotics (ISAPP) recommended the use of the term postbiotic in 2021, which is defined as “a preparation of inanimate microorganisms and/or their components that confers a health benefit on the host”. Postbiotics are bioactive metabolites such as organic acids, peptides/proteins, cell wall components, functional enzymes, short-chain fatty acids, vitamins, and phenols. These molecules mediate many positive effects such as immunomodulatory, antimicrobial, and antioxidant effects. These positive effects on maintaining health have enabled the identification of many new postbiotic proteins such as p40, p75, and HM0539. In this review, the postbiotic proteins p40, p75, and HM0539 derived from lactobacilli and their functional effects are systematically summarized. The p40 protein, in particular, has been shown to support gut barrier activity and reduce inflammation, potentially through mechanisms involving epidermal growth factor receptor-dependent signaling. Additionally, p40 and p75 proteins exhibit protective effects on intestinal epithelial tight junctions, suggesting their therapeutic potential in preventing intestinal damage and diseases such as colitis. HM0539 enhances intestinal barrier integrity, exhibits antiinflammatory properties, and protects against bacterial infection, suggesting its possible as a therapeutic for inflammatory bowel disease. This review may contribute to future studies on the therapeutic use of p40, p75, and HM0539 postbiotic proteins in inflammatory gastrointestinal system diseases. Full article

The gut–kidney axis represents the complex interactions between the gut microbiota and kidney, which significantly impact the progression of chronic kidney disease (CKD) and overall patient health. In CKD patients, imbalances in the gut microbiota promote the production of uremic toxins, such as indoxyl sulfate and p-cresyl sulfate, which impair renal function and contribute to systemic inflammation. Mechanisms like endotoxemia, immune activation and oxidative stress worsen renal damage by activating pro-inflammatory and oxidative pathways. Insights into these mechanisms highlight the impact of gut-derived metabolites, bacterial translocation, and immune response changes on kidney health, suggesting new potential approaches for CKD treatment. Clinical applications, such as dietary interventions, prebiotics, probiotics and fecal microbiota transplantation, are promising in adjusting the gut microbiota to alleviate CKD symptoms and slow disease progression. Current research highlights the clinical relevance of the gut–kidney axis, but further study is essential to clarify these mechanisms’ diagnostic biomarkers and optimize therapeutic interventions. This review emphasizes the importance of an integrated approach to CKD management, focusing on the gut microbiota as a therapeutic target to limit kidney injury. Full article

Cancer persists as a significant global health challenge, claiming millions of lives annually despite remarkable strides in therapeutic innovation. Challenges such as drug resistance, toxicity, and suboptimal efficacy underscore the need for novel treatment paradigms. In this context, the repurposing of antibiotics as anti-cancer agents has emerged as an attractive prospect for investigation. Diverse classes of antibiotics have exhibited promising anti-cancer properties in both in vitro and in vivo studies. These mechanisms include the induction of apoptosis and cell cycle arrest, generation of reactive oxygen species, and inhibition of key regulators of cell proliferation and migration. Additional effects involve the disruption of angiogenesis and modulation of pivotal processes such as inflammation, immune response, mitochondrial dynamics, ferroptosis, and autophagy. Furthermore, antibiotics have demonstrated the potential to enhance the efficacy of conventional modalities like chemotherapy and radiotherapy, while alleviating treatment-induced toxicities. Nevertheless, the integration of antibiotics into oncological applications remains contentious, with concerns centered on their disruption of gut microbiota, interference with immunotherapeutic strategies, contribution to microbial resistance, and potential association with tumorigenesis. This narrative review explores the mechanisms of antibiotics’ anti-cancer activity, addresses controversies about their dual role in cancer biology, and envisions future perspectives that include the development of novel derivatives and innovative frameworks for their incorporation into cancer treatment paradigms. Full article

Identifying biomarkers of mycotoxin effects in chickens will provide an opportunity for early intervention to reduce the impact of mycotoxicosis. This study aimed to identify whether serum enzyme concentrations, gut integrity, and liver miRNAs can be potential biomarkers for fumonisin B1 (FB1), deoxynivalenol (DON), and zearalenone (ZEA) toxicity in broiler birds as early as 14 days after exposure. A total of 720 male broiler chicks were distributed to six treatment groups: T1: control group (basal diet), T2 (2 FB1 + 2.5 DON + 0.9 ZEA), T3 (5 FB1 + 0.4 DON + 0.1 ZEA), T4 (9 FB1 + 3.5 DON + 0.7 ZEA), T5 (17 FB1 + 1.0 DON + 0.2 ZEA), and T6 (21 FB1 + 3.0 DON + 1.0 ZEA), all in mg/kg diet. On d14, there were no significant differences in the body weight gain (BWG) of mycotoxin treatment groups when compared to the control (p > 0.05), whereas on d21, T6 birds showed significantly reduced BWG compared to the control (p < 0.05). On d14, birds in T6 showed significant upregulation of liver miRNAs, gga-let-7a-5p (14.17-fold), gga-miR-9-5p (7.05-fold), gga-miR-217-5p (16.87-fold), gga-miR-133a-3p (7.41-fold), and gga-miR-215-5p (6.93-fold) (p < 0.05) and elevated serum fluorescein isothiocyanate-dextran (FITC-d) concentrations, aspartate aminotransferase (AST), and creatine kinase (CK) levels compared to the control (p < 0.05). On d21, T2 to T6 birds exhibited reduced serum phosphorus, glucose, and potassium, while total protein, FITC-d, AST, and CK levels increased compared to control (p < 0.05). These findings suggest that serum FITC-d, AST, CK, and liver miRNAs could serve as biomarkers for detecting mycotoxin exposure in broiler chickens. Full article

The gut–brain axis plays an integral role in maintaining overall health, with growing evidence suggesting its impact on the development of various neuropsychiatric disorders, including depression. This review explores the complex relationship between gut microbiota and glutamate (Glu) regulation, highlighting its effect on brain health, particularly in the context of depression following certain neurological insults. We discuss how microbial populations can either facilitate or limit Glu uptake, influencing its bioavailability and predisposing to neuroinflammation and neurotoxicity. Additionally, we examine the role of gut metabolites and their influence on the blood–brain barrier and neurotransmitter systems involved in mood regulation. The therapeutic potential of microbiome-targeted interventions, such as fecal microbiota transplantation, is also highlighted. While much research has explored the role of Glu in major depressive disorders and other neurological diseases, the contribution of gut microbiota in post-neurological depression remains underexplored. Future research should focus on explaining the mechanisms linking the gut microbiota to neuropsychiatric outcomes, particularly in conditions such as post-stroke depression, post-traumatic brain-injury depression, and epilepsy-associated depression. Systematic reviews and human clinical studies are needed to establish causal relationships and assess the efficacy of microbiome-targeted therapies in improving the neuropsychiatric sequalae after neurological insults. Full article

Background/Objectives: Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder associated with gut dysbiosis. To investigate the association between gut microbiota and T2DM in a Saudi Arabian population. Methods: We conducted a comparative analysis of fecal microbiota from 35 individuals, including both T2DM patients and healthy controls. 16S rRNA gene sequencing was employed to characterize the microbial community structure. Results: Our findings revealed significant differences in microbial composition between the two groups. The T2DM group exhibited a higher abundance of Firmicutes and lower levels of Bacteroidetes compared to the healthy control group. At the genus level, T2DM patients showed a decrease in butyrate-producing bacteria such as Bacteroides and Akkermansia, while an increase in Ruminococcus and Prevotella was observed. Additionally, the T2DM group had a higher abundance of Faecalibacterium, Agathobacter, and Lachnospiraceae, along with a lower abundance of Bacteroides. Conclusions: These results suggest that alterations in gut microbiota composition may contribute to the development of T2DM in the Saudi Arabian population. Further large-scale studies are needed to validate these findings and explore potential therapeutic interventions targeting the gut microbiome. Full article