RESUMEN

The human gastrointestinal microbiota, densely populated with a diverse array of microorganisms primarily from the bacterial phyla Bacteroidota, Bacillota, and Actinomycetota, is crucial for maintaining health and physiological functions. Dietary fibers, particularly pectin, significantly influence the composition and metabolic activity of the gut microbiome. Pectin is fermented by gut bacteria using carbohydrate-active enzymes (CAZymes), resulting in the production of short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate, which provide various health benefits. The gastrointestinal microbiota has evolved to produce CAZymes that target different pectin components, facilitating cross-feeding within the microbial community. This review explores the fermentation of pectin by various gut bacteria, focusing on the involved transport systems, CAZyme families, SCFA synthesis capacity, and effects on microbial ecology in the gut. It addresses the complexities of the gut microbiome's response to pectin and highlights the importance of microbial cross-feeding in maintaining a balanced and diverse gut ecosystem. Through a systematic analysis of pectinolytic CAZyme production, this review provides insights into the enzymatic mechanisms underlying pectin degradation and their broader implications for human health, paving the way for more targeted and personalized dietary strategies.

RESUMEN

Short-chain fatty acids (SCFAs) - acetate, propionate, and butyrate - are important bacterial fermentation metabolites regulating many important aspects of human physiology. Decreases in the concentrations of any or multiple SCFAs are associated with various detrimental effects to the host. Previous research has broadly focused on gut microbiome produced SCFAs as a group, with minimal distinction between acetate, propionate, and butyrate independently, each with significantly different host effects. In this review, we comprehensively delineate the roles of these SCFAs with emphasis on receptor affinity, signaling pathway involvement, and net host physiologic effects. Butyrate is highlighted due to its unique role in gastrointestinal-associated functions, especially maintaining gut barrier integrity. Butyrate functions by promoting epithelial tight junctions, serving as fuel for colonocyte ATP production, and modulating the immune system. Interaction with the immune system occurs locally in the gastrointestinal tract and systemically in the brain. Investigation into research conducted on butyrate production pathways and specific bacterial players involved highlights a unique risk associated with use of gram-positive targeted antibiotics. We review and discuss evidence showing the relationship between the butyrate-producing gram-positive genus, Roseburia, and susceptibility to commonly prescribed, widely used gram-positive antibiotics. Considering gut microbiome implications when choosing antibiotic therapy may benefit health outcomes in patients.

Asunto(s)

Butiratos , Ácidos Grasos Volátiles , Microbioma Gastrointestinal , Humanos , Microbioma Gastrointestinal/fisiología , Ácidos Grasos Volátiles/metabolismo , Animales , Butiratos/metabolismo , Bacterias/metabolismo , Bacterias/clasificación , Bacterias/genética , Tracto Gastrointestinal/microbiología , Tracto Gastrointestinal/metabolismo , Antibacterianos

RESUMEN

Alzheimer's disease (AD) is a neurodegenerative disease that is known to accumulate amyloid-ß (Aß) and tau protein. Clinical studies have not identified pathogenesis mechanisms or produced an effective cure for AD. The Aß monoclonal antibody lecanemab reduces Aß plaque formation for the treatment of AD, but more studies are required to increase the effectiveness of drugs to reduce cognitive decline. The lack of AD therapy targets and evidence of an association with an acute neuroinflammatory response caused by several bacteria and viruses in some individuals has led to the establishment of the infection hypothesis during the last 10 years. How pathogens cross the blood-brain barrier is highly topical and is seen to be pivotal in proving the hypothesis. This review summarizes the possible role of the gut microbiome in the pathogenesis of AD and feasible therapeutic approaches and current research limitations.

Asunto(s)

Enfermedad de Alzheimer , Microbioma Gastrointestinal , Enfermedad de Alzheimer/microbiología , Enfermedad de Alzheimer/tratamiento farmacológico , Enfermedad de Alzheimer/metabolismo , Humanos , Animales , Péptidos beta-Amiloides/metabolismo , Barrera Hematoencefálica/metabolismo , Barrera Hematoencefálica/microbiología , Proteínas tau/metabolismo

RESUMEN

Large amounts of waste activated sludge are generated daily worldwide, posing significant environmental challenges. Anaerobic fermentation is a promising method for sludge disposal, but it has two technical bottlenecks: the availability of short-chain fatty acids (SCFAs)-producing substrates and SCFAs consumption by methanogenesis. This study proposes a pretreatment strategy combining sodium percarbonate (SPC) and magnetite (Fe3O4) to address these issues. Under optimized conditions (20 mg Fe3O4/g TSS and 15 mg SPC/g TSS), SCFAs production increased to 3244.10 ± 216.31 mg COD/L, about 3.06 times the control (1057.29 ± 35.06 mg COD/L) and surpassing reported treatments. The combined pretreatment enhanced the disruption of extracellular polymeric substances, increased the release of biodegradable matters, improved acidogenesis enzyme activities, and inhibited methanogenesis. Additionally, it increased NH4+-N release in favor of the recovery of phosphorus from sludge residual. This study demonstrates an efficient pretreatment for high SCFAs production and resource recovery from WAS.

Asunto(s)

Carbonatos , Ácidos Grasos Volátiles , Fermentación , Óxido Ferrosoférrico , Aguas del Alcantarillado , Eliminación de Residuos Líquidos , Ácidos Grasos Volátiles/metabolismo , Anaerobiosis , Eliminación de Residuos Líquidos/métodos , Acetatos/metabolismo , Reactores Biológicos

RESUMEN

While the gut microbiome has been intensively investigated for more than twenty years already, its role in various disorders remains to be unraveled. At the same time, questions about what changes in the gut microbiota can be considered as normal or pathological and whether communities are able to recover after exposure to negative factors (diseases, medications, environmental factors) are still unclear. Here, we describe changes in the gut microbiota composition and the content of short-chain fatty acids in adult healthy volunteers (n = 15) over a 24 month-period. Intraindividual variability in gut microbial composition was 40%, whereas the short chain fatty acids profile remained relatively stable (2-year variability 20%, inter-individual 26%). The changes tend to accumulate over time. Nevertheless, both short-term and long-term changes in the gut microbiome composition were significantly smaller within individuals than interindividual differences (two-year interindividual variability was 75%). Seasonal changes in gut microbiota were found more often in autumn and spring involving the content of minor representatives (less than 1.5% of the community in average) in the phyla Actinobacteriota, Firmicutes and Proteobacteria.

RESUMEN

The beneficial effects of probiotics for the improvement of metabolic disorders have been studied intensively; however, these effects are evident in a probiotic strain-specific and disease-specific manner. Thus, it is still essential to evaluate the efficacy of each strain against a target disease. Here, we present an anti-obese and anti-diabetic probiotic strain, Lactiplantibacillus plantarum APsulloc331261 (GTB1™), which was isolated from green tea and tested for safety previously. In high-fat-diet-induced obese mice, GTB1™ exerted multiple beneficial effects, including significant reductions in adiposity, glucose intolerance, and dyslipidemia, which were further supported by improvements in levels of circulating hormones and adipokines. Lipid metabolism in adipose tissues was restored through the activation of PPAR/PGC1α signaling by GTB1™ treatment, which was facilitated by intestinal microbiota composition changes and short-chain fatty acid production. Our findings provide evidence to suggest that GTB1™ is a potential candidate for probiotic supplementation for comprehensive improvement in metabolic disorders.

RESUMEN

As a food contaminant that can be quickly absorbed through the gastrointestinal system, furan has been shown to disrupt the intestinal flora and barrier. Investigation of the intestinal toxicity mechanism of furan is of great significance to health. We previously identified the regulatory impact of salidroside (SAL) against furan-provoked intestinal damage, and the present work further explored whether the alleviating effect of SAL against furan-caused intestinal injury was based on the intestinal flora; three models, normal, pseudo-germ-free, and fecal microbiota transplantation (FMT), were established, and the changes in intestinal morphology, barrier, and inflammation were observed. Moreover, 16S rDNA sequencing observed the variation of the fecal flora associated with inflammation and short-chain fatty acids (SCFAs). Results obtained from the LC-MS/MS suggested that SAL increased furan-inhibited SCFA levels, activated the mRNA expressions of SCFA receptors (GPR41, GPR43, and GPR109A), and inhibited the furan-activated TLR4/MyD88/NF-κB signaling. Analysis of protein-protein interaction further confirmed the aforementioned effects of SAL, which inhibited furan-induced barrier damage and intestinal inflammation.

Asunto(s)

Bacterias , Ácidos Grasos Volátiles , Furanos , Microbioma Gastrointestinal , Glucósidos , Fenoles , Transducción de Señal , Receptor Toll-Like 4 , Microbioma Gastrointestinal/efectos de los fármacos , Glucósidos/farmacología , Fenoles/farmacología , Receptor Toll-Like 4/metabolismo , Receptor Toll-Like 4/genética , Animales , Transducción de Señal/efectos de los fármacos , Furanos/farmacología , Masculino , Ácidos Grasos Volátiles/metabolismo , Humanos , Ratones , Bacterias/genética , Bacterias/clasificación , Bacterias/aislamiento & purificación , Bacterias/metabolismo , Bacterias/efectos de los fármacos , Mucosa Intestinal/metabolismo , Mucosa Intestinal/efectos de los fármacos , FN-kappa B/metabolismo , FN-kappa B/genética , Rhodiola/química , Inflamación/metabolismo , Inflamación/tratamiento farmacológico , Ratones Endogámicos C57BL

RESUMEN

Short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, modulate immune cell functions, particularly macrophages. This review explores the potential therapeutic applications of SCFAs in pulmonary fungal infections, a critical concern due to their high mortality rates and antifungal resistance. SCFAs enhance macrophage functions by promoting phagosome-lysosome fusion, increasing reactive oxygen species production, and balancing cytokine responses. Pulmonary fungal infections, caused by pathogens like Aspergillus fumigatus, are prevalent in immunocompromised patients, including those with diabetes, chronic obstructive pulmonary disease, and those on high-dose corticosteroids. SCFAs have shown promise in improving macrophage function in these contexts. However, the application of SCFAs must be balanced against potential side effects, including gut microbiota disruption and metabolic disorders. Further research is needed to optimize SCFA therapy for managing pulmonary fungal infections.

RESUMEN

The microbiota-gut-brain axis (MGBA) represents a sophisticated communication network between the brain and the gut, involving immunological, endocrinological, and neural mediators. This bidirectional interaction is facilitated through the vagus nerve, sympathetic and parasympathetic fibers, and is regulated by the hypothalamic-pituitary-adrenal (HPA) axis. Evidence shows that alterations in gut microbiota composition, or dysbiosis, significantly impact neurological disorders (NDs) like anxiety, depression, autism, Parkinson's disease (PD), and Alzheimer's disease (AD). Dysbiosis can affect the central nervous system (CNS) via neuroinflammation and microglial activation, highlighting the importance of the microbiota-gut-brain axis (MGBA) in disease pathogenesis. The microbiota influences the immune system by modulating chemokines and cytokines, impacting neuronal health. Synbiotics have shown promise in treating NDs by enhancing cognitive function and reducing inflammation. The gut microbiota's role in producing neurotransmitters and neuroactive compounds, such as short-chain fatty acids (SCFAs), is critical for CNS homeostasis. Therapeutic interventions targeting the MGBA, including dietary modulation and synbiotic supplementation, offer potential benefits for managing neurodegenerative disorders. However, more in-depth clinical studies are necessary to fully understand and harness the therapeutic potential of the MGBA in neurological health and disease.

Asunto(s)

Alergia e Inmunología , Humanos , Animales , Microbiología

RESUMEN

Ulcerative colitis (UC) is an autoimmune disease in which the immune system attacks the colon, leading to ulcer development, loss of colon function, and bloody diarrhea. The human gut ecosystem consists of almost 2000 different species of bacteria, forming a bioreactor fueled by dietary micronutrients to produce bioreactive compounds, which are absorbed by our body and signal to distant organs. Studies have shown that the Western diet, with fewer short-chain fatty acids (SCFAs), can alter the gut microbiome composition and cause the host's epigenetic reprogramming. Additionally, overproduction of H2S from the gut microbiome due to changes in diet patterns can further activate pro-inflammatory signaling pathways in UC. This review discusses how the Western diet affects the microbiome's function and alters the host's physiological homeostasis and susceptibility to UC. This article also covers the epidemiology, prognosis, pathophysiology, and current treatment strategies for UC, and how they are linked to colorectal cancer.

Asunto(s)

Colitis Ulcerosa , Neoplasias Colorrectales , Dieta Occidental , Epigénesis Genética , Microbioma Gastrointestinal , Humanos , Colitis Ulcerosa/microbiología , Colitis Ulcerosa/metabolismo , Colitis Ulcerosa/genética , Neoplasias Colorrectales/microbiología , Neoplasias Colorrectales/metabolismo , Dieta Occidental/efectos adversos , Animales

RESUMEN

OBJECTIVE: To observe the effects of acupuncture on blood pressure, fecal short-chain fatty acids (SCFAs) and toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-κB (NF-κB) signaling pathway in spontaneously hypertensive rats (SHR), and to explore the mechanism of acupuncture for anti-hypertension. METHODS: Twenty-four male SHR of SPF grade were randomly divided into a model group, a western medication group, an acupuncture group and a sham acupuncture group, with 6 rats in each group, and 6 male Wistar-Kyoto rats were selected as the blank group additionally. Hydrochlorothiazide solution was given by gavage in the western medication group; acupuncture was applied at bilateral "Renying" (ST 9) and "Zusanli" (ST 36) in the acupuncture group, 20 min a time; acupuncture was applied at the non-meridian and non-acupoint points close to bilateral "Renying" (ST 9) and "Zusanli" (ST 36) in the sham acupuncture group, 20 min a time. The intervention was adopted once a day for 4 weeks continuously in each group. The systolic blood pressure (SBP) of the caudal artery was measured before intervention and after 1, 2, 3 and 4 weeks of intervention. After intervention, the morphology of colonic tissue was observed by HE staining; the fecal level of SCFAs was detected by gas chromatography; the serum levels of interleukin (IL)-6, IL-1ßand tumor necrosis factor-α (TNF-α) were detected by ELISA; the protein expression of TLR4, MyD88 and NF-κB p65 in the mesenteric artery was detected by Western blot. RESULTS: Compared with the blank group, in the model group, the SBP was increased (P<0.05), significant pathological changes could be found in the colonic tissue, the fecal SCFAs level was decreased (P<0.05), the serum levels of IL-6, IL-1ß and TNF-α were increased (P<0.05), the protein expression of TLR4, MyD88 and NF-κB p65 in the mesenteric artery was increased (P<0.05). Compared with the model group, the SBP after 2, 3 and 4 weeks of intervention was decreased (P<0.05), the serum levels of IL-6, IL-1ß and TNF-α were decreased (P<0.05) in the acupuncture group and the western medication group; the mucosal epithelium of colonic tissue was intact, the number of intestinal glands was abundant, the fecal SCFAs level was increased (P<0.05), and the protein expression of TLR4, MyD88 and NF-κB p65 in the mesenteric artery was decreased (P<0.05) in the acupuncture group. Compared with the sham acupuncture group, the SBP after 2, 3 and 4 weeks of intervention was decreased (P<0.05), the fecal SCFAs level was increased (P<0.05), the serum levels of IL-6, IL-1ß and TNF-α were decreased (P<0.05), the protein expression of TLR4, MyD88 and NF-κB p65 in the mesenteric artery was decreased (P<0.05) in the acupuncture group. CONCLUSION: Acupuncture at bilateral "Renying" (ST 9) and "Zusanli" (ST 36) can effectively play an anti-hypertensive role in SHR. Its mechanism may be related to regulating fecal SCFAs level and inhibiting the TLR4/MyD88/NF-κB signaling pathway.

Asunto(s)

Terapia por Acupuntura , Ácidos Grasos Volátiles , Heces , Factor 88 de Diferenciación Mieloide , FN-kappa B , Ratas Endogámicas SHR , Ratas Endogámicas WKY , Transducción de Señal , Receptor Toll-Like 4 , Animales , Receptor Toll-Like 4/metabolismo , Receptor Toll-Like 4/genética , Factor 88 de Diferenciación Mieloide/metabolismo , Factor 88 de Diferenciación Mieloide/genética , Masculino , Ratas , FN-kappa B/metabolismo , Humanos , Heces/química , Ácidos Grasos Volátiles/metabolismo , Hipertensión/terapia , Hipertensión/metabolismo , Hipertensión/fisiopatología , Presión Sanguínea , Puntos de Acupuntura

RESUMEN

The production of short-chain fatty acids (SCFAs) is constrained by substrate availability and the increased fractional pressure of H2 emitted by acidogenic/fermentative bacteria during anaerobic fermentation of waste activated sludge (WAS). This study introduced a novel approach employing zero-valent iron (ZVI)-activated sulfite pretreatment combined with H2-consuming sulfate-reducing bacteria (SRB) mediation to improve SCFAs, especially acetate production from WAS fermentation. Experimental results showed that the combined ZVI-activated sulfite and incomplete-oxidative SRB (io-SRB) process achieved a peak SCFAs production of 868.11 mg COD/L, with acetate accounting for 80.55 %, which was 7.90- and 2.18-fold higher than that obtained from raw WAS fermentation, respectively. This could be firstly attributed to the SO4- and OH generated by ZVI-activated sulfite, which significantly promoted WAS decomposition, e.g., soluble proteins and carbohydrates increased 14.3- and 10.8-fold, respectively, over those in raw WAS. The biodegradation of dissolved organic matter was subsequently enhanced by the synergistic interaction and H2 transfer between anaerobic fermentation bacteria (AFB) and io-SRB. The positive and negative correlations among AFB, nitrate-reducing bacteria (NRB) and the io-SRB consortia were revealed by molecular ecological network (MEN) and Mantel test. Moreover, the expression of functional genes was also improved, for instance, in relation to acetate formation, the relative abundances of phosphate acetyltransferase and acetate kinase was 0.002 % and 0.005 % higher than that in the control test, respectively. These findings emphasized the importance of sulfate radicals-based oxidation pretreatment and the collaborative relationships of multifunctional microbes on the value-added chemicals and energy recovery from sludge fermentation.

Asunto(s)

Ácidos Grasos Volátiles , Fermentación , Aguas del Alcantarillado , Sulfitos , Eliminación de Residuos Líquidos , Aguas del Alcantarillado/microbiología , Sulfitos/metabolismo , Ácidos Grasos Volátiles/metabolismo , Eliminación de Residuos Líquidos/métodos , Sulfatos/metabolismo , Hidrógeno/metabolismo , Bacterias/metabolismo , Hierro/metabolismo

RESUMEN

Nitrate photolysis has become an efficient, low-cost and promising technology for emerging contaminants removal, while its performance and mechanism for waste activated sludge (WAS) treatment is still unknown. This study innovatively introduced nitrate photolysis for WAS disintegration, and investigated the effect of nitrate addition (150-375 mg N/L) for short-chain fatty acids (SCFAs) production during anaerobic fermentation (AF). The results showed that nitrate photolysis significantly promoted the SCFAs production from WAS, and peaked at 280.7 mg/g VSS with 7-d fermentation with 150 mg N/L addition (150N-UV), which increased by 8.8-35.0 % and 10.7-23.3 % compared with other photolysis groups and sole nitrate groups. Effective release of the soluble organics was observed in the nitrate photolysis groups during AF, especially soluble proteins, reaching 1505.4 mg COD/L at 9 d in 150N-UV group, promoted by 7.0∼15.7 % than nitrate/nitrate photolysis groups. The model compounds simulation experiment further demonstrated the positive effect of nitrate photolysis on organics hydrolysis and SCFAs accumulation. The result of the radical capture and quenching verified the reactive oxygen species contributed more compared with reactive nitrogen species. Functional group analysis confirmed the effective bioconversion of the macromolecular organics during the fermentation. Moreover, the nitrate photolysis enhanced the enrichment of the functional consortia, including anaerobic fermentation bacteria (AFB), e.g., Fnoticella, Romboutsia, Gracilibacter and Sedimentibacter, and nitrate reducing bacteria (NRB), e.g., Acinerobacter and Ahniella. The macrogenetic analysis further revealed that glycolysis, amino acid metabolism, acetate metabolism and nitrogen metabolism were the dominating metabolic pathways during fermentation, and the abundance of the relevant genes were enhanced in 150N-UV group.

Asunto(s)

Ácidos Grasos Volátiles , Fermentación , Nitratos , Fotólisis , Aguas del Alcantarillado , Anaerobiosis , Ácidos Grasos Volátiles/metabolismo , Eliminación de Residuos Líquidos , Reactores Biológicos

RESUMEN

BACKGROUND: Although the pathogenesis of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), has not been fully elucidated, accumulating researches suggest that intestinal microbiota imbalance contributes to the development of IBD in patients and animal models. RDP58, a peptide-based computer-assisted rational design, has been demonstrated to be effective in protecting against a wide range of autoimmune and inflammatory diseases. However, the underlying mechanism by which RDP58 protects against IBD mediated by intestinal microbiota has yet to be elucidated. METHODS: The colitis model was induced by continuously administering 2.5 % (wt/vol) dextran sodium sulfate (DSS) solution for 7 days. The manifestations of colon inflammation were assessed via daily weight changes, colon length, tumor necrosis factor-alpha (TNF-α) level, disease activity index (DAI) score, pathology score, and intestinal barrier permeability. Intestinal microbiota analysis was carried out by 16S-rRNA sequencing. Colonic short chain fatty acids (SCFAs) and regulatory T cells (Tregs) were also detected. To further confirm the protective effect of RDP58 on intestinal microbiota, broad-spectrum antibiotic cocktail (ABX) treatment and fecal microbial transplantation (FMT) experiment were performed. RESULTS: Oral administration of RDP58 ameliorated DSS-induced mice colitis by altering the diversity and composition of intestinal microbiota. Notably, RDP58 significantly upregulated SCFAs-producing microbiota, thereby promoting the generation of Tregs. ABX and FMT were performed to verify the above mechanism. CONCLUSIONS: RDP58 ameliorated DSS-induced colitis through altering intestinal microbiota and enhancing SCFAs and Tregs production in intestinal microbiota dependent manner, potentially provide a novel therapy for IBD.

Asunto(s)

Colitis , Sulfato de Dextran , Microbioma Gastrointestinal , Ratones Endogámicos C57BL , Linfocitos T Reguladores , Animales , Microbioma Gastrointestinal/efectos de los fármacos , Colitis/inducido químicamente , Colitis/tratamiento farmacológico , Colitis/microbiología , Colitis/inmunología , Administración Oral , Linfocitos T Reguladores/inmunología , Ratones , Modelos Animales de Enfermedad , Colon/patología , Colon/microbiología , Colon/efectos de los fármacos , Colon/inmunología , Masculino , Factor de Necrosis Tumoral alfa/metabolismo , Trasplante de Microbiota Fecal , Humanos , Ácidos Grasos Volátiles/metabolismo , Oligopéptidos

RESUMEN

Diarrheagenic Escherichia coli (DEC) is the main cause of diarrhea in children under five years old. The virulence of DEC is tightly regulated by environmental signals influenced by the gut microbiota and its metabolites. Short-chain fatty acids (SCFAs) are the main metabolic product of anaerobic fermentation in the gut, but their role in DEC diarrhea has not yet been established. In this study, we determine the levels of acetate, propionate, and butyrate in stool samples from children with diarrhea caused by DEC, and we identify bacteria from the fecal gut microbiota associated with the production of SCFAs. The microbiota and SCFAs levels in stool samples obtained from 40 children with diarrhea and 43 healthy children were determined by 16S rRNA gene sequencing and HPLC, respectively. Additionally, shotgun metagenomics was used to identify metagenome-assembled genomes (MAGs) in a subgroup of samples. The results showed significantly higher levels of all SCFAs tested in diarrheal samples than in healthy controls. The abundance of Streptococcus sp., Limosilactobacillus, Blautia, Escherichia, Bacteroides, Megamonas, and Roseburia was higher in the DEC group than in healthy individuals. Functional analysis of bacteria and their main metabolic pathways made it possible to identify species MAGs that could be responsible for the detected SCFAs levels in DEC-positive diarrhea. In conclusion, based on our results and published data, we suggest that SCFAs may be important in the crosstalk between the microbiota and DEC pathogens in the gut.

RESUMEN

The gastrointestinal tract is home to trillions of diverse microorganisms collectively known as the gut microbiota, which play a pivotal role in breaking down undigested foods, such as dietary fibers. Through the fermentation of these food components, short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate are produced, offering numerous health benefits to the host. The production and absorption of these SCFAs occur through various mechanisms within the human intestine, contingent upon the types of dietary fibers reaching the gut and the specific microorganisms engaged in fermentation. Medical literature extensively documents the supplementation of SCFAs, particularly butyrate, in the treatment of gastrointestinal, metabolic, cardiovascular, and gut-brain-related disorders. This review seeks to provide an overview of the dynamics involved in the production and absorption of acetate, propionate, and butyrate within the human gut. Additionally, it will focus on the pivotal roles these SCFAs play in promoting gastrointestinal and metabolic health, as well as their current therapeutic implications.

RESUMEN

BACKGROUD: Central nervous system (CNS) diseases pose a serious threat to human health, but the regulatory mechanisms and therapeutic strategies of CNS diseases need to be further explored. It has been demonstrated that the gut microbiota (GM) is closely related to CNS disease. GM structure disorders, abnormal microbial metabolites, intestinal barrier destruction and elevated inflammation exist in patients with CNS diseases and promote the development of CNS diseases. More importantly, GM remodeling alleviates CNS pathology to some extent. AIM OF REVIEW: Here, we have summarized the regulatory mechanism of the GM in CNS diseases and the potential treatment strategies for CNS repair based on GM regulation, aiming to provide safer and more effective strategies for CNS repair from the perspective of GM regulation. KEY SCIENTIFIC CONCEPTS OF REVIEW: The abundance and composition of GM is closely associated with the CNS diseases. On the basis of in-depth analysis of GM changes in mice with CNS disease, as well as the changes in its metabolites, therapeutic strategies, such as probiotics, prebiotics, and FMT, may be used to regulate GM balance and affect its microbial metabolites, thereby promoting the recovery of CNS diseases.

RESUMEN

Heart failure (HF) is a significant health concern; early detection and prevention are crucial. Recent studies suggest that the gut microbiota and its metabolites may influence HF development and risk factors. We explored this relationship by examining changes in gut microbiota composition and metabolite levels in HF patients. HF patients often exhibit decreased alpha and beta diversity compared to controls, suggesting lower bacterial richness and community variation. Changes in specific bacterial phyla were observed, with decreases in Firmicutes (e.g., Ruminococcus) and Bacteroidetes (e.g., Prevotella) and increases in Proteobacteria (e.g., Escherichia, Shigella, and Klebsiella) and Actinobacteria. Gut-microbiota-related metabolites have been identified, potentially affecting various body systems, including the cardiovascular system. Among these are short-chain fatty acids (SCFAs), betaine, trimethylamine N-oxide (TMAO), phenylalanine, tryptophan-kynurenine, and phenylacetylgutamine (PAGIn). Although SCFAs positively affect our organisms, patients with HF have been observed to experience a decline in bacteria responsible for producing these chemical compounds. There have been indications of possible links between betaine, TMAO, phenylalanine, tryptophan-kynurenine, PAGIn, and heart failure. TMAO and phenylalanine, in particular, show promise as potential prognostic factors. However, their clinical significance has not yet been thoroughly evaluated and requires further investigation.