This study demonstrated the potential of ellagic acid-rich fruit byproducts, particularly pomegranate peel, as functional ingredients. During digestion, pomegranate peel exhibited superior antioxidant activity owing to its high phenolic content. Twenty-four phenolic compounds were released, with pomegranate peel maintaining higher bioactivity than chestnut and walnut peels. In vitro colonic fermentation with urolithin A-producing microbiota revealed that pomegranate peel stimulated butyrate synthesis (11.94 mM) and urolithin A production (6.31 μM), highlighting the prebiotic role of ellagic acid. Gut microbiota modulation by pomegranate peel increased Bacteroides and Bifidobacterium (a potential key for ellagic acid conversion) while suppressing Alistipes. Functional analyses confirmed its effect on carbohydrate, lipid, and amino acid metabolism. In contrast, chestnut and walnut peels exhibited lower bioactivity and microbial selectivity. These findings positioned pomegranate peel as a superior ingredient for gut health and microbial metabolism optimization, offering targeted nutritional benefits over conventional byproducts.

Tormentil rhizome was used for centuries in traditional medicine to treat gastrointestinal disorders. Its anti-inflammatory, antioxidant, and antibacterial properties, and unique taste, suggest its potential as a food additive for functional foods. The research aimed to determine gut metabolites of the extract, their impact on microbiota biodiversity, and interactions between them. Gut metabolites were obtained by ex vivo incubation of extract with fecal samples. Among the compounds, only catechin and its oligomers were metabolized by gut microbiota. Triterpenes remained unchanged, while ellagic acid derivatives were undetected in metabolized and unmetabolized forms. The extract also promoted bacteria growth from the Ruminococcaceae family (producers of short-chain fatty acids) and other families, increasing microbiota biodiversity. A mutual interaction occurred between Ruminococcaceae and metabolites, with bacteria influencing metabolite production and metabolites enhancing bacterial growth. The selective metabolism of tormentil rhizome and its interaction with gut microbiota may offer new strategies to improve gut health.

Cadmium (Cd) is a widespread environmental pollutant linked to liver injury and metabolic dysfunction, yet the gut-liver axis mechanisms remain unclear. We investigated chronic low-dose Cd exposure (100 nM CdCl2, 12 weeks) in mice using integrated metagenomic and metabolomic profiling. Despite intact intestinal morphology, Cd exposure induced hepatic inflammation, steatosis, and elevated transaminases. Shotgun metagenomics revealed gut microbiota shifts, with enrichment of Prevotella and depletion of Turicibacter. Fecal metabolomics showed disrupted bile acid detoxification and lipid remodeling. Functional analysis indicated upregulation of microbial fatty acid metabolism genes, suggesting compensatory but dysregulated responses. These findings demonstrate that chronic Cd exposure perturbs gut microbiota and metabolic outputs, driving liver injury via microbiota-mediated mechanisms. Our study highlights the gut-liver axis as a key target of Cd toxicity and points to microbiota-based interventions as potential therapies.

Multiple sclerosis (MS) is a chronic autoimmune disorder characterised by myelin degeneration in the central nervous system (CNS), leading to significant neurological impairment. Affecting approximately 2.8 million people globally and has a multifactorial aetiology involving genetic predispositions and environmental factors, particularly dietary influences. This review explores the emerging field of immuno-nutritional therapy as a novel approach for managing experimental autoimmune encephalomyelitis (EAE), a widely accepted animal model of MS. We highlight the therapeutic potential of key nutritional components, such as omega-3 fatty acids, polyphenols, and vitamins A and D, which have been shown to modulate immune responses and promote neuroprotection. These nutrients exert their effects by regulating cytokine profiles, enhancing regulatory T-cell (Treg) differentiation, and maintaining blood-brain barrier (BBB) integrity. Evidence suggests that dietary interventions can significantly modulate disease severity and progression in EAE, offering valuable insights into potential therapeutic strategies for MS patients. However, translating the findings from EAE models to human MS requires careful consideration of differences in immune responses and environmental factors. Future clinical trials designed to evaluate the long-term efficacy of dietary interventions across diverse MS populations are essential. By integrating immunomodulatory treatments with tailored nutritional strategies, there is a potential for innovative therapies that can alter disease trajectories and improve patient outcomes. A collaborative approach among nutrition scientists, immunologists, and neurologists could pave the way for effective immuno-nutritional therapies in MS management, enhancing the quality of life of those affected by this debilitating condition.

Chronic constipation (CC) and functional constipation (FC) are common gastrointestinal disorders that significantly affect quality of life. This study investigates the intestinal microbiota characteristics in CC and FC patients, revealing microbial imbalances characterized by reduced beneficial taxa, such as Acinetobacter, Blautia, Dorea formicigenerans, Eubacterium ramulus, and Halomonas, alongside increased levels of Alistipes, Holdemanella, Parabacteroides, Pseudomonas, Streptococcus, and so on. These findings highlight dysbiosis as a critical factor in constipation pathogenesis and provide a foundation for the bottom-up design of targeted probiotics and prebiotics. Potential therapeutic strategies include tailored probiotic formulations to replenish deficient taxa and the application of prebiotics to restore microbial balance. Additionally, the role of microbial metabolites, particularly short-chain fatty acids, and the microbiota-gut-brain axis offers further insight into mechanisms underlying symptom modulation. The integration of artificial intelligence enhances precision in probiotic design, enabling the prediction of strain-specific combinations optimized for therapeutic efficacy. This microbiota-centered approach underscores the potential for personalized interventions in addressing dysbiosis and advancing innovative management for CC and FC.

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by persistent hyperglycemia, oxidative stress, and inflammation, contributing to insulin resistance and long-term complications. Dietary antioxidants from plant sources, such as polyphenols, flavonoids, carotenoids, and phenolic acids, have been increasingly studied for their potential to modulate these pathophysiological mechanisms.

This review aims to summarize and critically analyze the current evidence on the biological effects, therapeutic potential, and translational challenges of plant-derived antioxidants in the prevention and management of T2DM.

This narrative review was conducted using peer-reviewed literature from PubMed, Scopus, and Web of Science. Emphasis was placed on mechanistic studies, clinical trials, bioavailability data, and advances in formulation technologies related to antioxidant compounds in the context of T2DM.

Plant antioxidants exert beneficial effects by modulating oxidative stress, reducing systemic inflammation, and improving insulin signaling pathways. However, their clinical application is limited by low bioavailability, chemical instability, and high interindividual variability. Recent developments, such as nanoencapsulation, synergistic functional food formulations, and microbiome-targeted strategies, have shown promise in enhancing efficacy. Additionally, personalized nutrition approaches and regulatory advances are emerging to support the integration of antioxidant-based interventions into diabetes care.

Plant-derived antioxidants represent a promising complementary tool for T2DM management. Nonetheless, their effective clinical use depends on overcoming pharmacokinetic limitations and validating their long-term efficacy in well-designed trials. Integrating food technology, microbiome science, and precision nutrition will be crucial to translate these compounds into safe, scalable, and personalized therapeutic options for individuals with or at risk of T2DM.

Plastic materials, ubiquitous in daily life, degrade into microplastics (MPs) that can accumulate in humans through the food chain, leading to health issues. While some antioxidants have been shown to mitigate the toxicity caused by MPs exposure, they are only effective at high doses, which can be harmful to human health when ingested in excess. Concurrently, Lactobacillus species have demonstrated the ability to adsorb onto micro- and nano-plastics (MNPs), with certain strains exhibiting high antioxidant activity. In this study, Lactobacillus plantarum strains with varying antioxidant capacities and affinities for polystyrene nanoparticles (PS-NPs) were utilized to investigate their effects on toxicity induced by exposure to PS-MPs. The results indicated that the antioxidant capabilities of Lactobacillus plantarum can reduce oxidative damage caused by PS-MPs exposure, and their ability to bind with PS-MNPs can reduce the body's PS-MPs content and increase fecal PS-MPs content, thereby reducing toxicity. Notably, the strain 89-L1, which possesses low antioxidant activity and low binding affinity for PS-MNPs, also reduced toxicity, potentially through repairing the intestinal barrier and modulating bile acid (BAs) metabolism. Our findings suggest that the mechanisms by which Lactobacillus plantarum reduces PS-MPs-induced toxicity extend beyond antioxidant and binding capabilities; the repair of the intestinal barrier and modulation of BAs metabolism also play significant roles in reducing toxicity caused by PS-MPs exposure and may act partially independently of these capacities. This study provides a theoretical basis for the future development of strategies for Lactobacillus plantarum to reduce toxicity caused by exposure to MPs.

INFOGEST became the standard digestion protocol to address inconsistencies in gastrointestinal tract (GIT) digestion protocols. However, sample collection, enzymatic inactivation methods, and storage conditions can significantly impact the accurate assessment of food compounds. This study investigates for the first time the impact of inactivation methods (thermal, pH-based, and specific inhibitors) and storage conditions (freezing and freeze-drying), following INFOGEST protocol on macronutrients of Pleurotus ostreatus biomass (used as a model food matrix). The results revealed that groups of macromolecules are differently affected by inactivation and storage methods. For α-glucans and glucans with different linkages than (1 → 3)(1 → 6)-β-glucans, enzyme inactivation seemed to prevent overestimation of enzymatic activity, with freezing emerging as the most promising storage method. For this carbohydrate group, no significant differences were found between inactivation strategies. The results suggested that freezing and thermal inactivation preserve peptide solubility. Additionally, freeze-drying may promote phenolic degradation and reduce antioxidant potential. Depending on the GIT phase, pH-based and specific inhibitors negatively impact these variables. The storage seemed to have no significant effect on fatty acids, enabling the selection of storage conditions based on the stability requirements of other macronutrient groups. Overall, thermal inactivation combined with freezing emerged as an effective, low-cost, and straightforward approach, minimizing post-digestion enzymatic activity and protecting food compounds from degradation. These findings enhance the reproducibility of digestion studies, facilitating inter-laboratory comparisons. Future studies should explore additional macronutrient-rich matrices, particularly those with diverse protein and lipid profiles, to expand the applicability of these findings.

Increased intestinal permeability can occur in patients with diabetes mellitus. Previous studies demonstrated a correlation between impaired intestinal barrier function, elevated blood glucose levels, and diminished protective capacity of intestinal epithelial cells. However, few studies have explored gut-barrier disruption using three-dimensional (3D) in vitro models. In this study, we developed and optimized a 3D intestinal organoid model that mimics diabetic conditions by exposing the organoids to high glucose (HG) and palmitic acid (PA) levels. Human intestinal organoids derived from samples of both healthy individuals and patients with diabetes mellitus were analyzed. We evaluated the transcript levels of tight junction proteins and inflammation-related genes in ex vivo mouse intestinal organoids cultured under HG and PA conditions for 48 h. Human intestinal organoids from patients with diabetes mellitus exhibited reduced expression of genes associated with intestinal function and barrier integrity compared with those from healthy individuals. In mouse intestinal organoids, PA treatment induced cytotoxicity and significantly reduced the expression of intestinal stem cells and tight junction proteins, including zonula occludens-1 and occludin, compared with the control and HG-treated groups. Furthermore, treatment with HG and PA resulted in increased levels of inflammatory factors compared with those in the control group. Our in vitro model using 3D intestinal organoids can be used to investigate the impact of diabetic conditions and provide insights into gut barrier disruption.

At the present stage, heavy metal pollution, led by environmental exposure to cadmium (Cd), has caused incalculable losses in animal husbandry. The potential value of caprylic acid as a medium- and long-chain fatty acid with a unique role in regulating lipid metabolism has attracted much attention. Our previous study found that octanoic acid levels were significantly reduced under Cd-exposed conditions in Hu Sheep, on the basis of which we investigated the protective effect of sodium octanoate, a derivative of octanoic acid, against Cd exposure in Hu Sheep in the present study. In this study, an animal model of Cd exposure in Hu Sheep was established. Comprehensive assessment of Cd-induced intestinal injury using hematoxylin and eosin (H&E) staining, immunostaining and carried out in-depth analyses combined with lipid metabolomics and transcriptomics. The results showed that Cd exposure triggered intestinal inflammation, barrier function damage and oxidative stress imbalance. Lipid metabolomics analysis showed that Cd exposure severely disrupted lipid metabolic processes, especially the glycerophospholipid metabolic pathway, suggesting that lipid metabolic disorders are closely related to intestinal injury. Notably, sodium octanoate could partially reverse the lipid metabolism abnormality by regulating the Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway, effectively alleviating the Cd toxicity, which provides a brand-new prevention and control strategy for Cd-induced intestinal injury in the livestock industry pollution-mediated disease.

Recent global burden of disease studies have shown that bacterial infections are responsible for over 13 million deaths worldwide, or 1 in every 8 deaths, each year. Enteric diarrheal infections, in particular, pose a significant challenge and strain on healthcare systems as many are difficult to address pharmaceutically, and thus rely primarily on the patient's own immune system and gut microbiome to fight the infection. Nonetheless, the specific mechanisms behind gut microbiome colonization resistance of enteric pathogens are not well defined and microbiome diversity is difficult to represent and study experimentally. To address this gap, we have constructed an agent-based computational model of the colonic epithelium cross section to investigate the colonic invasion of enteric pathogens. The model focuses on three main regions: epithelial layer, mucosal bilayer, and adjacent lumen, and utilizes four main cell types as agents: anaerobic bacteria, facultative anaerobic bacteria, human goblet cells, and pathogens. Utilizing this model, we are able to describe the healthy microbiome cell localization and dynamics from our mucosal bilayer. In addition, we are also able to investigate the impact of host dietary fiber consumption and simulate pathogen invasion. The model exemplifies the possibility and potential to explore key gut microbiome colonization resistance mechanisms and environmental impacts on the gut microbiome using computational methods.

Prenatal alcohol exposure (PAE) can severely impact fetal development, including alterations to the developing immune system. Immune perturbations, in tandem with gut dysbiosis, have been linked to brain and behavioral dysfunction, but this relationship is poorly understood in the context of PAE. This study takes an ontogenetic approach to evaluate PAE-induced alterations to brain and serum cytokine levels and both the composition and metabolic output of the gut microbiota. Using a well-established rat model of PAE, cytokine levels in the serum, prefrontal cortex, amygdala, and hypothalamus as well as gut microbiota composition and short-chain fatty acid (SCFA) levels were assessed at three postnatal (P) timepoints: P8 (infancy), P22 (weaning), and P38 (adolescence). Male PAE rats had increased cytokine levels in the amygdala and hypothalamus, but not prefrontal cortex, at P8. This altered neuroimmune function was not seen in the PAE females. The effect of PAE on central cytokine levels was reduced at P22/38, the same age at which PAE-induced alterations in serum cytokine levels emerge in both sexes. PAE reduced bacterial diversity in both sexes at P8, but only in females at P38, where a PAE-induced unique community composition emerged. Both sexes had alterations to specific bacterial taxa (e.g., Firmicutes), some of which are important in producing the SCFA butyric acid, which was decreased in PAE animals at P22. These results demonstrate that PAE leads to sex- and age-specific alterations in immune function, gut microbiota and SCFA production, highlighting the need to consider both age and sex in future work.

In this study, low molecular weight chondroitin sulfates (LMCSs) with different structures, named LMCSO, LMCSD, and LMCSH, were prepared by oxidative degradation, deamidation cleavage, and hydrothermal depolymerization, respectively. In vitro fermentation modeling was used to study the effects of CS and LMCSs on gut microbiota and metabolite composition. The degree of carbohydrate metabolism was in the order of CS > LMCSH > LMCSO > LMCSD. Significantly, GlcA in chondroitin-6-sulfate (CSC) was more readily utilized by gut microbiota during fermentation, and this trend was more pronounced in LMCSs. The LMCSs group notably increased microbial richness and evenness, especially in the LMCSD group. Bacteroides fragilis was identified as a potential primary degrader of CS and LMCSs through species-level analysis. The abundance of Escherichia-Shigella was reduced by LMCSs, and short-chain fatty acids production was enhanced, particularly by LMCSO, while the production of beneficial metabolites such as N-acetyl-D-Glucosamine 6-Phosphate (GlcNAc-6P), lactate, and progesterone was stimulated. Among these, the metabolism of the key metabolite GlcNAc-6P was significantly and positively correlated with the abundance of Bacteroides, Clostridium_sensu_stricto_1, and Parabacteroides. Exploring the mechanisms by which gut microbiota metabolize LMCSs with different structures can provide theoretical support for the targeted preparation of LMCSs that modulate the gut microbiota.

Sugarcane (Saccharum spp.) is an important cash crop widely grown in tropical and subtropical regions. In addition to being the main raw material for sugar and ethanol production, it is rich in a wide range of bioactive compounds with remarkable chemical diversity and biological activity. In recent years, sugarcane research has gradually increased due to the increased interest in natural medicines and functional foods. This paper reviews the chemical constituents and their potential bioactivities of sugarcane. These include flavonoids, flavonoid carbonyl glycosides, flavonols, dihydroflavonoids, dihydroflavonols, chalcones and flavanols. China's traditional Chinese medicine resources are facing serious problems in terms of sustainable development, causing a shortage aggravated by changes in the natural environment and species composition as well as uncontrolled human harvesting. Therefore, it is of great significance for the maintenance and development of traditional Chinese medicine resources to study such resources, which have medicinal value and crop potential, and discover new uses for them. In this review, we discuss the chemical composition of sugarcane and its potential bioactivities, explore its applications in the field of medicine and look for the direction of future research.

Background: Glutamate, a nutritionally non-essential amino acid, is a key intermediate in nitrogen metabolism. Despite more studies on its functional role in intestine health, it remains unknown how glutamate regulates nitrogen metabolism in animals fed a low-protein diet. Methods: Herein, we investigated the effects of glutamate supplementation on colonic amino acid transport, barrier protein expression, microbiota alterations, fecal nitrogen emissions, hepatic amino acid transport, and protein synthesis in weaned rats. Results: We found that protein restriction diminished the mucus thickness, reduced goblet cell numbers, and the expression of EAAT3, y+LAT2 in the colon. In contrast, glutamate supplementation reversed these effects, increasing the colon length and enhancing the expression of ZO-1, Occludin, and Claudin-1 in the colon. At the genus level, glutamate increased the abundance of Lactococcus and Clostridia_sensu_stricto_18. Additionally, glutamate supplementation resulted in an increased apparent nitrogen digestibility, reduced the ratio of fecal nitrogen to total nitrogen intake, and increased the ratio of fecal microbial nitrogen to total nitrogen intake. Protein restriction decreased the mRNA level of ATP1A1, EAAT3, SNAT9/2, and ASCT2, and the protein level of p-mTOR, mTOR, p-mTOR/mTOR, and p-p70S6K/p70S6K as well as p-4EBP1/4EBP1 in the liver. These effects were reversed by glutamate supplementation. Conclusions: In conclusion, glutamate supplementation upregulates amino acid transporters and barrier protein expression in the colon, modulates microbiota composition to reduce fecal nitrogen excretion, and enhances amino acid transport and protein synthesis in the liver by activating the mTOR/p70S6K/4EBP1 pathway, which influences nitrogen metabolism in weaned rats fed a low-protein diet.

2'-Fucosyllactose (2'-FL), an industrial breast milk oligosaccharide, is approved for use in infant formula and may reduce cow's milk protein allergenicity. To investigate whether glycosylation products of 2'-FL in dairy products (2'-FL-β-LG) increase its sensitization, we cross-linked β-LG with 2'-FL and used it to sensitize Balb/c mice, comparing it with nonglycosylated β-LG. Both 2'-FL-β-LG sensitization and oral 2'-FL intervention reduced allergic symptoms, specific antibodies (IgE, IgG, and IgG2a), inflammatory cytokine levels, and intestinal damage. 2'-FL also shifted T-cell differentiation, reduced cell surface expression of DC receptors, and enhanced gut microbial diversity. Oral 2'-FL showed the greatest efficacy, suggesting its potential for lowering milk allergenicity in formula.

Mesenteric torsion (MT) is a condition that affects several animal species and can lead to the animals' death. However, little is known about its etiology. Therefore, this study aimed to identify genomic regions and candidate genes associated with MT. Phenotypic and genotypic data from 405 pigs, including MT records and genealogy were used. In the model, contemporary group (sex, year, and week of weaning) was considered fixed effect, the linear effect of weaning weight as a covariate, while direct additive genetic effect was random. In the genome-wide association study, genomic windows explaining more than 0.3% of the genetic variance were considered significant. Fifty-two significant windows were identified, covering 299 genes located on 15 chromosomes. The HSD17B4, TNFAIP8, TENM4, CHD2, RGMA, OPRM1, PPARGC1A, CHIA, KCNJ2, KCNJ16, KCNJ15, ELN, SGO1, IL17A, IL17F, GATA4, OVOL2, GLI3, and RAP1A genes were considered candidates to MT since they are related to intestinal morphogenesis, feeding behavior, intestinal barrier, digestion, and intestinal motility. These processes could induce intestinal malformations, dysbiosis, excessive fermentation, delay intestinal transit, and obstruction. Our findings contribute to understanding the mechanisms involved in the occurrence of MT in pigs and may help to elucidate the etiology of intestinal torsion/volvulus in other mammals, including humans.

Alcoholic heart disease (AHD) is a severe cardiovascular condition linked to chronic alcohol consumption. This study investigates the effects of a high-fiber diet and acetate on gut microbiota and cardiac function in AHD mouse models. Sixty male C57BL/6 mice were divided into six groups, receiving either a control diet, high-fiber diet, or acetate supplementation alongside alcohol treatment. Results revealed that cardiac fibrosis and heart failure were notably improved in the AHD mice receiving high-fiber or acetate diets. Transcriptomic analyses indicated that dietary interventions modulated the expression of genes involved in lipid metabolism and the TGF-β signaling pathway. Additionally, 16S rRNA sequencing showed that the high-fiber diet and acetate altered gut microbiota composition, enhancing the abundance of beneficial bacteria such as Akkermansia muciniphila, Lactobacillus intestinalis, and Bacteroides acidifaciens. These microbes exhibited positive correlations with genes related to fat metabolism and TGF-β signaling, suggesting a potential mechanism for gut microbiota's role in AHD pathology. ROC analysis identified these bacteria as promising biomarkers for AHD detection. Overall, our findings underscore the therapeutic potential of dietary fiber and acetate in modulating gut microbiota and improving cardiac function in AHD, highlighting the intricate relationship between gut health and cardiovascular disease management.

Parkinson's Disease (PD) is a neurodegenerative disorder characterized by motor and non-motor symptoms, with emerging research suggesting a critical link between intestinal dysbiosis and PD progression. This review explores the pathophysiological mechanisms underlying PD, such as alpha-synuclein aggregation, mitochondrial dysfunction, neuroinflammation, and oxidative stress, while focusing on the impact of gut dysbiosis on intestinal barrier function and its role in reduced neurochemical production. The clinical features of PD, including dopamine, serotonin, and GABA deficiencies, are examined, with a focus on how dysbiosis contributes to neurotransmitter depletion. Current treatments of PD, such as levodopa and dopamine agonists, are discussed alongside gut health therapies such as probiotics, prebiotics, and Fecal Microbiota Transplantation (FMT). Future therapeutic directions, including synbiotics, engineered microbes, phage therapy, and the integration of machine learning (ML) and artificial intelligence (AI), are explored. The chapter also considers preventive strategies, such as lifestyle adjustments and early gut health monitoring using modern diagnostic tools and biosensors. Furthermore, a strong need for continued research into the gut-brain axis (GBA) to develop more effective, gut-targeted therapies for managing PD is discussed.

Pectin has multiple functions and is widely used in the food industry. It is an acidic heteropolysaccharide found in most plants, mainly consisting of two regions: homogalacturonan (HG) and rhamnogalacturonan-I (RG-I). HG and RG-I rich pectin have unique structures and functional properties, which can be obtained through specific preparation methods. Some emerging physics assisted preparation strategies are more advantageous for preparing specific structures with higher purity and efficiency than traditional preparation methods. HG and RG-I rich pectin have unique processing and functional properties, but sometimes a proper ratio of HG and RG-I pectin may have better effects than individuals. Therefore, it is speculated that there may be some synergistic effects between the two pectin structures. A comprehensive understanding of the preparation, structure, and functional relationship of HG and RG-I rich pectin is crucial for the efficient preparation of pectin with targeted functions.

Hypertension is a common chronic disease driven by multiple physiological mechanisms, primarily the overactivation of the renin-angiotensin system (RAS). Gamma-aminobutyric acid (GABA), a nonprotein amino acid, has well-documented health benefits, including antihypertensive and calming effects. This study evaluates the blood pressure-lowering effects of Lactiplantibacillus plantarum DPUL-F233 bacterial powder in spontaneously hypertensive rats (SHRs). The bacterial powder was produced using optimized fermentation and freeze-drying techniques. In the oral administration experiment on SHRs, the group treated with a high dose of bacterial powder via long-term gavage showed a significant reduction in blood pressure compared to the untreated group. Specifically, the final measurements of diastolic and systolic blood pressure were reduced to 206.0 ± 2.35 mm Hg and 145.0 ± 6.78 mm Hg, respectively. The angiotensin-converting enzyme I/Angiotensin II/AT1R axis was downregulated, while the angiotensin-converting enzyme II/Angiotensin 1-7/MasR axis was upregulated, rebalancing the RAS signaling pathway. The high-dose group also demonstrated protective effects on the heart and kidneys, with significant improvements observed in reducing cardiac hypertrophy and kidney damage. Additionally, molecular simulation studies indicated potential inhibition of ACE I by GABA. The results suggest that GABA-rich L. plantarum DPUL-F233 powder has significant potential as a natural antihypertensive supplement, particularly for use in functional food development.

This study aims to investigate the effects of selenium Broussonetia papyrifera polysaccharide (Se-BPP) on growth performance, immune regulation, intestinal barrier function, and gut microbiota in cyclophosphamide (CTX)-induced immunosuppressed chicks. A total of 120 one-day-old male yellow-feathered broilers were randomly divided into five groups: normal control group (NC), model control group (MC), low-dose Se-BPP group (Se-L), high-dose Se-BPP group (Se-H), and Astragalus polysaccharide (APS) group The Se-L and Se-H groups were supplemented with 0.1 % or 0.2 % Se-BPP, respectively, while the APS group was supplemented with 0.2 % APS. On days 22, 24, and 26, the NC group received intramuscular injections of 80 mg/kg saline, while the other groups received the same dose of CTX to induce immunosuppression in the chicks. The results showed that CTX caused growth retardation, immunosuppression, intestinal damage, and alterations in gut microbiota structure. Supplementation with Se-BPP improved average daily gain and reduced feed-to-gain ratio, promoting growth in immunosuppressed chicks. Se-BPP increased the immune organ index and serum content of IgG, IgM, IgA, SOD, GSH-Px, CAT, IL-2, IL-4, IL-6, IL-10, and INF-γ, thus alleviating the immunosuppression and oxidative stress caused by CTX. Additionally, Se-BPP enhanced the mRNA expression levels of ZO-1, Claudin 1, and MUC2 and increased villus height in the jejunum, effectively mitigating intestinal damage induced by CTX. Although the effect of Se-BPP on alpha diversity of the gut microbiota was not significant, it increased the abundance of beneficial bacteria such as Ruminococcus and Lactobacillus. In brief, this study demonstrated that adding Se-BPP to the diet could improve immunosuppression, intestinal damage, and microbiota disturbances in yellow-feather broiler chickens challenged with CTX, enhancing their production performance.

Probiotics are effective for improving poultry health. Probiotic Bacillus cereus strains are widely used to improve animal health by stimulating the immune system. In this study, we obtained a B. cereus 13 (BC13) strain that functions in acid, high-temperature, and bile salt resistance. It also degrades starch, cellulose, and other proteins. To better understand the probiotic effects of BC13, we added the strain to the diet of broilers and observed its effects. We found that BC13 significantly improved the growth performance of broilers. The levels of total antioxidant capacity, superoxide dismutase, and glutathione peroxidase were increased, and the concentration of malondialdehyde was reduced by BC13. Supplementation with BC13 enhanced immune function by increasing the levels of secretory immunoglobulin A (sIgA) in the jejunum mucosa; IgA, IgM, and IgG in the serum; mRNA levels of Zo-1, claudin and occludin of the jejunal mucosa; and increased villus height/crypt depth of the jejunum. Furthermore, BC13 improved the composition of intestinal microbes, especially at the genus level of Akkermansia. The addition of BC13 increased the levels of acetic, butyric, valeric, and propionic acids. These results emphasise the potential of BC13 as a probiotic dietary supplement to improve the antioxidant capacity, intestinal barrier function, and gut microbial composition to enhance body health.

The aim of this study was to evaluate the effects of lactic acid and glyceryl lactate on growth performance, antioxidant capacity, and intestinal health in piglets. This study included 240 castrated male piglets (initial body weight: 7.50 ± 0.54 kg) assigned to four groups: CON (basal diet), LA (basal diet + 0.5% lactic acid), GL (basal diet + 0.5% glyceryl lactate), and LG (basal diet + 0.5% lactic acid + 0.5% glyceryl lactate). Each group had six replicates of 10 piglets. The trial lasted 28 days. Compared with the control group, the GL and LG groups showed enhanced growth performance and reduced diarrhea rate in piglets. The LA and LG groups showed decreased intestinal chyme pH and increased digestive enzyme activities. Moreover, the GL and LG groups displayed elevated jejunal mRNA levels of the tight junction protein occludin and mucin MUC2, enhanced expression levels of Nrf2 signaling pathway genes, increased activities of the antioxidant enzymes GPX and CAT, and reduced MDA content. Acidifier supplementation also modulated cecal bacterial abundance and short-chain fatty acid (SCFA) content. Genera such as Faecalibaculum, Nocardiopsis, Collinsella, CAG269, Allobaculum, and Enterococcus were affected. In conclusion, glyceryl lactate and its combination with lactic acid improved piglet growth performance by enhancing intestinal barrier function, antioxidant capacity, microbial community structure, and SCFA production.

The gut plays a crucial role in digestion and immunity, so its balance is essential to overall health. This balance relies on dynamic interactions between intestinal epithelial cells, immune cells, and crypt stem cells. Inflammatory bowel disease (IBD), which consists of ulcerative colitis and Crohn's disease, is a chronic relapsing inflammatory disease of the gastrointestinal tract closely related to immune dysfunction. Stem cells, known for their ability to self-renew and differentiate, play an important role in repairing damaged intestinal epithelium and maintaining homeostasis in vivo. Macrophages are key gatekeepers of intestinal immune homeostasis and have a significant impact on IBD. Current research has focused on the link between epithelial cells and stem cells, but interactions with macrophages, which have been recognized as attractive targets for the development of new therapeutic approaches to disease, have been less explored. Recently, the developing field of immunometabolism has reinforced that metabolic reprogramming is a key determinant of macrophage function and subsequent disease progression. The aim of this review is to explore the role of the macrophage-stem cell axis in the maintenance of intestinal homeostasis and to summarize potential approaches to treating IBD by manipulating the cellular metabolism of macrophages, as well as the main opportunities and challenges faced. In summary, our overview provides a framework for understanding the critical role of macrophage immunometabolism in maintaining gut health and potential therapeutic targets.

The gut microbiome comprises a vast community of microbes inhabiting the human alimentary canal, playing a crucial role in various physiological functions. These microbes generally live in harmony with the host; however, when dysbiosis occurs, it can contribute to the pathogenesis of diseases, including osteoporosis. Osteoporosis, a systemic skeletal disease characterized by reduced bone mass and increased fracture risk, has attracted significant research attention concerning the role of gut microbes in its development. Advances in molecular biology have highlighted the influence of gut microbiota on osteoporosis through mechanisms involving immunoregulation, modulation of the gut-brain axis, and regulation of the intestinal barrier and nutrient absorption. These microbes can enhance bone mass by inhibiting osteoclast differentiation, inducing apoptosis, reducing bone resorption, and promoting osteoblast proliferation and maturation. Despite these promising findings, the therapeutic effectiveness of targeting gut microbes in osteoporosis requires further investigation. Notably, gut microbiota has been increasingly studied for their potential in early diagnosis, intervention, and as an adjunct therapy for osteoporosis, suggesting a growing utility in improving bone health. Further research is essential to fully elucidate the therapeutic potential and clinical application of gut microbiome modulation in the management of osteoporosis.

Heart failure with preserved left ventricular ejection fraction (HFpEF) is a disease that affects multiple organs throughout the body, accounting for over 50% of heart failure cases. HFpEF has a significant impact on individuals' life expectancy and quality of life, but the exact pathogenesis remains unclear. Emerging evidence implicates low-grade systemic inflammation as a crucial role in the onset and progression of HFpEF. Gut microbiota dysregulation and associated metabolites alteration, including short-chain fatty acids, trimethylamine N-oxides, amino acids, and bile acids can exacerbate chronic systemic inflammatory responses and potentially contribute to HFpEF. In light of these findings, we propose the hypothesis of a "gut microbiota-inflammation-HFpEF axis", positing that the interplay within this axis could be a crucial factor in the development and progression of HFpEF. This review focuses on the role of gut microbiota dysregulation-induced inflammation in HFpEF's etiology. It explores the potential mechanisms linking dysregulation of the gut microbiota to cardiac dysfunction and evaluates the therapeutic potential of restoring gut microbiota balance in mitigating HFpEF severity. The objective is to offer novel insights and strategies for the management of HFpEF.

Diarrhea is usually observed in newborn Hu lambs, while severe diarrhea may lead to the stunted growth and even death in lambs, necessitating the common practice of antibiotic administration to newborns. In order to explore the application of the effective probiotics and/or prebiotic treatment in animal feed to lessen the recline on antibiotics, 27 newborn of Hu lambs were equally allocated into three groups: control group (Con), probiotics group (Pro) receiving Lactiplantibacillus plantarum N-1 (LPN-1), and synbiotics group (Syn) receiving LPN-1 combined with isomaltose-oligosaccharide (IMO), and raised till 60 days of age.

Compared with the Con, the incidence of severe diarrhea was lower in both two treatment groups, accompanied by a significant reduction in terramycin administration frequency (P < 0.05). The daily feed intake in newborns significantly increased after probiotics or synbiotics treatment (P < 0.05), leading to the substantial increment in average daily gain by 48.28% and heart girth (P < 0.05), as well as enhancements in height (P < 0.01) at 60 days of the age in synbiotics treatment group. Applying probiotics and synbiotics exhibited the enhanced rumen weight (P < 0.05), and synbiotics further promoted the spleen development (P < 0.05). The inclusion of probiotics and synbiotics significantly modified the gut microbial composition of Hu lambs (P < 0.01), with an increase in Butyrivibrio proteoclasticus and Pseudoruminococcus massiliensis, which were associated with starch and sucrose metabolism. Additionally, the Syn group exhibited an upsurge in the number of species associated with amino acid metabolism and cellulolysis, as well as the raised short-chain fatty acids levels in the newborn gut (P < 0.05).

This study demonstrated that LPN-1 and IMO had an enhanced effect to improve the growth performance and decrease the reliance on antibiotics by promoting the feed intake, balancing the gut microbiota and increasing the short-chain fatty acids content in Hu lambs.

Intestinal health disorders significantly contribute to the development of type 2 diabetes mellitus (T2DM). Sugar substitutes such as mogroside V (MOG), stevioside (ST), sucralose (TGS), and erythritol (ERT), are increasingly used in T2DM management as alternatives to sucrose (SUC). However, their effects on intestinal health in T2DM have not been fully compared. In the present study, we established a T2DM mouse model using a high-fat diet and streptozotocin injection. These mice were treated with equal doses of SUC, MOG, ST, TGS, or ERT for 4 weeks to evaluate the effects of these sugar substitutes on intestinal health in T2DM. T2DM mice exhibited increased intestinal permeability, reduced goblet cell numbers, elevated pro-inflammatory cytokine levels, and alterations in both gut microbiota and metabolite composition. After 4 weeks of treatment, MOG showed the most significant benefits. MOG activates the PI3K/AKT pathway, enhancing the expression of tight junction proteins, which improves intestinal barrier function and reduces permeability. This is accompanied by NF-κB inhibition, leading to reduced pro-inflammatory cytokine production and increased mucus secretion. These changes help maintain healthy gut microbiota and metabolites, preventing pathogenic bacteria from entering the bloodstream. ST downregulates NF-κB to alleviate intestinal inflammation and improves gut microbiota and metabolic homeostasis in T2DM. ERT has less beneficial effects. TGS and SUC reduce intestinal inflammation and have a better effect on the duodenum. However, TGS has a negative effect on the colon microbiota and metabolites, whereas SUC has a negative effect on the colon microbiota alone. MOG improved intestinal health in T2DM by modulating the PI3K/AKT and NF-κB pathways, whereas ST primarily modulated NF-κB to alleviate intestinal inflammation. Both treatments were effective, with MOG showing the best performance. Therefore, MOG can be considered a viable alternative to SUC for T2DM management.

Quorum sensing (QS) is a process by which bacteria sense their population density and regulate behavior accordingly. QS not only regulates bacterial virulence but also directly influences host cells. Previous studies have shown that QS is strongly associated with piglet intestinal health, but the mechanism is not yet clear. For the first time, we have confirmed in a piglet animal model that OdDHL directly damages intestinal cells in weaned piglets, disrupting the intestinal barrier. We also provide a preliminary exploration of the underlying mechanism of these effects. TUNEL assays confirmed that damage to the piglet intestinal barrier coincided temporally and spatially with dysregulated apoptosis. Lipid rafts, key components of the cell membrane, are involved in many biological processes, including the activation of apoptosis-related proteins. Following the disruption of the lipid raft structure in IPEC-J2 cells, the apoptosis rate under OdDHL stimulation decreased by 50%. These data demonstrate that lipid rafts mediate the attachment of OdDHL to porcine intestinal cells; then, OdDHL induces apoptosis in porcine intestinal cells through the mitochondrial and death receptor pathways, thereby compromising the integrity of the porcine intestinal barrier. This study provides foundational insights into the role of QS in piglet intestinal diseases.

Parkinson's disease (PD) is one of the most common neurodegenerative diseases. Constipation is a prodromal symptom of PD. It is important to investigate the pathogenesis of constipation symptoms in PD. Rotenone has been successfully used to establish PD animal models. However, the specific mechanism of rotenone-induced constipation symptoms is not well understood. In this work, we found that constipation symptoms appeared earlier than motor impairment in mice gavaged with a low dose of rotenone (30 mg/kg·BW). Rotenone not only caused loss of dopaminergic neurons and accumulation of α-synuclein, but also significantly reduced serum 5-HT levels and 5-HTR4 in the striatum and colon. The mRNA expression of aquaporins, gastrointestinal motility factors (c-Kit, Cx43, smMLCK and MLC-3) in mouse colon was also significantly regulated by rotenone. In addition, both colon and brain showed rotenone-induced inflammation and barrier dysfunction; the PI3K/AKT pathway in the substantia nigra and colon was also significantly inhibited by rotenone. Importantly, the structure, composition and function of the gut microbiota were also significantly altered by rotenone. Some specific taxa were closely associated with motor and constipation symptoms, inflammation, and gut and brain barrier status in PD mice. Akkermansia, Staphylococcus and Lachnospiraceae_UCG-006 may play a role in exacerbating constipation symptoms, whereas Acinetobacter, Lactobacillus, Bifidobacterium, Solibacillus and Eubacterium_xylanophilum_groups may be beneficial in stimulating gastrointestinal peristalsis, maintaining motor function and alleviating inflammation and barrier damage in mice. In conclusion, low-dose rotenone can cause parkinsonism with constipation symptoms in mice by disrupting the intestinal microecosystem and inhibiting the PI3K-AKT pathway and gastrointestinal motility.

Ziziphi Spinosae Semen (ZSS), a homology of medicine and a type of seed, has been widely used to improve sleep quality. The present study aimed to assess the effects of ZSS flavonoid (ZSSF) extracted and isolated from ZSS on gut microbiota and hypothalamus metabolomic profiles in a chronic restraint stress (CRS)-induced anxiety mouse model. ZSSF was prepared using microporous resin chromatography, and seven compounds were determined by UPLC-MS. ZSSF treatment dramatically reduced anxiety-like behaviors, exerted sedative-hypnotic effects, increased hippocampal 5-HT and 5-HTP, and enhanced intestinal barrier function through inhibiting colon ZO-1, Claudin-1, and Occludin expression and reducing TNF-α, IL-6, and IL-1β levels. Compared with the CRS group, the diversity of gut microbiota in ZSSF-group mice was increased, with an increase in Bacteroidetes and a decrease in Firmicutes, and it was accompanied by an increase in fecal SCFAs. Hypothalamus metabolomics and lipidomics were performed to achieve 25 differential metabolites and 44 lipids, respectively. Serum metabolomics showed a total of 13 metabolites associated with anxiety were remarkably regulated by ZSSF. Weighted correlation network analysis (WGCNA) showed that glycerophospholipids (GPs) as well as phenylalanine, tyrosine, and L-tryptophan in peripheral and central parts were significant metabolites, which contributed to the pharmacological action of ZSSF. The mRNA expression of TPH2 and DDC key enzymes associated with tryptophan metabolism were upregulated, and PLA2G12A, LACT, and PLA2G6 key enzymes associated with GP metabolism were downregulated in ZSSF compared with CRS. Briefly, ZSSF improved tryptophan and GP metabolism and regulated the gut microbiome. This study may lay a theoretical basis for potentially developing ZSSF as a natural functional food ingredient for the improvement of anxiety and sleep disorders.

To explore the mechanism of Zhuyang Tongbian Decoction (ZTD) in treating functional constipation (FC) by observing its effects on intestinal flora composition, the metabolic function of gut microbiota, fecal short-chain fatty acid (SCFA) levels, and serum concentrations of TLR4, NF-κB, TNF-α, and IL-6 in patients with FC.

40 patients with FC were randomly divided into the control group and the treatment group, 20 cases in each group. And 20 healthy volunteers were recruited during the same period. The control group was administered lactulose, while the treatment group was treated with ZTD. 16s RNA sequencing technology was used to compare the changes in the structure and diversity of the intestinal flora of patients before and after treatment. Changes in the levels of SCFAs in faeces and the levels of TLR4, NF-κB, TNF-α and IL-6 in serum were analysed. Metagenomics sequencing assessed microbiota metabolic functions.

The treatment group showed a significant increase in the relative abundance of beneficial bacteria, including Bifidobacterium, Lactobacillus, and Faecalibacterium_prausnitzii (P < 0.05), whereas Desulfobacterota and Ruminococcus were significantly reduced (P < 0.05). Notably, fecal acetic and propionic acid levels were significantly higher in the treatment group (P < 0.05). Serum biomarkers TLR4, NF-κB, TNF-α, and IL-6 decreased significantly (P < 0.05). Metagenomics sequencing showed that Carbohydrate metabolism, Metabolism of cofactors and vitamins, and C5- Branched dibasic acid metabolism were significantly increased in functional abundance (P < 0.05).

ZTD notably improves intestinal flora composition and gut microbiota metabolic function, regulates SCFA levels, and reduces inflammation markers in FC patients. The strain Faecalibacterium_prausnitzii shows significant potential in regulation of intestinal inflammation and may play a crucial role in the treatment efficacy of ZTD for FC.

The gut microbiota plays a crucial role in safeguarding host health and driving the progression of intestinal diseases. Despite recent advances in the remarkable correlation between dysbiosis and extraintestinal cancers, the underlying mechanisms are yet to be fully elucidated. Pathogenic microbiota, along with their metabolites, can undermine the integrity of the gut barrier through inflammatory or metabolic pathways, leading to increased permeability and the translocation of pathogens. The dissemination of pathogens through the circulation may contribute to the establishment of an immune-suppressive environment that promotes carcinogenesis in extraintestinal organs either directly or indirectly. The oncogenic cascade always engages in the disruption of hormonal regulation and inflammatory responses, the induction of genomic instability and mutations, and the dysregulation of adult stem cell proliferation. This review aims to comprehensively summarize the existing evidence that points to the potential role of dysbiosis in the malignant transformation of extraintestinal organs such as the liver, breast, lung, and pancreas. Additionally, we delve into the limitations inherent in current methodologies, particularly the challenges associated with differentiating low loads gut-derived microbiome within tumors from potential sample contamination or symbiotic microorganisms. Although still controversial, an understanding of the contribution of translocated intestinal microbiota and their metabolites to the pathological continuum from chronic inflammation to tumors could offer a novel foundation for the development of targeted therapeutics.

Atrial cardiomyopathy is a multifaceted heart disease characterized by structural and functional abnormalities of the atria and is closely associated with atrial fibrillation and its complications. Its etiology involves a number of factors, including genetic, infectious, immunologic, and metabolic factors. Recent research has highlighted the critical role of the gut microbiota in the pathogenesis of atrial cardiomyopathy, and this is consistent with the gut-heart axis having major implications for cardiac health. The aim of this work is to bridge the knowledge gap regarding the interactions between the gut microbiota and atrial cardiomyopathy, with a particular focus on elucidating the mechanisms by which gut dysbiosis may induce atrial remodeling and dysfunction. This article provides an overview of the role of the gut microbiota in the pathogenesis of atrial cardiomyopathy, including changes in the composition of the gut microbiota and the effects of its metabolites. We also discuss how diet and exercise affect atrial cardiomyopathy by influencing the gut microbiota, as well as possible future therapeutic approaches targeting the gut-heart axis. A healthy gut microbiota can prevent disease, but ecological dysbiosis can lead to a variety of symptoms, including the induction of heart disease. We focus on the pathophysiological aspects of atrial cardiomyopathy, the impact of gut microbiota dysbiosis on atrial structure and function, and therapeutic strategies exploring modulation of the microbiota for the treatment of atrial cardiomyopathy. Finally, we discuss the role of gut microbiota in the treatment of atrial cardiomyopathy, including fecal microbiota transplantation and oral probiotics or prebiotics. Our study highlights the importance of gut microbiota homeostasis for cardiovascular health and suggests that targeted interventions on the gut microbiota may pave the way for innovative preventive and therapeutic strategies targeting atrial cardiomyopathy.

Stilbenoids are a class of naturally occurring phenolic compounds found in various plant species, characterized by a stilbene backbone with diverse substituents that confer a range of biological activities. These compounds exhibit antioxidant, anti-inflammatory, and antimicrobial properties, making them promising candidates for improving intestinal health. The intestinal tract plays a critical role in nutrient digestion, absorption, and immune defense, and maintaining its integrity is vital for animal growth. Stilbenoids contribute to gut health by enhancing intestinal morphology, supporting mucosal immune responses, regulating gut microbiota composition, modulating metabolic pathways, and maintaining mitochondrial health. This review provides a comprehensive analysis of key stilbenoids, including resveratrol, pterostilbene, piceatannol, and oxyresveratrol, focusing on their biological effects and regulatory mechanisms. By highlighting their roles in mitigating intestinal inflammation and promoting gut function, this review provides a basis for the practical application of stilbenoids in animal health and husbandry.

Short-chain fatty acids (SCFAs), produced through fermentation of dietary fibers by gut bacteria, play a central role in modulating cardiovascular function and heart failure (HF) development. The progression of HF is influenced by intestinal barrier dysfunction and microbial translocation, where SCFAs serve as key mediators in the gut-heart axis. This review examines the complex metabolic interactions between SCFAs and other gut microbiota metabolites in HF, including their relationships with trimethylamine N-oxide (TMAO), aromatic amino acids (AAAs), B vitamins, and bile acids (BAs). We analyze the associations between SCFA production and clinical parameters of HF, such as left ventricular ejection fraction (LVEF), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and glomerular filtration rate (GFR). Gaining insights into metabolic networks offers new potential therapeutic targets and prognostic markers for managing heart failure, although their clinical significance needs further exploration.

Population aging has become a primary global public health issue, and the prevention of age-associated diseases and prolonging healthy life expectancies are of particular importance. Gut microbiota has emerged as a novel target in various host physiological disorders including aging. Comprehensive understanding on changes of gut microbiota during aging, in particular gut microbiota characteristics of centenarians, can provide us possibility to achieving healthy aging or intervene pathological aging through gut microbiota-directed strategies.

This review aims to summarize the characteristics of the gut microbiota associated with aging, explore potential biomarkers of aging and address microbiota-associated mechanisms of host aging focusing on intestinal barrier and immune status. By summarizing the existing effective dietary strategies in aging interventions, the probability of developing a diet targeting the gut microbiota in future is provided.

This review is focused on three key notions: Firstly, gut microbiota has become a new target for regulating health status and lifespan, and its changes are closely related to age. Thus, we summarized aging-associated gut microbiota features at the levels of key genus/species and important metabolites through comparing the microbiota differences among centenarians, elderly people and younger people. Secondly, exploring microbiota biomarkers related to aging and discussing future possibility using dietary regime/components targeted to aging-related microbiota biomarkers promote human healthy lifespan. Thirdly, dietary intervention can effectively improve the imbalance of gut microbiota related to aging, such as probiotics, prebiotics, and postbiotics, but their effects vary among.

While artificial sweeteners are Generally Regarded as Safe (GRAS), the scientific community remains divided on their safety status. The previous assumption that artificial sweeteners are inert within the body is no longer valid. Artificial sweeteners, known for their high intense sweetness and low or zero calories, are extensively used today in food and beverage products as sugar substitutes and are sometimes recommended for weight management and Type 2 Diabetes Mellitus (T2DM) patients. The general omission of information about the concentration of artificial sweeteners on market product labels makes it challenging to determine the amounts of artificial sweeteners consumed by people. Despite regulatory authorization for their usage, such as from the United States Food and Drug Administration (FDA), concerns remain about their potential association with metabolic diseases, such as T2DM, which the artificial sweeteners were supposed to reduce. This review discusses the relationship between artificial sweetener consumption and the risk of developing T2DM. With the increasing number of recent scientific studies adding to the debate on this subject matter, we assessed recent literature and up-to-date evidence. Importantly, we highlight future research directions toward furthering knowledge in this field of study.

Hypertension is a prevalent cardiovascular disease. Exercise is widely recognized as an effective treatment for hypertension, and it may also influence the composition of the intestinal microflora. However, it remains unclear whether exercise can specifically regulate the intestinal microflora in the context of hypertension treatment. In this study, tail blood pressure in spontaneously hypertensive rats (SHR) was measured using a blood pressure meter after exercise intervention and fecal bacteria transplantation following exercise. Blood lipid levels were assessed using an automatic biochemical analyzer, and 16S rRNA sequencing was employed to analyze the intestinal microflora. Histological examinations of ileal tissue were conducted using HE and Masson staining. Intestinal permeability, inflammatory status, and sympathetic activity were evaluated by measuring the levels of diamine oxidase, D-lactic acid, C-reactive protein, interleukin-6, tumor necrosis factor-α, lipopolysaccharide, norepinephrine, angiotensin II, cyclic adenosine monophosphate, and cyclic guanosine monophosphate. Exercise was found to reduce blood pressure and blood lipid levels in SHR. It also improved the composition of the intestinal microflora, as evidenced by a reduced Firmicutes/Bacteroidetes ratio, an increase in bacteria that produce acetic and butyric acid, and higher Chao 1 and Shannon diversity indices. Furthermore, exercise reduced the thickness of the fibrotic and muscular layers in the ileum, increased the goblet cell/villus ratio and villus length, and decreased intestinal permeability, inflammatory markers, and sympathetic nerve activity. The intestinal microbial flora regulated by exercise demonstrated similar effects on hypertension. In conclusion, exercise appears to regulate the intestinal microflora, and this exercise-induced change in flora may contribute to improvements in hypertension in rats.

Sleep deprivation is a prevalent issue in contemporary society, with significant ramifications for both physical and mental well-being. Emerging scientific evidence illuminates its intricate interplay with the gut-brain axis, a vital determinant of neurological function. Disruptions in sleep patterns disturb the delicate equilibrium of the gut microbiota, resulting in dysbiosis characterized by alterations in microbial composition and function. This dysbiosis contributes to the exacerbation of neurological disorders such as depression, anxiety, and cognitive decline through multifaceted mechanisms, including heightened neuroinflammation, disturbances in neurotransmitter signalling, and compromised integrity of the gut barrier. In response to these challenges, there is a burgeoning interest in therapeutic interventions aimed at restoring gut microbial balance and alleviating neurological symptoms precipitated by sleep deprivation. Probiotics, dietary modifications, and behavioural strategies represent promising avenues for modulating the gut microbiota and mitigating the adverse effects of sleep disturbances on neurological health. Moreover, the advent of personalized interventions guided by advanced omics technologies holds considerable potential for tailoring treatments to individualized needs and optimizing therapeutic outcomes. Interdisciplinary collaboration and concerted research efforts are imperative for elucidating the underlying mechanisms linking sleep, gut microbiota, and neurological function. Longitudinal studies, translational research endeavours, and advancements in technology are pivotal for unravelling the complex interplay between these intricate systems.