Search Results (288)

Aims: The effects of two Lactiplantibacillus plantarum strains and their probiotics on loperamide-induced constipation in mice were compared, and the possible mechanisms of the two strains in alleviating constipation were explored. Methods: KM mice were divided into the normal group, model group, positive control group, LTJ53 group, LP11824 group, HK-LTJ53 group and HK-LP11824 group. Loperamide was used to induce constipation in the mice. The study examined changes in defecation time, intestinal propulsion rate, gastric emptying rate, gastrointestinal peptides, colon histology, expression of intestinal barrier function genes, gut microbiota, and short-chain fatty acids (SCFAs). Results: Both live and postbiotic forms of L. plantarum significantly shortened defecation time, improved gastric emptying and intestinal motility, increased the levels of 5-hydroxytryptamine (5-HT), gastrin (GAS) and motilin (MTL), decreased the level of vasoactive intestinal peptide (VIP), restored colon morphology, upregulated the expression of Zonula Occludens-1 (ZO-1), mucin 2 (MUC2) and aryl hydrocarbon receptor (AhR), and downregulated the expression of aquaporin 4 (AQP4). They can also regulate the composition of the gut microbiota and alter the levels of SCFAs. Strain-specific effects were observed: LTJ53 was more effective in improving weight loss and gastric emptying, while LP11824 showed stronger efficacy in promoting small intestinal motility. Conclusions: L. plantarum and its postbiotics can relieve constipation through regulating the intestinal flora, enhancing gastrointestinal motility, adjusting the levels of neurotransmitters, and improving the intestinal barrier function. The specific effects of the two strains can support the selection of function-oriented precise intervention. Full article

Male infertility contributes to approximately half of all infertility cases, with a substantial proportion remaining idiopathic. Emerging evidence implicates the gut microbiome as a regulator of male reproductive health through a proposed gut–testis axis. Few studies have shown that gut microbial dysbiosis may impair sperm quality via multiple mechanisms, including disruption of endocrine function (e.g., reduced testosterone production), alterations in microbial-derived metabolites, and impaired testicular energy metabolism. Increased intestinal permeability and systemic inflammation may further compromise the blood–testis barrier, while translocation of bacterial endotoxins may also contribute to testicular damage. Collectively, these processes can disrupt spermatogenesis and negatively affect sperm parameters, such as concentration, motility, and morphology. Interventions that restore microbial balance, including dietary modulation, have shown potential in reversing these effects and improving reproductive outcomes. This review summarizes and evaluates current literature linking gut microbial dysbiosis to male reproductive dysfunction. Key methodological limitations and knowledge gaps are highlighted, providing a foundation for advancing the development of gut microbiome-based interventions to improve male reproductive health. Full article

Background/Objectives: Paediatric intestinal pseudo-obstruction (PIPO) is a disorder of gut motility in childhood, frequently leading to intestinal failure (IF). Consensus on optimum nutrition management (oral, enteral, intravenous feeding exclusively or in combination) is lacking. Our aim was to investigate the current approach to the nutrition support of children (<18 years) with PIPO managed in Gastroenterology centres in the United Kingdom (UK) and long-term mode of feeding. Methods: An electronic questionnaire was sent to the members of the British Society of paediatric Gastroenterology, Hepatology and Nutrition (BSPGHAN). The data collected (October–November 2023) included patient demographics, disease phenotype, age at symptom onset and mode/type of feeding. Results: A total of 36 patients fulfilled criteria for PIPO; 22/36 (61.1%) patients were female, and 25/36 (69.4%) were white British. A total of 15/36 (41.6%) became symptomatic during the neonatal period and 23/36 (63.8%) within the first year of life. A total of 5/36 (13.9%) was eating a normal solid diet: 2/36 (5.5%) of these never required artificial feeding, 2/36 (5.5%) were started on a normal diet after short-term parenteral nutrition (PN) in the first year of life, and 1/36 (2.8%) re-established oral eating after 10 years of total PN following small bowel transplantation. A total of 31/36 (86.1%) required permanent artificial feeding (enteral and/or parenteral) after an average time of symptoms of 14 months. A total of 2/36 (5.5%) was exclusively on enteral nutrition (EN), and 4/36 (11.1%) was on total PN. A total of 25/36 (69.4%) received a combination of PN and oral diet (normal, or bite and dissolve, or normal but minimal intake) and/or EN. Conclusions: The results show that how and with what children with PIPO are fed in the UK varies widely. Larger studies are needed to make evidence-based recommendations on the best nutrition approach. Full article

Chronic kidney disease (CKD), a progressive disorder leading to renal dysfunction, remains a significant global health issue. This study investigated whether Lactiplantibacillus plantarum HY7718 modulates gut–kidney axis-associated inflammatory, gastrointestinal, and microbial alterations in a mouse model of adenine-induced chronic kidney disease. We examined fibrosis- and inflammation-related gene expression in mouse tissues and analyzed the gut microbiota via next-generation sequencing. HY7718 supplementation was associated with reduced expression of genes related to renal fibrosis (Col1a1, Acta2) and vascular inflammation (Icam-1, Vcam-1). Further, HY7718 suppressed intestinal inflammatory responses, including downregulation of pro-inflammatory cytokines (Tnf, Il-1β, Il-6) and TLR4/MyD88/NF-κB signaling pathway genes in the colon tissues. Gastrointestinal function was also improved, with significant upregulation of gastric motility-related genes and increased digestive enzyme activity. The gut microbiota composition was altered by HY7718, with reduced abundance of pro-inflammatory taxa such as Mucispirillum and Deferribacterota, whereas beneficial genera like Lactiplantibacillus were enriched. These microbial shifts were associated with reduced intestinal inflammatory and renal fibrosis-related markers. Overall, the findings indicate that HY7718 supplementation modulates gut–kidney axis-associated inflammatory, gastrointestinal, and microbial alterations in adenine-induced CKD mice and supports further investigation of this strain in CKD-related settings. Full article

Background: Functional dyspepsia (FD) is a disorder of gut–brain interaction characterized by heterogeneous pathophysiological mechanisms, including altered gastric motility, visceral hypersensitivity, low-grade inflammation, impaired mucosal defence, and oxidative stress. Multi-target botanical strategies may represent a rational approach for addressing this complexity. Methods: This study evaluated the mechanistic rationale supporting a botanical formulation containing Zingiber officinale, Cynara scolymus, and Citrus limon extracts, here referred to as DyspepCyn^®. A focused narrative review was conducted to summarize the available mechanistic and clinical evidence for the three botanicals. In addition, the formulation was characterized through solubility testing in aqueous and biorelevant simulated gastrointestinal media, together with antioxidant assessment using ORAC and DPPH assays. Results: DyspepCyn^® showed favourable dispersion and solubility behaviour across simulated gastrointestinal conditions, with complete solubilization up to approximately 700 mg/100 mL in water and up to approximately 800 mg/100 mL in simulated intestinal fluids. No precipitation was observed in the tested media. The formulation also showed measurable antioxidant activity, with an ORAC value of 365 µmol Trolox equivalents/g and a DPPH radical scavenging EC₅₀ of 32 µg/mL. Conclusions: DyspepCyn^® combines botanicals with complementary actions on gastric motility, postprandial digestive processes, mucosal protection, and oxidative stress. The observed physicochemical stability and antioxidant capacity support the mechanistic rationale for this multi-target botanical strategy in FD. Clinical studies are required to confirm its efficacy in patients with FD. Full article

This study aimed to investigate the effects of supplementing with an essential oil blend and ascorbic acid on performance, semen characteristics, antioxidant status, gut microbiota, immunity, and gene expression in heat-stressed male rabbits. One hundred and forty male New Zealand White rabbits, aged 6 months, were randomly distributed into four dietary groups: the control group receiving basal feed (CON), the group receiving an essential oil blend (EOB, 200 mg/kg), the group receiving ascorbic acid (ASA, 1000 mg/kg), and the group receiving an essential oil blend and ascorbic acid (MAO). The experimental period lasted for eight weeks. The MAO mixture supported rabbits’ tolerance to heat stress by enhancing stress markers, as demonstrated by decreased glucose and HSP70 and increased triiodothyronine (T3). In addition, increased body weight, carcass weight, and nutrient digestibility, but reduced mortality rate, were observed in rabbits fed the MAO mixture. Additionally, semen density and volume, as well as sperm progressive motility and normality, were enhanced in rabbits fed the MAO mixture. Furthermore, MAO mixture supplementation decreases plasma cholesterol, triglycerides, AST, urea, and creatinine levels, while raising HDL and total protein levels. Adding MAO mixture contributed to an increase in plasma SOD and GPx levels, as well as seminal fluid TAC and GSH levels. Additionally, the incorporation of MAO increases IgA, IgG, and IL-10 levels while decreasing IL-6 and TNF-α levels. Adding the MAO mixture reduced C. perfringens and E. coli, as well as increased the expression of the MUC-2, CAT-1, and CLDN-1 genes. Combining an essential oil blend and ascorbic acid may contribute to improvements in performance, semen quality, immune response, antioxidant capacity, and gut health in heat-stressed male rabbits. Full article

Opioid-induced constipation (OIC) represents a prevalent adverse effect of opioid analgesics, affecting 60–90% of patients and significantly compromising quality of life. This review delineates the multifactorial pathogenesis of OIC. Peripheral μ-opioid receptor (MOR) activation suppresses enteric neuronal excitability, inhibits intestinal motility and secretion, and impairs rectoanal function. Notably, the colon appears to exhibit a distinctive lack of tolerance to opioids. Enteric glial cell activation has been implicated in neuroinflammation, while interstitial cells of Cajal show impaired pacemaker function. Central mechanisms are increasingly recognized to involve the brain–gut axis. Furthermore, opioid-induced barrier disruption, microbiota dysbiosis, and LPS/TLR4-mediated inflammation are proposed to interact and may contribute to a self-reinforcing cycle. Animal models have been instrumental in dissecting these mechanisms. However, they present limitations in reproducibility, clinical phenotype fidelity, and translational validity, particularly regarding microbiome composition and neuroimmune responses. Future research should prioritize the development of standardized, physiologically relevant animal models incorporating multi-omics approaches, and validate mechanism-based therapeutic strategies, including peripherally acting MOR antagonists and microbiota-targeted interventions, for precision management of OIC. Full article

Background/Objectives: Constipation is a common gastrointestinal problem in older adults and is associated with reduced quality of life, functional decline, frailty, and an increased risk of delirium and cognitive impairment. Its pathogenesis is multifactorial, involving age-related changes in gastrointestinal motility, neural regulation, comorbidities, and polypharmacy. However, this condition has traditionally been regarded as a localized gastrointestinal disorder, which may not fully reflect its systemic clinical significance in older populations. While prior narrative reviews have described multifactorial contributors to constipation, none have formally applied a geriatric syndrome framework to integrate these dimensions. This review proposes a three-criterion operational definition—multifactorial pathogenesis, association with functional decline and frailty, and contribution to adverse systemic outcomes—to characterize constipation in older adults as a “systemic geriatric syndrome,” and evaluates available evidence against each criterion. Methods: A narrative literature search was conducted using PubMed to identify relevant studies published between 1 January 2023, and 31 December 2025. MeSH terms included “Constipation” [Major Topic] and “Aged” [MeSH Terms]. Eligible articles included English-language original studies, systematic reviews, and clinical or epidemiological studies involving individuals aged ≥65 years. Results: Diagnosis in older adults is often complicated by secondary causes, including medications and neurological disorders, as well as atypical symptom presentations in individuals with cognitive impairment. Key pathophysiological mechanisms include reductions in interstitial cells of Cajal, impaired smooth muscle contractility, dysfunction of the enteric and autonomic nervous systems, and gut microbiota dysbiosis, which may promote chronic low-grade inflammation. Major contributing factors include physical inactivity, sarcopenia, dehydration, inappropriate defecation posture, and polypharmacy, particularly opioids and anticholinergic agents. Importantly, these factors interact through the brain–gut–microbiota axis, contributing not only to gastrointestinal dysfunction but also to systemic outcomes such as frailty, cognitive decline, and increased healthcare burden, thereby supporting a multidimensional disease framework. Conclusions: The available evidence collectively supports the plausibility of framing constipation in older adults as a systemic geriatric syndrome, though formal validation of this classification requires further longitudinal and mechanistic research. Comprehensive and individualized management strategies, extending beyond simple laxative use, are essential to reduce complications and preserve functional health in aging populations. Further studies are required to validate this framework. Full article

Background: Constipation is a common gastrointestinal (GI) state for which probiotics have shown promise as a relief. This study examined the laxative effects of the strain Bifidobacterium animalis subsp. lactis CECT 8145 (BPL1^®) in a loperamide-induced rat model of constipation. Methods: Fifty-nine rats were divided into control and loperamide-induced constipation groups. Animals received a 3-day intervention with either placebo or probiotic BPL1^® at two doses: 1.5 × 10⁸ CFU (colony-forming units) (low) and 3 × 10⁹ CFU (high). The study assessed several parameters to determine the probiotic’s effect, including: stool and gut characteristics, gastrointestinal transit time (GTT), gene expression and gut microbiome composition. Results: While loperamide significantly decreased stool number, weight and humidity, BPL1^® supplementation effectively restored these parameters, being more pronounced at a high dose. Microbiome analysis showed that BPL1^® at a low dose reduced the abundance of Muribaculaceae and Muribaculum gordoncarteri, associated with constipation. In addition, Muribaculaceae abundance was negatively correlated with stool humidity. Functional microbiome profiling indicated that BPL1^® suppressed pathways related to mucin degradation, vancomycin resistance and isoleucine biosynthesis while promoting L-lactate and pyridoxal-P (vitamin B6) biosynthesis, which may support gut motility and barrier integrity. Conclusions:Bifidobacterium animalis subsp. lactis BPL1^® exhibits potential as a functional probiotic for relieving constipation through improving stool excretion and consistency, inducing taxonomic changes and beneficial functional modulation of the intestinal microbiome. These findings justify further investigation into the mechanisms of BPL1^® as a probiotic for constipation management. Full article

Background: Retrograde cricopharyngeus dysfunction (RCPD) is a recently described upper esophageal sphincter motility disorder caused by the inability of the cricopharyngeus muscle to relax, prohibiting belching. While clinical features and treatment have been reported, early-life experiences remain unclear. This study aimed to explore childhood experiences, comorbidities, and family history in adults reporting symptoms consistent with RCPD. Methods: This cross-sectional survey included adults recruited through an online community focused on RCPD who reported cardinal symptoms consistent with RCPD. The survey collected and descriptively analyzed demographics, symptom profile, family history, neonatal and childhood experiences, psychological factors, and physician visits. Results: Of 225 respondents, 207 met inclusion criteria (mean age 32 years; 69% female). Nearly all experienced abdominal bloating (98%), gurgling noises (98%), flatulence (90%), and inability to belch (100%). Painful hiccupping, a newer described symptom, was reported by 80%. Symptoms began before age 25 in 97%, and 29% reported a first-degree relative affected. Common early-life experiences included emetophobia (39%), anxiety (38%), and difficulty being burped as an infant (20%). No statistically significant crude differences were detected in symptom severity, frequency, gender, or age of onset by presence of experiences. Only 36% felt that any physician understood their condition, and 18% reported their gastroenterologist improved their symptoms. Conclusions: Psychological early-life experiences and family history were common, but exploratory analyses did not detect statistically significant differences in symptom burden by their presence. These findings provide a foundation for future studies investigating the disorder’s pathophysiology. Limited physician recognition highlights the need for greater clinical awareness of this emerging esophageal motility disorder. Full article

Background/Objectives: Enteric glial cells (EGCs) are key players in regulating enteric neurons and gastrointestinal functions including disturbed gut motility in diabetic patients. Enteric neuronal damage has been shown in type 1 diabetes, but EGCs’ vulnerability to hyperglycaemic insults requires more investigation. Therefore, we aimed to study the quantitative changes in the EGC network enmeshing enteric plexuses, intestinal smooth muscle and mucosa in streptozotocin-induced acute (1-week) and chronic (10-weeks) diabetic rat models. Methods: Fluorescent immunohistochemistry using Sox10 glial and HuC/HuD pan-neuronal markers, immunogold electron microscopy and ELISA were performed on different gut segments. Results: In the submucosal ganglia of the ileum and colon, the density of Sox10-immunoreactive EGCs was significantly reduced in acute and increased in chronic hyperglycaemic rats without any changes in the duodenum. In the myenteric ganglia, regionally distinct alterations of glial density were noted in acute hyperglycaemia; however, a remarkable decrease was observed in chronic animals. Alterations of neuronal density did not follow the pattern of glial changes, resulting in shifts in the glia/neuron ratio. The presence of Sox10-HuC/HuD-immunoreactive cells and their diabetes-related quantitative changes were also revealed in enteric plexuses. The density of Sox10-labelling gold particles was significantly increased in the duodenal myenteric glia of diabetic rats. Muscular EGC density increased only in the colon after acute hyperglycaemia and changed in all segments after chronic hyperglycaemia. Glial fibrillary acidic protein levels decreased in the small intestine of chronic hyperglycaemic rats. Conclusions: Our present findings reveal time-dependent and regionally distinct changes in the EGC network in response to hyperglycaemia, contributing to diabetic enteric neuropathy and gut motility disturbances. Full article

The gut microbiota is a crucial component of a tiger’s health and plays a significant role in adapting to changes in food and the environment. Although extensive studies have been carried out on the gut microbiota of tigers, investigating the responses of gut microbial composition and function to preadaptation to wild predation patterns under captive conditions is particularly significant for South China tigers, given that it is the only tiger subspecies existing solely in captive settings at present. Here, we performed shotgun metagenomic sequencing for a comprehensive analysis of the gut microbiota of South China tigers assigned to two dietary groups (live prey group, LP group; frozen meat group, FM group), thereby generating abundant valuable data for this endangered subspecies. The results indicated that the core intestinal microbial composition was similar between the two dietary groups. Differential analysis revealed associations between dietary treatments and microbial abundance in the intestines of South China tigers. Functional gene analysis revealed that the LP group exhibited upregulation of genes and pathways related to antimicrobial resistance, bacterial infection-related disease, cell motility and proliferation, while the FM group displayed efficient energy metabolism. A total of 1251 antibiotic resistance genes (ARGs) were identified in the gut microbiome of South China tigers. The core resistome mainly included resistance to peptides, glycopeptides, tetracyclines, fluoroquinolones, and macrolides. In addition, the differences in ARGs between the LP group and FM group may be related to a broader range of animal tissues of live prey and the processing conditions of frozen meat. In summary, although feeding live prey did not change the core framework of the gut microbiota in South China tigers, it was associated with differences in microbial abundance, metabolic pathways, and antibiotic resistance gene profiles. Full article

Gallbladder diseases spanning cholelithiasis, cholecystitis, and gallbladder cancer represent a clinically heterogeneous continuum in which type 2 diabetes mellitus (T2DM) acts as a key metabolic modifier. Conventional models centered on bile supersaturation alone do not sufficiently account for the persistent inflammation and inter-individual variability frequently observed in practice. Here, we synthesize emerging evidence implicating the gut microbiota–bile acid (BA) axis as an integrative mechanism linking metabolic dysregulation, barrier dysfunction, and biliary pathobiology in the diabetic host. Hyperglycemia and insulin resistance, together with impaired mucosal resilience, are associated with shifts in microbial community structure and BA-transforming functions (e.g., bile salt hydrolase and 7α-dehydroxylation), favoring a more hydrophobic BA pool. These changes may disrupt BA receptor signaling, including FXR–FGF15/19 and TGR5-related pathways, thereby amplifying metabolic inflammation, promoting lithogenic bile formation, and impairing gallbladder motility. In parallel, barrier vulnerability may facilitate microbial translocation and LPS-driven immune activation, reinforcing a feed-forward loop that supports the gallstone–inflammation–carcinogenesis trajectory. Translationally, microbiome- and BA-oriented strategies (dietary patterns, bile acid therapeutics, and targeted microbiome modulation) are promising adjuncts, yet precision management should explicitly consider medication- and weight loss–related confounding—particularly with incretin-based therapies—to optimize biliary outcomes across disease stages. Full article

Energy homeostasis arises from a complex interplay between gut-derived hormones, the central nervous system, and pancreatic function. Beyond the classical incretin axis, a broad spectrum of gut peptides acts in concert to coordinate appetite regulation, nutrient sensing, gastric motility, and systemic bioenergetic balance. Perturbation of this network contributes to metabolic disorders such as obesity, type 2 diabetes, and cachexia, underscoring its pivotal role in physiological and pathological energy regulation. This review provides an integrated analysis of the mechanisms through which gut–brain–pancreas communication maintains metabolic homeostasis, with particular attention to the dynamic cross-talk between peripheral endocrine signals and central regulatory circuits. Alterations in these pathways are examined in relation to their impact on energy expenditure and substrate utilisation, alongside recent translational efforts exploiting multi-receptor peptide agonism and combinatorial hormonal modulation to restore metabolic equilibrium. Emerging therapeutic approaches increasingly aim to engage multiple bioenergetic pathways simultaneously, supported by advances in peptide engineering and molecular design. By conceptualising metabolic regulation as a coordinated network rather than a linear hormonal cascade, this article delineates a physiological and translational framework for next-generation interventions targeting bioenergetic dysfunction in human disease. Full article

Objective: To investigate the therapeutic effects and safety profile of Wanshi Shachong Xiaoji Pills (WSXPs) on a functional dyspepsia (FD) mouse model and to preliminarily explore its potential mechanism and impact on associated hepatic metabolism. Methods: An FD model was established in mice using L-arginine. Gastrointestinal motility was assessed by measuring gastric emptying and intestinal propulsion rates. Serum levels of gastrointestinal hormones (MTL, GAS, VIP, CCK) and gut microbiota composition were analyzed. A one-month repeated-dose toxicity study was conducted in normal mice to evaluate safety. The effects of WSXPs on lipid metabolism and inflammation were further examined in a hepatocyte steatosis model in vitro, and network pharmacology was employed to predict potential mechanisms. Results: WSXPs significantly alleviated FD symptoms by improving gastrointestinal motility, bidirectionally regulating gut hormone levels, and increasing the abundance of beneficial bacteria (Akkermansia muciniphila). Long-term administration showed no significant toxicity. In vitro, WSXPS reduced lipid accumulation and inflammation in hepatocytes. Network analysis identified the PI3K-Akt signaling pathway as a potentially central common target, providing a hypothesis for future mechanistic studies. Conclusions: WSXPs effectively improve FD symptoms, modulates gut microbiota, and exhibits potential benefits on hepatic lipid metabolism in vitro, possibly via the PI3K-Akt pathway. This hepatocyte-level finding, combined with its in vivo efficacy in FD, suggests a promising avenue for future research into its potential applications in metabolic-associated conditions. This study provides a scientific foundation for the further development and clinical application of WSXPs in treating FD. Full article