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        <title>Frontiers in Physiology | Gastrointestinal Sciences section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/physiology/sections/gastrointestinal-sciences</link>
        <description>RSS Feed for Gastrointestinal Sciences section in the Frontiers in Physiology journal | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-12T22:41:54.509+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1808663</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1808663</link>
        <title><![CDATA[Lacticaseibacillus rhamnosus HN001 enhances intestinal barrier function and protects the blood-brain barrier from inflammatory disruption in vitro]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Dulantha Ulluwishewa</author><author>Ajitpal Purba</author><author>Vincent Fegan</author><author>Narsaa Na</author><author>Simon J. O’Carroll</author><author>Rachel C. Anderson</author>
        <description><![CDATA[The integrity of the intestinal epithelial and blood-brain barriers is critical for maintaining homeostasis along the gut-brain axis as these interfaces regulate the passage of inflammatory mediators into systemic circulation and their access to the brain. Disruption of these barriers can lead to neuroinflammatory processes implicated in mood disturbances. Lacticaseibacillus rhamnosus HN001 has been associated with improved mood outcomes in clinical and preclinical studies, however the mechanistic basis for these effects is unclear. Here, we investigated whether HN001 enhances intestinal and blood-brain barrier function in a two-stage in vitro gut-brain axis model. Differentiated Caco-2 epithelial monolayers were co-cultured with HN001 (Stage-1; intestinal epithelial barrier), and the conditioned basal medium from this stage was subsequently applied to hCMEC/D3 endothelial monolayers (Stage-2; blood-brain barrier). HN001 increased transepithelial electrical resistance in Caco-2 monolayers under both aerobic and apical-anaerobic conditions. This was accompanied by transcriptional modulation of tight-junction signaling, including upregulation of OCLN and sealing claudins, and downregulation of the pore-forming claudin CLDN2. Conditioned basal medium collected from HN001-treated Caco-2 intestinal epithelial monolayers improved barrier resistance in hCMEC/D3 brain endothelial monolayers and mitigated IL-1β-induced barrier disruption. The protective effect was not accompanied by changes in IL-1β-stimulated secretion of IL-6, IL-8, MCP-1, TNF-α or IL-1β, indicating that HN001-derived signals regulate blood-brain barrier function independently of the cytokines measured here. Together, these findings indicate that HN001 supports both the intestinal barrier and the blood-brain barrier integrity within the gut-brain axis. By regulating these barrier interfaces, HN001 may reduce susceptibility to neuroinflammation, suggesting a potential mechanistic basis for its previously reported psychobiotic benefits.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1788389</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1788389</link>
        <title><![CDATA[From body composition to reflux esophagitis: an interpretable machine learning model based on CT-derived features]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Tianyi Wang</author><author>Lu Chen</author><author>Yajie Li</author><author>Qi Zhang</author><author>Xilong Ou</author><author>Qin Lu</author>
        <description><![CDATA[BackgroundThe prevalence of gastroesophageal reflux disease (GERD) has been increasing in China. Previous studies link sarcopenia and visceral adiposity to GERD, but most models lack CT-based body composition data. This study aims to improve the identification of Reflux esophagitis (RE) by applying machine learning (ML) to third lumbar vertebra cross-sectional CT (L3-CT) images for quantitative analysis of muscle and fat mass.MethodsParticipants underwent comprehensive abdominal CT and gastroscopy. Body composition parameters, including skeletal muscle mass (SM), total fat mass (FM), fat-free mass (FFM), visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and intermuscular adipose tissue (IMAT), were derived from the L3-CT images. Six ML models were developed: Random Forest (RF), Extreme Gradient Boosting (XGBoost), Logistic Regression (LR), K-Nearest Neighbors (KNN), Support Vector Machine (SVM), and Artificial Neural Network (ANN). Model performance was evaluated using the area under the receiver operating characteristic curve (AUROC). Shapley Additive exPlanations (SHAP) values were used to interpret the RF model.ResultsA total of 324 subjects were included, with 135 diagnosed with RE. The prevalence of low skeletal muscle mass index (low SMI) was significantly higher in the RE group compared to controls (52.6% vs. 36.5%, P < 0.01). The top six variables in the RF importance matrix were IMAT, visceral-to-subcutaneous fat ratio (VSR), age, VAT, SAT, and hiatal hernia. In the validation set, RF (AUC = 0.829, 95% CI: 0.731–0.905) and LR (AUC = 0.829, 95% CI: 0.736–0.909) demonstrated the best discriminative performance for RE. SHAP summary plots illustrated the positive and negative contributions of the top 20 features, while SHAP dependence plots explained the impact of individual variables on the RF model output.ConclusionThis study reveals a significant association between low SMI and RE. ML models identified key body composition factors, providing insights for targeted screening and clinical assessment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1813824</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1813824</link>
        <title><![CDATA[Pancreatitis: correcting CFTR expression and function as a promising effective treatment]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Paramita Sarkar</author><author>Wei-Yin Lin</author><author>Ava Movahed Abtahi</author><author>Woo Young Chung</author><author>Shmuel Muallem</author>
        <description><![CDATA[The two principal cell types of the exocrine pancreas, acinar and ductal cells, serve distinct but complementary roles. Acinar cells synthesize and secrete digestive enzymes, whereas duct cells secrete fluid and bicarbonate (HCO3-). Ductal secretion protects the pancreas by producing an alkaline fluid that prevents premature digestive enzyme activation and facilitates their transport to the intestine. A critical step in this protective mechanism is protein kinase A–mediated activation of the luminal Cl- channel, cystic fibrosis transmembrane conductance regulator (CFTR). In this context, increasing evidence indicates that impaired CFTR function represents a common pathological feature across all forms of pancreatitis, the most prevalent disease of the exocrine pancreas. Acute and chronic pancreatitis are inflammatory disorders characterized by pancreatic ductal injury that initiates recurrent inflammatory episodes and subsequent acinar cell damage, for which effective treatments remain lacking. Accordingly, this review aims to summarize current evidence supporting alterations in CFTR expression and activity as key events in pancreatitis pathogenesis. Furthermore, given the availability of safe and effective CFTR correctors and potentiators currently approved for the treatment of cystic fibrosis, we argue that these agents warrant strong consideration as potential therapeutic strategies for pancreatitis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1785500</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1785500</link>
        <title><![CDATA[Ductal epithelial MXD3 promotes disease progression in acute pancreatitis through Wnt/β-catenin-mediated inflammation and injury]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xianru Jia</author><author>Bingbing Cui</author><author>Xuejin Liu</author>
        <description><![CDATA[IntroductionAcute pancreatitis (AP) is a severe inflammatory disease where epithelial injury and dysregulated repair are central to pathogenesis, yet the underlying transcriptional mechanisms remain poorly understood.MethodsThis study employed an integrated approach to identify and characterize the transcription factor MXD3 as a master regulator of AP progression. Using single-cell RNA sequencing in a ceruleininduced rat AP model, we delineated a pathogenic epithelial trajectory from ciliated through non-ciliated to a proliferative state, with MXD3 emerging as the most significantly upregulated transcription factor in the proliferative cluster. Subsequent validation in pancreatic ductal epithelial-specific MXD3 knockout rats revealed profound protection against AP, manifesting as reduced histological damage, diminished fibrosis, attenuated neutrophil infiltration (MPO+ cells), and decreased expression of pro-inflammatory cytokines (IL-6, TNF-α, IL-1β).ResultsMechanistically, we demonstrated that MXD3 directly activates the Wnt/β-catenin pathway, as evidenced by increased non-phospho β-catenin, its nuclear accumulation, and transcriptional upregulation of canonical targets (cMyc, Cyclin D1, Axin2). Furthermore, functional rescue experiments confirmed the pathway’s necessity, wherein the β-catenin inhibitor ICG-001 substantially reversed MXD3-driven apoptosis, necrosis, and pro-inflammatory cytokine secretion (IL-1β, IL-6, MCP-1) in vitro.ConclusionsOur findings establish a novel MXD3- Wnt/β-catenin axis as a crucial mechanism governing epithelial pathology in AP, revealing MXD3 as a promising therapeutic target for this debilitating condition.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1787963</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1787963</link>
        <title><![CDATA[Epigenetic signatures and cellular stress response pathways in metabolic dysfunction-associated steatotic liver disease: a personalized medicine perspective]]></title>
        <pubdate>2026-04-30T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Fabian M. Cortés-Mancera</author><author>Marianne G. Rots</author><author>Han Moshage</author><author>Johanna C. Arroyave-Ospina</author>
        <description><![CDATA[Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease around the world, with at least 40% global prevalence. Although genetic susceptibility contributes to disease risk, it does not fully explain the marked interindividual variability in disease onset, severity, and progression. Increasing evidence indicates that epigenetic mechanisms act as critical mediators between genetic predisposition and environmental exposures, shaping hepatic stress responses and metabolic dysfunction in MASLD. Epigenetic regulation, including DNA methylation and histone modifications, plays a fundamental role in maintaining metabolic homeostasis and coordinating cellular responses to metabolic, oxidative, and organellar stress, e.g., endoplasmic reticulum stress. Dysregulation of these processes has been consistently associated with hepatic steatosis, inflammation, fibrosis, and disease progression. Moreover, epigenetic control of circadian rhythms and molecular clock pathways further link metabolic imbalance to liver dysfunction and biological aging. Importantly, epigenetic signatures are stable, positioning them as attractive biomarkers for disease diagnosis, prognosis, and patient stratification, but also potentially reversible, making them promising targets for therapeutic intervention. Advances in epigenomic profiling and translational research are increasingly supporting the integration of epigenetic information into personalized medicine approaches for MASLD. In this review, we synthesize current experimental and translational evidence on epigenetic alterations involved in MASLD pathophysiology, with a particular focus on their role in cellular stress response pathways. We discuss the potential of epigenetic signatures as biomarkers and therapeutic targets, highlighting their relevance for the development of precision-based strategies in the management of MASLD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1766078</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1766078</link>
        <title><![CDATA[Bioactive compounds as therapeutic modulators of metabolic syndrome: targeting inflammation and gut microbiota regulation]]></title>
        <pubdate>2026-04-28T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Magdalene Eno Udobi</author><author>Mercy Bella-Omunagbe</author><author>Israel Sunmola Afolabi</author><author>Shalom Nwodo Chinedu</author>
        <description><![CDATA[Food bioactives, including polyphenols, flavonoids, omega-3 fatty acids, and glucosinolates, play a crucial role in preventing metabolic syndrome by modulating chronic inflammation, gut microbiota homeostasis, and metabolic processes. These compounds influence key molecular pathways implicated in metabolic dysfunction and systemic inflammation. This review explores the mechanisms through which food bioactives contribute to metabolic health, emphasizing their role in inflammation regulation, gut microbiota modulation, and insulin sensitivity. A comprehensive literature review was conducted using databases such as PubMed, Scopus, and Web of Science. Relevant peer-reviewed articles, meta-analyses, and clinical trials published in the last two decades were analyzed, focusing on bioactives’ biochemical actions and therapeutic potential in Metabolic syndrome. The study showed that bioactives mitigate inflammation by inhibiting NF-κB signaling and NLRP3 inflammasome activation, reducing pro-inflammatory cytokines (TNF-α, IL-6, IL-1β). They also modulate gut microbiota, promoting beneficial bacteria (e.g., Akkermansia muciniphila) and enhancing gut barrier integrity via increased expression of tight junction proteins. Short-chain fatty acids (SCFAs) derived from microbial metabolism contribute to systemic anti-inflammatory effects. Clinical studies indicate that polyphenol-rich diets, such as the Mediterranean diet, improve metabolic syndrome parameters by lowering inflammatory markers, enhancing lipid profiles, and improving insulin sensitivity. Despite promising findings, challenges such as poor bioavailability and variability in gut microbiome responses hinder clinical application. Strategies like nanoencapsulation and microbiome-targeted nutrition may optimize bioactive efficacy. Overall, food bioactives represent a promising strategy for metabolic health. Future research should focus on enhancing bioavailability, personalized nutrition, and large-scale clinical trials to establish optimal dosing and long-term benefits.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1817832</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1817832</link>
        <title><![CDATA[Assessment of gut-brain interactions: reframing DGBI symptoms from visceral hypersensitivity to computational interoceptive overfitting]]></title>
        <pubdate>2026-04-15T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Dakai Zeng</author><author>He Zeng</author><author>Zi Lin</author><author>Wen-Jing Yan</author>
        <description><![CDATA[For decades, disorders of gut-brain interaction (DGBI) have been ensnared in an epistemological bottleneck, clinically managed as diagnoses of exclusion despite the absence of structural pathology on conventional endoscopy. Traditional bottom-up models of visceral hypersensitivity fail to explain the profound subjective-objective symptom mismatches observed in clinical practice. This Perspective proposes a radical paradigm shift: leveraging the Predictive Processing (PP) framework to reconceptualize DGBI as a hierarchical computational dysfunction termed “interoceptive overfitting”. We postulate that rigid, high-precision threat priors force the salience network (dACC and aIns) to misallocate pathologically high precision weighting to baseline physiological noise, such as healthy 3-cycles-per-minute (cpm) gastric slow waves. This top-down failure synthesizes illusory pain and triggers genuine autonomic disruption via active inference, creating a self-fulfilling loop of GI micro-sabotage. We present a clinical roadmap utilizing high-resolution body surface gastric mapping (BSGM) and Ecological Momentary Assessment (EMA) to identify “Probabilistic Mismatch Points” within a multimodal diagnostic matrix that accounts for non-rhythmic peripheral modulators. To resolve therapeutic stagnation, we propose closed-loop digital therapeutics (DTx) designed to recalibrate the brain’s predictive engine through validation-correction loops, targeted extinction learning, and dual-stream telemetry. This computational framework provides a rigorously scientific blueprint to resolve therapeutic stagnation in DGBI.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1764088</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1764088</link>
        <title><![CDATA[A model for Crohn’s disease post-ileal resection fibrosis development using human ileal enteroids and myofibroblasts]]></title>
        <pubdate>2026-04-15T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jun Hwan Yoo</author><author>Yoon Jeong Choi</author><author>Iryna V. Pinchuk</author><author>Don W. Powell</author><author>Nicholas C. Zachos</author><author>Mark Donowitz</author>
        <description><![CDATA[BackgroundFibrosis and inflammation frequently emerge soon after ileal resection for strictures in Crohn’s disease (CD).ObjectiveThis study examined the profibrotic and proinflammatory effects of conditioned media from TNF and IFN-γ (T+I)-exposed healthy and inactive CD ileal enteroids (CDiE) on subepithelial myofibroblasts (SEMF), modeling early post-ileal resection conditions in CD.MethodsIleal enteroids from healthy subjects (HE) and inactive CD patients (CDiE) were exposed to T+I for 6 hours, followed by an 18-hour conditioning period. Conditioned media were collected and applied to human intestinal myofibroblasts (HIMF) from healthy and inactive CD ileum for 24 hours to assess proinflammatory and profibrotic gene expression.ResultsT+I exposure induced epithelial damage and cell death in CDiE, while reducing proliferation and decreasing occludin and F-actin expression in both HE and CDiE. TEER (transepithelial electrical resistance) declined in CDiE but remained stable in HE. Conditioned media from T+I-exposed enteroids altered HIMF-HC (healthy control) and HIMF-CD mRNA expression, upregulating proinflammatory genes (IL1B, IL6, MCP1, and IKBA) while downregulating profibrotic genes (COL1A1, ACTA2, TGFB, and SRF).ConclusionCytokine-exposed HE- and CDiE-derived conditioned media promoted inflammation while suppressing fibrosis-associated gene expression in subepithelial myofibroblasts. Our results suggest that damaged intestinal crypts in early CD inflammation may not directly trigger certain fibrogenic markers in vitro. This model of the early post-ileal resection state provides a platform to identify key targets for preventing fibrosis progression and potentially reducing the need for repeat ileal surgery in CD patients.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1745668</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1745668</link>
        <title><![CDATA[Combined use of EUS, ESD, and laparoscopic techniques in the diagnosis and treatment of a mucinous adenocarcinoma of the ascending colon originating from the submucosal layer: a case report]]></title>
        <pubdate>2026-04-10T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Zongyao Liu</author><author>Yanling Li</author><author>Rong Tan</author><author>Ainizhati Abudusaimaiti</author><author>Shengjuan Hu</author><author>Ximei Li</author>
        <description><![CDATA[This report describes a 53-year-old woman admitted for evaluation of a space-occupying lesion in the ascending colon detected one year earlier and recent right lower quadrant pain. Initial colonoscopy revealed a 2.0 × 2.0 cm submucosal elevated lesion with surface ulceration near the ileocecal valve. Biopsy showed inflammatory mucosa with abundant mucin but no malignancy, and CT revealed no definite abnormalities. One year later, the lesion enlarged to 3.5 × 3.0 cm with increased ulceration. Endoscopic ultrasound (EUS) demonstrated a hypoechoic submucosal mass, and endoscopic submucosal dissection (ESD) was performed. During ESD, a jelly-like substance raised suspicion of a mucinous neoplasm, leading to laparoscopic resection of the ileocecal region and ascending colon. Pathology confirmed mucinous adenocarcinoma originating from the submucosal layer. This rare presentation differs from typical colorectal cancers that arise from the epithelial layer. The combined use of EUS, ESD, and laparoscopic surgery facilitated accurate diagnosis and effective treatment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1794931</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1794931</link>
        <title><![CDATA[The attenuated incretin effect is associated with glucose intolerance in patients with hepatitis B-related acute-on-chronic liver failure]]></title>
        <pubdate>2026-03-27T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Meichuan Li</author><author>Han Hu</author><author>Yujuan Liu</author><author>Xiaohuan Wu</author><author>Yin Zhang</author><author>Ying Li</author><author>Fangwan Yang</author><author>Yan Li</author><author>Shide Lin</author>
        <description><![CDATA[ObjectiveThe pathogenesis of glucose homeostasis disturbance in acute-on-chronic liver failure (ACLF) remains poorly defined. This study aimed to investigate the association between incretin effect (IE) and glucose intolerance in patients with hepatitis B virus-related ACLF (HBV-ACLF).MethodsIn this prospective study, 25 patients with HBV-ACLF were stratified by glucose tolerance: normal glucose tolerance (NGT, n=7), pre-diabetes (pre-DM, n=9), and diabetes mellitus (DM, n=9). All participants underwent paired oral (OGTT) and intravenous glucose tolerance test (IVGTT) within 72 hours of admission. Dynamic profiles of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and insulin were analyzed. The IE, calculated from insulin area under the curve (AUC) differences, was compared across groups.ResultsPatients with pre-DM and DM exhibited significantly reduced insulin sensitivity and early-phase insulin secretion, alongside elevated insulin resistance, compared to the NGT group. While GLP-1 and GIP responses post-OGTT remained significantly higher than post-IVGTT across all groups, the GIP secretory response was markedly blunted in DM patients compared to those with NGT. Critically, the incremental insulin response during OGTT versus IVGTT was abolished in DM patients but preserved in pre-DM and NGT. Consequently, IE was progressively and significantly reduced from NGT (58.5 ± 9.2%) to pre-DM (44.5 ± 7.5%) to DM (25.8 ± 8.7%) (P < 0.01). These differences remained statistically significant after adjustment for age, sex, body mass index, Model for End-Stage Liver Disease-Sodium score and C-reactive protein.ConclusionThe attenuated IE is associated with the severity of glucose intolerance, and the development of DM is associated with a blunted GIP secretory response in patients with HBV-ACLF.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1778235</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1778235</link>
        <title><![CDATA[Artificial intelligence-driven gastrointestinal functional assessment: multimodal imaging, digital biomarkers, and real-time monitoring]]></title>
        <pubdate>2026-03-25T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Liucheng Li</author><author>Fang Lv</author><author>Chen Du</author><author>Lianjun Yang</author><author>Chengzhou Pa</author><author>Yunrui Dai</author>
        <description><![CDATA[Gastrointestinal (GI) functional disorders and chronic inflammatory diseases impose a substantial health burden, yet their assessment remains challenging because symptoms reflect dynamic interactions among motility, visceral sensation, immune–microbiome regulation, and brain–gut signaling. Artificial intelligence (AI) is rapidly reshaping GI functional medicine by enabling scalable, quantitative interpretation of complex data generated from multimodal imaging, physiological sensing, and real-world patient monitoring. This review synthesizes advances across three tightly connected pillars that map onto a physiology-informed “assessment-to-action” loop: (i) AI-assisted multimodal GI imaging for quantitative phenotyping and integrated diagnosis; (ii) AI-enabled discovery and validation of digital biomarkers that capture dynamic GI function in naturalistic settings; and (iii) real-time monitoring platforms that support early warning, longitudinal assessment, and adaptive management. We summarize representative applications in functional GI disorders, inflammatory bowel disease (IBD), and GI oncology, highlighting methodological themes including multimodal fusion, temporal modeling, uncertainty estimation, and explainable AI. We then discuss barriers to translation—standardization and interoperability, external validation under dataset shift, privacy and governance, and workflow integration—and outline practical directions for building clinically trustworthy AI systems for GI functional assessment. Collectively, physiology-centered AI approaches have the potential to transform GI care from episodic testing to longitudinal, mechanism-aware monitoring and personalized intervention.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1735342</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1735342</link>
        <title><![CDATA[Impact of arm position and load on upper and lower esophageal sphincter pressures]]></title>
        <pubdate>2026-03-19T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Petr Bitnar</author><author>Adam Kurka</author><author>Andrew Busch</author><author>Tereza Stehnova</author><author>Katerina Madle</author><author>Jan Stovicek</author><author>Alena Kobesova</author>
        <description><![CDATA[BackgroundThe diaphragm contributes to respiration, postural stabilization, and regulation of esophageal sphincter pressures through its crural portion. Although its dual respiratory–postural role is established, the effects of physical load and arm position on esophageal sphincter pressures remain unclear. This study investigated how postural demand and external load influence upper (UES) and lower (LES) esophageal sphincter pressures under varying stabilization conditions.MethodsTwenty-eight healthy adults underwent high-resolution manometry (HRM) to measure UES and LES pressures in standing, supine leg raise, and during standing while holding 3, 6, and 9 kg loads with arms alongside the body or raised to 45° shoulder flexion. Paired-samples t-tests and one-way ANOVA were applied, with effect sizes calculated.ResultsLES pressure significantly increased in the supine leg raise and when loads were held with arms elevated at 45° shoulder flexion (p < 0.001), indicating enhanced activation of the esophagogastric high-pressure zone involving the crural diaphragm. No significant LES change occurred when weights were held parallel to the body. UES pressure significantly increased only during the supine leg raise (p < 0.001), whereas load magnitude had no effect in standing.ConclusionEsophageal sphincter pressures are modulated by posture and load, supporting an integrated respiratory–postural–sphincteric function of the diaphragm. LES pressure rises with increasing postural demand, consistent with crural diaphragm recruitment, while UES responses appear position-dependent. These findings extend current understanding of the diaphragm’s coordinated role in esophagogastric junction and upper sphincter control.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1791638</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1791638</link>
        <title><![CDATA[Epigenetic reprogramming in metabolic dysfunction–associated steatotic liver disease: from metabolic memory to precision medicine]]></title>
        <pubdate>2026-03-19T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Basile Njei</author><author>Yazan A. Al-Ajlouni</author>
        <description><![CDATA[BackgroundMetabolic dysfunction associated steatotic liver disease (MASLD) is the most common chronic liver disease worldwide and is characterized by substantial heterogeneity in clinical presentation, disease progression, and treatment response. Conventional metabolic risk factors do not fully explain this variability. Epigenetic regulation has emerged as a central mechanism linking metabolic stress to sustained alterations in hepatic gene expression and long-term disease behavior.MethodsThis narrative review synthesizes evidence from human observational studies, interventional studies, systematic reviews, and experimental research examining epigenetic regulation in MASLD. Key epigenetic mechanisms reviewed include DNA methylation, histone modifications, and noncoding RNA mediated regulation, with emphasis on physiological relevance and translational implications.ResultsEpigenetic alterations in MASLD are closely associated with chronic metabolic stress and influence pathways involved in lipid metabolism, insulin resistance, inflammation, mitochondrial dysfunction, and fibrogenesis. These changes contribute to disease persistence, progression, and heterogeneity, including lean disease phenotypes. Evidence suggests partial reversibility of epigenetic programming following lifestyle modification, metabolic improvement, and surgical intervention. Circulating microRNAs and DNA methylation signatures show promise as noninvasive tools for disease phenotyping, risk stratification, and monitoring, although clinical validation remains limited.ConclusionsEpigenetic reprogramming represents a core biological process in MASLD that integrates metabolic exposures with long term hepatic outcomes. Improved understanding of epigenetic plasticity and stability across disease stages may inform earlier intervention strategies and support the development of precision medicine approaches in this heterogeneous condition.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1795419</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1795419</link>
        <title><![CDATA[Targeted therapeutics for pancreatitis]]></title>
        <pubdate>2026-03-13T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Tareq Alsaleh</author><author>John George</author>
        <description><![CDATA[ImportanceAcute pancreatitis (AP) can result in significant morbidity and mortality. Its complications include persistent organ failure, necrosis, and death. Recurrent episodes of AP may also result in chronic pancreatitis (CP), a fibroinflammatory condition characterized by chronic pain and endocrine and exocrine failure. Despite improved supportive care, approved disease-modifying targeted therapies for AP or CP are lacking.ObservationsMechanistic studies identify early pathways within acinar and ductal cells that lead to injury, providing potential therapeutic targets before necrosis and other complications develop. Sustained cytosolic calcium elevation drives premature enzyme activation and mitochondrial failure, maintained by store-operated calcium entry through Orai1. Calcium overload promotes increased mitochondrial permeability, ATP depletion, and necrotic cell death. Potential early interventions include Orai1 inhibition (CM4620/Auxora with early-phase human safety data and phase 2b signals), mitochondrial pore inhibition (NIM811) and other mitochondrial protectants. When systemic inflammation escalates, preclinical containment targets include NLRP3 inflammasome signaling, neutrophil extracellular traps, damage-associated molecular pattern signaling (including HMGB1), and upstream cytokine shedding via ADAM17/TACE. Pragmatic strategies under study, such as early high-energy feeding, test whether modifiable supportive inputs can shift early severity trajectories. In chronic pancreatitis, long-term disease modification centers on targeting pancreatic stellate cells, which are critical drivers of fibrosis. Furthermore, the highly morbid chronic pain of CP can be modified through treatment of neuroimmune pain sensitization. The emerging clinical pipeline includes repurposed anti-fibrotic or immunomodulatory agents (pirfenidone, paricalcitol, tocilizumab, proglumide), genotype-matched therapy (CFTR modulation in selected populations), and cell-based approaches.Conclusion and RelevanceThe current targeted therapeutic landscape in pancreatitis is promising, but difficulties lie in trial enrichment as the timing of drug administration is critically dependent on the timeline of disease. Therefore, progress will depend on matching treatment timing to target biology, identifying patients using practical early severity and inflammatory features, and using endpoints that reflect disease modification (organ failure, necrosis, recurrence, fibrosis progression, pancreatic function, and pain trajectories). Trial designs matching these therapeutics to their target biology will help understand the real clinical value of mechanism-based regimens across the AP–RAP–CP continuum.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1776210</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1776210</link>
        <title><![CDATA[Patient-centered gastrointestinal function assessment technologies: a paradigm shift from traditional approaches to non-invasive innovations]]></title>
        <pubdate>2026-03-12T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Qian Zhu</author><author>Qian Li</author><author>Yan Zan</author><author>Yuchen Lu</author><author>Liangjun Xia</author><author>Youbing Xia</author><author>Tiancheng Xu</author>
        <description><![CDATA[Gastrointestinal function assessment has assumed an increasingly pivotal role in diagnosing and managing digestive system disorders, yet the widespread clinical application of conventional techniques remains constrained by ionizing radiation exposure, high procedural invasiveness, and heavy reliance on specialized equipment—limitations severely compromising patient acceptance and service accessibility. Guided by the patient-centered care paradigm, this paper systematically reviews the evolution of such assessment technologies, delineating the intrinsic limitations of radionuclide imaging, invasive manometry, and traditional electrogastrography in terms of safety, comfort, and accessibility, while synthesizing research progress and clinical evidence of non-invasive modalities like stable isotope breath tests, surface electrogastrographic mapping, wireless motility capsules, and wearable monitors. It also explores AI’s potential in integrating multi-dimensional physiological signals to support clinical decision-making and examines translational barriers from technical validation to routine practice. Accumulating evidence shows emerging non-invasive technologies provide clinically actionable insights while alleviating patient burden, but most current studies focus on diagnostic accuracy validation, lacking high-quality evidence for their benefits in guiding treatment or improving long-term prognosis. Future research should prioritize patient outcomes, rigorously assess technologies’ applicability and value in real-world settings, and facilitate innovation transformation from parameter measurement to patient-centric care and from laboratory to clinical practice.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1795494</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1795494</link>
        <title><![CDATA[Reconceptualizing negative endoscopy as a positive contextual indicator for disorders of gut-brain interaction]]></title>
        <pubdate>2026-03-12T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Wumiao Zhang</author><author>He Zeng</author><author>Qian-Nan Ruan</author><author>Dakai Zeng</author>
        <description><![CDATA[In the contemporary landscape of gastroenterology, the “negative” endoscopy—an examination revealing no gross structural, mucosal, or biochemical abnormalities—is frequently perceived by both clinicians and patients as a diagnostic non-event, a failure to identify a cause, or an ambiguous dead-end. This perspective paper argues for a fundamental epistemological and clinical paradigm shift: a negative endoscopic result, when combined with appropriate biopsy protocols and clinical history, should not be classified merely as the absence of organic disease but as positive, corroborative evidence acting as a contextual indicator supporting a diagnosis of a Disorder of Gut-Brain Interaction (DGBI). By integrating the verified absence of macroscopic “hardware” damage (structural pathology) with the presence of characteristic symptom patterns, clinicians can support the diagnosis of a “software” malfunction (visceral hypersensitivity and altered central processing). This report provides a detailed analysis of the physiological mechanisms of the brain-gut axis that underpin this argument, dissects the psychological impact of diagnostic labeling versus invalidation, and proposes a comprehensive novel clinical workflow—the “Affirm-Explain-Transform” (AET) model—to convert the negative endoscopy from a source of clinical ambiguity into a potent therapeutic tool.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1703887</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1703887</link>
        <title><![CDATA[Prolactin and oxytocin as modulators of intestinal contractility and glucose uptake]]></title>
        <pubdate>2026-02-26T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Perla Alejandra Figueroa-Carrasco</author><author>Aída Jimena Velarde-Salcedo</author><author>Carmen Gonzalez</author>
        <description><![CDATA[IntroductionProlactin (PRL) and oxytocin (OT) are bioactive hormones naturally present in maternal milk that support neonatal development, contribute to immune regulation and gut maturation in infants, and promote growth and cell differentiation in the small intestine. However, the individual and combined roles of these hormones in intestinal function remain unclear. This study aims to elucidate the physiological effects of PRL and OT on intestinal motility, nitric oxide (NO) production, and glucose uptake to better understand their influence during early development.MethodsPrecontracted intestinal segments were placed in physiological solution, connected to isometric transducers, and exposed to various concentrations of PRL, OT, or PRL + OT, and changes in contractile responses were recorded. Glucose uptake was measured using everted sacs, and NO production was measured via the Griess method. PRL, OT, and PRL + OT modulated intestinal contractile activity, with effects varying by segment. OT induced higher NO levels than PRL at cumulative concentrations.Results and discussionA single concentration of PRL or OT mostly preserved the contraction vs. % of the maximal contraction induced by KCl (100%), while PRL + OT reduced it and NO production in the duodenum and jejunum, but not in the ileum. Individually, PRL and OT increased glucose uptake, while their combination inhibited it, suggesting a modulatory mechanism regulating nutrient absorption. These findings support the role of PRL and OT as maternal milk-derived regulators of intestinal functions.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1739744</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1739744</link>
        <title><![CDATA[Effect of enteral nutrition support combined with prone position mechanical ventilation on respiratory function, nutritional status, and inflammatory response in patients with severe pneumonia]]></title>
        <pubdate>2026-02-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Li Xu</author><author>Ling Xie</author><author>Huijuan Wang</author>
        <description><![CDATA[ObjectiveThis study aims to investigate the efficacy of enteral nutrition support combined with prone position mechanical ventilation in patients with severe pneumonia.MethodsThis retrospective cohort study included 55 patients with severe pneumonia, who were allocated to a control group (n = 35) receiving conventional mechanical ventilation combined with early enteral nutrition support, and an observation group (n = 20) receiving prone position mechanical ventilation combined with early enteral nutrition support. The intervention lasted for 1 week. Changes in blood gas indicators were compared before and after the intervention. Improvement in nutritional status and inflammatory indicators, including serum prealbumin (PAB), albumin (ALB), haemoglobin (HGB) and C-reactive protein (CRP), and procalcitonin (PCT), were assessed. The incidence of adverse events during the intervention was compared between groups. This study was approved by the Ethics Review Committee of our hospital, and written informed consent was obtained from all participants.ResultsAfter the intervention, both groups showed increased PaO2, SpO2, and PaO2/FiO2 levels and decreased PaCO2 levels, with more pronounced improvement observed in the observation group. Nutritional indicators (PAB, ALB, and HGB) improved in the observation group. CRP and PCT levels were reduced in both groups, with the observation group demonstrating lower levels. The observation group showed a lower incidence of adverse events than the control group (15.00% vs. 42.86%).ConclusionEnteral nutrition support combined with prone position mechanical ventilation reduces the incidence of adverse events, improves respiratory function and nutritional status, and alleviates inflammatory response in patients with severe pneumonia.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1762846</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1762846</link>
        <title><![CDATA[Endoscopic excision for internal and mixed hemorrhoids: a retrospective case series of short-term outcomes]]></title>
        <pubdate>2026-02-19T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Qi Xu</author><author>Bingfeng Qiu</author><author>Tangzhou Xu</author><author>Dandan Zhuang</author><author>Junhan Qu</author>
        <description><![CDATA[ObjectiveThis study aimed to investigate the short-term clinical outcomes and safety of endoscopic excision for the management of internal and mixed hemorrhoids.MethodsA retrospective analysis was conducted on 20 patients with Grade II to Grade IV internal or mixed hemorrhoids who underwent endoscopic excision at Zhoushan Hospital between January 2024 and December 2024. All patients had complete follow-up data.ResultsAt 3 and 6 months after surgery, the treatment effectiveness rate was 100%, and both postoperative satisfaction and acceptance rates were 100%. No severe postoperative complications occurred, and no bleeding or infection was observed. Mild pain developed in three patients, a transient sensation of anal heaviness and distension occurred in one patient, and temporary urinary retention occurred in one patient, which resolved after local hot compress therapy. Postoperative pathological examinations confirmed that the resected anorectal masses demonstrated changes consistent with hemorrhoidal tissue.ConclusionEndoscopic excision for internal and mixed hemorrhoids is a safe and effective therapeutic approach. It provides significant symptom relief, yields high postoperative satisfaction and acceptance among patients, and allows for definitive pathological confirmation of the nature of the resected anorectal tissue.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1747341</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1747341</link>
        <title><![CDATA[The role of bile acid-activated receptor TGR5 in inflammation and liver diseases]]></title>
        <pubdate>2026-02-17T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Hongyan Xiang</author><author>Huanyu Xiang</author><author>Shuyun Wang</author><author>Peiyu Wu</author><author>Zhidan Luo</author><author>Jie Zhang</author>
        <description><![CDATA[Takeda G-protein-coupled receptor 5 (TGR5), a bile acid receptor, has been recognized as an important signal molecule with roles extending far beyond bile acid homeostasis. Its activation has been shown to ameliorate metabolic disorders and suppress inflammatory responses through diverse mechanisms. Expressed widely in both parenchymal and non-parenchymal cells of the liver, TGR5 plays a central role in hepatic physiology and disease. This review consolidates current evidence on the involvement of TGR5 in various liver pathologies, including metabolic dysfunction-associated steatohepatitis, cholestatic diseases, liver fibrosis, and hepatocellular carcinoma. Additionally, we summarize the regulatory functions of TGR5 in immune cells and inflammatory signaling pathways. We emphasize TGR5 as a promising therapeutic target for a range of chronic liver diseases, given its pivotal role in modulating inflammation and metabolism. Future research should focus on developing tissue-specific TGR5 agonists to enhance therapeutic efficacy and reduce systemic side effects, as well as elucidating its context-dependent dual roles in hepatocarcinogenesis to ensure safe clinical application.]]></description>
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