American journal of physiology. Gastrointestinal and liver physiology最新文献

{"title":"Gut neuropeptide involvement in Parkinson's disease.","authors":"Hayley N Templeton, Stuart A Tobet, Luke A Schwerdtfeger","doi":"10.1152/ajpgi.00383.2024","DOIUrl":"10.1152/ajpgi.00383.2024","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a neurodegenerative disorder affecting over 10 million people. A key pathological feature of PD is the accumulation of misfolded α-synuclein (aSyn) protein in the substantia nigra pars compacta. Aggregation of aSyn can form Lewy bodies that contribute to dopaminergic neuron degeneration and motor symptoms, such as tremor, rigidity, and bradykinesia. Beyond the central nervous system, aSyn aggregates have been detected in the gastrointestinal (GI) tract, suggesting a link between peripheral aSyn and nonmotor PD symptoms. GI symptoms, often preceding motor symptoms by up to 20 years, highlight the bidirectional communication between the central nervous system and the enteric nervous system (gut-brain axis) in PD. Although microbiome alterations and intestinal inflammation have been associated with PD, functional impacts on gut-brain signaling or aSyn aggregation remain unclear. Intestinal neuropeptides are key modulators of gut-brain communication, alter immune response to pathogens and environmental toxins, and may contribute to the function of the luminal gut barrier. Dysregulation of gut neuropeptide signaling, including vasoactive intestinal peptide, neuropeptide Y, calcitonin gene-related peptide, ghrelin, cholecystokinin, glucagon-like peptide 1, and substance P, have been associated with pathologic effects of PD in animal models. Despite their potential role in pathogenesis and disease modulation, gut neuropeptide roles in PD are underexplored. This article reviews current knowledge surrounding microbial metabolite and immune influences on gut neuropeptide signaling, aSyn aggregation in the enteric nervous system, and downstream neuroimmune pathway alterations within the context of PD and its mouse models.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G716-G733"},"PeriodicalIF":3.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12128169/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Host-microbial interactions in the esophagus.","authors":"Nonyelum Ebigbo, Rhonda F Souza","doi":"10.1152/ajpgi.00079.2025","DOIUrl":"10.1152/ajpgi.00079.2025","url":null,"abstract":"<p><p>Host-microbial interactions within the gastrointestinal tract are increasingly recognized as contributors to health and disease, yet our understanding of these interactions in the esophagus remains limited. Dysbiosis of the esophageal microbiome has been linked to esophageal disorders, but the precise mechanisms underlying microbial contributions to esophageal pathophysiology remain speculative. This review explores the mechanisms by which the esophageal microbiome modulates mucosal immunity, epithelial barrier integrity, and inflammatory responses. We highlight key host receptors that mediate these interactions and microbial metabolites that influence the local immune environment and epithelial function. By synthesizing current knowledge on how the microbiome impacts esophageal health, we identify significant knowledge gaps and propose areas for future research.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G848-G860"},"PeriodicalIF":3.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spontaneous ileitis and postsurgical murine models of enteric hyperoxaluria.","authors":"Karim Jaber, Nadim Zaidan, Melody Ho, Xiaozhong Xiong, Rashmi Mishra, Ambika Nair, Arnav Mishra, Yi Chu, Mohamad Mokadem, Lama Nazzal","doi":"10.1152/ajpgi.00043.2025","DOIUrl":"10.1152/ajpgi.00043.2025","url":null,"abstract":"<p><p>Enteric hyperoxaluria, a risk factor for kidney stone disease, often arises from malabsorptive bariatric surgeries or inflammatory bowel diseases. Current murine models for studying this condition are limited, necessitating new approaches. This study aims to establish two novel and distinct mouse models to investigate enteric hyperoxaluria: one simulating Roux-en-Y gastric bypass surgery and the other Crohn's ileitis. In the first model, diet-induced obese C57BL/6J male mice underwent either sham or bypass surgery, followed by 3 wk on a high-fat, oxalate-enriched diet. In the second model, SAMP1/YitFc and AKR mice were gradually introduced to high-fat diets, later supplemented with oxalate while reducing fat content. Samples of urine, blood, and feces were collected to assess oxalate, creatinine, and fecal lipid profiles. Results showed hyperoxaluria and increased stool fat content, indicating fat malabsorption, in both SAMP1 and bypass mice compared with controls. Kidney injury was also observed. These findings confirm the successful establishment of enteric hyperoxaluria in both models, highlighting the role of dietary oxalate, intestinal inflammation, and fat malabsorption in disease progression. These models provide valuable tools for exploring cellular and molecular mechanisms in enteric hyperoxaluria and may inform future therapeutic strategies.<b>NEW & NOTEWORTHY</b> This study is among the first to establish an enteric hyperoxaluria (EH) phenotype in two different and novel mouse models secondary to Roux-en-Y gastric bypass and ileitis. It also elucidates key factors affecting EH using the SAMP1 mice, revealing the significant roles of GI tract inflammation, fat malabsorption, and dietary fat in developing hyperoxaluria.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G760-G773"},"PeriodicalIF":3.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liver bypass in the development of pathogen-associated pulmonary vascular disease: contribution of mesocaval and portosystemic shunts.","authors":"Claudia Lucia Martins Silva, Prasanth N Puthanveetil, Suellen Darc Oliveira","doi":"10.1152/ajpgi.00409.2024","DOIUrl":"10.1152/ajpgi.00409.2024","url":null,"abstract":"<p><p>Portosystemic and mesocaval shunts are aberrant vascular connections that bypass hepatic detoxification process, directly linking the portal to the systemic circulation. These shunts, whether congenital or acquired, might play a pivotal role in the pathogenesis of systemic inflammatory diseases, such as schistosomiasis-associated pulmonary hypertension (Sch-PH) by facilitating the dissemination of pathogen-derived eggs and antigens from the gut and mesentery into the lungs. Beyond the translocation of <i>Schistosoma mansoni</i> eggs, emerging evidence implicates that gut-lung microbiome dysbiosis contributes to the development of pulmonary hypertension (PH) in the preclinical animal model of Sch-PH. Sch-PH emerges as a chronic complication of schistosomiasis and evolves silently, progressively increasing the mean pulmonary arterial pressure and vascular resistance, leading to right heart hypertrophy, failure, and significant morbidity and mortality. Chronic schistosomiasis is often linked to the development of portal hypertension, which significantly contributes to the formation of the porto/mesocaval shunt as a compensatory response that can have far-reaching implications on pulmonary vascular physiology. In addition, portal hypertension compromises the integrity of the intestinal barrier, exacerbating peritoneal and mesenteric inflammation, potentially facilitating microbial and metabolite entrance into the systemic circulation. This article briefly discusses the mechanisms by which porto/mesocaval shunts contribute to PH, especially Group I PH, focusing on the interplay between portosystemic shunting, microbial translocation, and systemic dissemination of proinflammatory metabolites.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G791-G800"},"PeriodicalIF":3.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary 3-aminobenzoic acid enhances intestinal barrier integrity and attenuates experimental colitis.","authors":"Miho Tanaka, Takahiko Toyonaga, Fumiyuki Nakagawa, Takeo Iwamoto, Yudai Hasegawa, Akira Komatsu, Natsuki Sumiyoshi, Naoki Shibuya, Ayaka Minemura, Tadashi Ariyoshi, Asami Matsumoto, Kentaro Oka, Masayuki Shimoda, Masayuki Saruta","doi":"10.1152/ajpgi.00406.2024","DOIUrl":"10.1152/ajpgi.00406.2024","url":null,"abstract":"<p><p>Disruption of intestinal epithelial integrity and increased permeability is central to the pathogenesis of ulcerative colitis (UC). In this study, we identified 3-aminobenzoic acid (3-ABA), a dietary component abundant in azuki beans, soybeans, and chickpeas as a regulator of epithelial permeability and inflammation in the colon. Screening 119 gut microbial metabolites revealed the ability of 4-ABA, a structural isomer of 3-ABA, to enhance barrier function in Caco2 cells. Further analysis of structural isomers identified 3-ABA as the most effective, significantly increasing transepithelial electrical resistance and reducing epithelial permeability. Using liquid chromatography-mass spectrometry, 3-ABA was detected in dietary beans and human fecal samples. Fecal 3-ABA levels were significantly lower in patients with UC compared with healthy individuals. Metagenomic and functional prediction analyses revealed dysbiosis in patients with UC, characterized by an enrichment of bacterial genes involved in ABA degradation. Gene expression analysis of 3-ABA-stimulated Caco2 cells demonstrated upregulation of tight junction molecules, such as CLDN1 and TJP1, enhancing epithelial barrier integrity. In a dextran sodium sulfate-induced colitis mouse model, rectal 3-ABA administration ameliorated colitis by enhancing epithelial barrier function and reducing inflammation. These findings highlight 3-ABA's potential as a dietary therapeutic agent for UC, offering a novel strategy to enhance intestinal integrity and mitigate inflammation.<b>NEW & NOTEWORTHY</b> Increased intestinal epithelial permeability is central to the pathogenesis of ulcerative colitis (UC). 3-Aminobenzoic acid (3-ABA), a dietary component abundant in beans, decreased epithelial permeability and attenuated colonic inflammation in a mouse experimental colitis model. Reduced fecal 3-ABA levels in patients with UC were associated with dysbiosis-driven accelerated degradation. These findings highlight the therapeutic potential of 3-ABA in UC by targeting colonic epithelium.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G801-G810"},"PeriodicalIF":3.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Lacticaseibacillus rhamnosus GG-</i>Driven Remodeling of Arginine Metabolism Mitigates Gut Barrier Dysfunction.","authors":"Jayson M Antonio, Yue Liu, Panan Suntornsaratoon, Abby Jones, Jayanth Ambat, Ajitha Bala, Joshua Kanattu, Juan Flores, Sheila Bandyopadhyay, Ravij Upadhyay, Jagannatham Naidu Bhupana, Xiaoyang Su, Wei Vivian Li, Nan Gao, Ronaldo P Ferraris","doi":"10.1152/ajpgi.00366.2024","DOIUrl":"https://doi.org/10.1152/ajpgi.00366.2024","url":null,"abstract":"<p><p>Inflammatory bowel diseases (IBD) and gut barrier impairment are associated with changes in dietary tryptophan and arginine metabolism, but mechanisms of barrier perturbation and restoration are unclear. We show here that the widely consumed probiotic <i>Lacticaseibacillus rhamnosus</i> GG (LGG) enhances gut barrier functions in part through stimulating the intestinal arginine metabolic pathway, and this mechanism depends on the sufficiency of dietary tryptophan in the host. Specifically, LGG markedly upregulates argininosuccinate lyase (ASL), the enzyme that breaks down argininosuccinate into arginine. ASL expression is markedly reduced during experimental colitis with an accumulation of serum argininosuccinate. LGG colonization in mice reduces serum argininosuccinate, a metabolite that inversely correlates with tight junction gene expression, impairs barrier function and exacerbates DSS colitis. We show that LGG-derived indoles as well as arginine metabolites enhanced <i>Asl</i> and <i>Nos2</i> expression, linking microbial metabolism to nitric oxide production and epithelial homeostasis. IBD patients have increased <i>ASS1</i> and decreased <i>ASL</i> expression, suggesting a metabolic bottleneck driving ASA accumulation. We propose that signaling pathways underlying LGG and tryptophan mediated ASL upregulation can be useful therapeutic targets to normalize arginine metabolism in select IBD patients.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gly-βMCA modulates bile acid metabolism to reduce hepatobiliary injury in <i>Mdr2</i> KO mice.","authors":"Mohammad Nazmul Hasan, Huaiwen Wang, Wenyi Luo, Yanhong Du, Tiangang Li","doi":"10.1152/ajpgi.00044.2025","DOIUrl":"https://doi.org/10.1152/ajpgi.00044.2025","url":null,"abstract":"<p><p>Cholestasis results from impaired bile flow that causes hepatic bile acid accumulation and injury. Alleviating bile acid hepatobiliary toxicity is a major therapeutic goal in cholestasis. Our recent study revealed a potent anti-cholestasis effect of glycine-conjugated β-muricholic acid (Gly-βMCA) in <i>Cyp2c70</i> KO mice with humanized hydrophobic bile acid composition. To better understand the mechanisms and human relevance of the therapeutic benefits of Gly-βMCA, we investigated the effects of Gly-βMCA on bile acid metabolism and biliary injury in <i>Mdr2</i> KO mice, a cholestasis model with a hydrophilic murine bile acid composition. Gly-βMCA significantly reduced serum alkaline phosphatase (ALP), ductular reaction, and liver cytokine expression in female mice but offered little benefits in male mice. Consistently, Gly-βMCA reduced hepatic bile acids and total bile acid pool size in female but not male mice, due to its ability to promote fecal bile acid excretion. However, the endogenous taurine-conjugated MCA (T-MCA) limited the ability of Gly-βMCA to further enrich the bile acid pool with Gly-βMCA-derived T-MCA to reduce bile acid hydrophobicity. Overall, Gly-βMCA showed diminished therapeutic efficacy in <i>Mdr2</i> KO mice than in <i>Cyp2c70</i> KO mice, which may be due to differences in bile acid hydrophobicity and disease etiology in the two cholestasis models. These findings suggest that the benefits of Gly-βMCA are mediated by its unique pharmacokinetics that allows for simultaneous reduction of bile acid pool size and hydrophobicity. Gly-βMCA may be a promising therapy for treating human cholestasis, despite its reduced efficacy in improving the toxicity profile of murine bile acid pool.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut-Heart Axis: Cardiac Remodeling and Heart Failure in the Context of Inflammatory Bowel Disease and Dysbiosis.","authors":"Thierry Kochkarian, Hania I Nagy, Qingjie Li","doi":"10.1152/ajpgi.00016.2025","DOIUrl":"https://doi.org/10.1152/ajpgi.00016.2025","url":null,"abstract":"<p><p>Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are debilitating and complex chronic gastrointestinal disorders that affect not only the gut but also extraintestinal organs, including the heart. The gut-heart crosstalk has garnered increasing attention in recent years; however, the molecular mechanisms underlying this complex interplay remain poorly understood. This review explores the gut-heart axis, focusing on how IBD disrupts gut microbiota homeostasis and promotes cardiac remodeling through systemic inflammation and various mediators, ultimately contributing to the onset or progression of heart failure. IBD compromises the integrity of the intestinal barrier, allowing microbial metabolites such as trimethylamine N-oxide and phenylacetylglutamine, along with inflammatory cytokines and microRNAs (miRNA) (e.g., miR-155, miR-21, let-7a), to enter the circulation and contribute to cardiac remodeling and heart failure. We identify dysfunction of nucleotide-binding oligomerization domain-containing protein 2 as a critical link between gut immunity and cardiovascular pathology. Additionally, we discuss emerging microbiome-based therapeutic strategies, including fecal microbiota transplantation and IL-23 inhibitors, aimed at restoring gut homeostasis and mitigating cardiovascular risk. By integrating molecular mechanisms, clinical evidence, and therapeutic approaches, this review underscores the pivotal role of gut dysbiosis in cardiac dysfunction and offers new perspectives for managing cardiac dysfunction in patients with IBD.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomarkers of Intestinal Permeability are Linked to Incident Cardiovascular Diseases and Cardiovascular Events: A Review of Prospective Studies.","authors":"Alexis R Quirk, Jenna K Schifferer, Katherine A Maki, Austin T Robinson, Bryant H Keirns","doi":"10.1152/ajpgi.00120.2025","DOIUrl":"https://doi.org/10.1152/ajpgi.00120.2025","url":null,"abstract":"<p><p>Intestinal hyperpermeability, which refers to translocation of microbial factors into the bloodstream, is associated with many chronic diseases. Increased intestinal permeability may contribute to the pathophysiology of these diseases by promoting systemic inflammation. While early work on the health implications of increased intestinal permeability focused on diseases of the gastrointestinal tract, subsequent preclinical and cross-sectional data identified that various types of cardiometabolic and cardiovascular diseases (<b>CVD</b>s) are linked to gut barrier dysfunction. More recently, a body of epidemiological studies have emerged, indicating that elevated biomarkers of intestinal permeability are prospectively linked to incident CVD and CVD events, such as myocardial infarction and stroke, even after controlling for traditional CVD risk factors. In this brief review, we discuss gut barrier function in health and disease, highlight methodologies employed to assess intestinal permeability, and review the emerging literature demonstrating that measures of intestinal permeability predict future CVD across several populations.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crural and costal diaphragm function during emesis.","authors":"Jasmine J Park, Giovanni Tagliabue, Michael Ji, Ravinder K Mittal, Paul A Easton","doi":"10.1152/ajpgi.00354.2024","DOIUrl":"https://doi.org/10.1152/ajpgi.00354.2024","url":null,"abstract":"<p><p><b>Background:</b> Together the costal and crural diaphragm constitute the primary respiratory muscle in mammals, but functionally they are distinct. The crural segment has additional gastrointestinal function, wrapped around the esophagus at the esophagogastric junction, contributing to the esophageal sphincter. Emesis is an expulsive process that requires coordinated action of multiple muscles to rapidly force out gastric contents. <b>Objective:</b> The simultaneous mechanical action and neural activation of the diaphragm segments during the process of emesis, especially expulsion, is uncertain. Detailed divergence of the crural diaphragm to sphincter function during emesis has not been studied. <b>Methods:</b> In 6 awake, spontaneously breathing canines, electrical activity and corresponding muscle shortening of costal and crural diaphragm were measured at five phases of emesis (rest, early prodrome, mid prodrome, late prodrome, expulsion) induced by apomorphine. <b>Results:</b> Overall, baseline muscle length decreased and baseline EMG increased progressively from rest through prodrome for both costal and crural, but at expulsion, the crural segment diverged, lengthening abruptly. Shortening and EMG activity per breath for costal changed slightly throughout emesis; crural shortening and EMG activity increased abruptly at expulsion. The divergent action of crural during expulsion developed sequentially through each breath. Also, neuromechanical coupling of the segments reversed at expulsion, with contractility of the crural surpassing that of the costal. <b>Conclusion:</b> These measurements confirm a disparate action of crural diaphragm, compared to costal, to facilitate expulsion. During the process of emesis, while the costal persists as an obligatory respiratory muscle, the crural converts from respiratory muscle to opening sphincter.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}