Gastrointestinal motility

胃肠运动
  • 文章类型: Journal Article
    最近的调查强调,实验和临床,装有阿拉伯呋喃糖苷酶的益生菌菌株,特别是abfA和abfB,有利于规律的肠道运动,从而抵消便秘。通过分析在存在益生菌B.longumW11的阿拉伯聚糖的情况下的基因表达和增殖反应,该菌株先前被验证为抗便秘益生菌,我们推测其对阿拉伯聚糖的反应机制可以有效解释其临床作用。我们的方法将来可用于选择具有阿拉伯呋喃糖苷酶相关抗便秘作用的益生菌。
    Recent investigations have highlighted, both experimentally and clinically, that probiotic strains equipped with arabinofuranosidase, in particular abfA and abfB, favor regular intestinal motility, thus counteracting constipation. By analyzing the gene expression and the proliferative response in the presence of arabinan of the probiotic B. longum W11, a strain previously validated as an anti-constipation probiotic, we have speculated that its response mechanism to arabinan can effectively explain its clinical action. Our approach could be used in the future to select probiotics endowed with arabinofuranosidase-related anti-constipation effects.
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  • 文章类型: Journal Article
    柚皮素(NRG)广泛存在于柑橘类水果中,具有抗炎作用,低血糖,和免疫调节作用。先前的研究表明,NRG促进小鼠便秘模型的胃肠运动,但是很少有系统的评估其对正常动物的影响。本研究首先阐明了NRG对胃排空和小肠推进的促进作用(p<0.01)。NRG还可以调节胃肠激素的释放,包括增强胃泌素(GAS)和胃动素(MTL)(p<0.01),同时减少血管活性肠肽(VIP)的分泌(p<0.01)。使用NRG刺激孤立的胃,十二指肠,和结肠显示出与体内观察到的相似的促进作用(p<0.01)。Westernblot分析表明,这种作用可能是通过增加干细胞因子(SCF)及其受体(c-Kit)在这三个片段中的表达而介导的。从而调节它们的下游途径。值得注意的是,NRG还可以增加有益细菌(Planococcaceae,酸化拟杆菌,梭菌_UCG-014)在肠道中并减少有害细菌(葡萄球菌)的数量。这些发现为NRG的应用提供了新的依据。
    Naringenin (NRG) is widely found in citrus fruits and has anti-inflammatory, hypoglycemic, and immunomodulatory effects. Previous studies have shown that NRG promotes gastrointestinal motility in mice constipation models, but there are few systematic evaluations of its effects on normal animals. This study first clarified the promotive effects of NRG on gastric emptying and small intestine propulsion (p < 0.01). NRG can also regulate the release of gastrointestinal hormones, including enhancing gastrin (GAS) and motilin (MTL) (p < 0.01), while reducing vasoactive intestinal peptide (VIP) secretion (p < 0.01). Using NRG to stimulate the isolated stomach, duodenum, and colon showed similar promotive effects to those observed in vivo (p < 0.01). A Western blot analysis indicated that this effect may be mediated by increasing the expression of stem cell factor (SCF) and its receptor (c-Kit) in these three segments, thus regulating their downstream pathways. It is worth noting that NRG can also increase the proportion of beneficial bacteria (Planococcaceae, Bacteroides acidifaciens, Clostridia_UCG-014) in the intestine and reduce the quantity of harmful bacteria (Staphylococcus). These findings provide a new basis for the application of NRG.
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  • 文章类型: Journal Article
    胃肠道功能在营养吸收和整体消化健康中起着关键作用。胃排空异常与2型糖尿病密切相关。影响血糖调节并引起胃肠道症状。本研究旨在调查和比较分段运输时间,运动性指数,格陵兰因纽特人和有或没有2型糖尿病的丹麦个体之间的微环境。我们包括了44名格陵兰因纽特人,其中23人患有2型糖尿病,以及年龄和性别匹配的丹麦人。分段运输时间,运动性,和腔环境使用SmartPill®测量。格陵兰对照显示较短的胃排空时间(GET)(163分钟),与2型糖尿病的格陵兰人相比,胃的中位pH(2.0pH)和十二指肠中位收缩(18.2mmHg)更高(GET:235分钟,pH:1.9,中位十二指肠收缩18.4mmHg)和丹麦对照(GET:190,pH:1.2中位十二指肠收缩17.5mmHg)。尽管有类似的抗糖尿病管理努力,胃肠道生理学的变化是明显的,强调糖尿病的复杂性及其与种族的相互作用,暗示潜在的饮食甚至遗传影响,强调个性化糖尿病管理方法的必要性。最后,这项研究为未来的研究开辟了可能性,鼓励研究与遗传学相关的潜在机制,饮食,和胃生理学,因为对因素的理解可以导致更有效的,为不同人群的糖尿病护理和改善消化系统健康量身定制的策略。
    Gastrointestinal function plays a pivotal role in nutrient absorption and overall digestive health. Abnormal gastric emptying is closely linked to type 2 diabetes, impacting blood glucose regulation and causing gastrointestinal symptoms. This study aims to investigate and compare segmental transit times, motility indices, and micromilieu between Greenlandic Inuit and Danish individuals with and without type 2 diabetes. We included forty-four Greenlandic Inuit, twenty-three of whom had type 2 diabetes, and age and gender-matched Danish individuals. Segmental transit time, motility, and luminal environment were measured using the SmartPill®. Greenlandic controls displayed shorter gastric emptying time (GET) (163 min), higher gastric median pH (2.0 pH) and duodenal median contractions (18.2 mm Hg) compared to Greenlanders with type 2 diabetes (GET: 235 min, pH:1.9, median duodenal contraction 18.4 mm Hg) and Danish controls (GET: 190, pH:1.2 median duodenal contraction 17.5 mmHg). Despite similar anti-diabetic management efforts, variations in gastrointestinal physiology were evident, highlighting the complexity of diabetes and its interaction with ethnicity, suggesting potential dietary or even genetic influences, emphasising the necessity for personalised diabetes management approaches. Finally, the study opens possibilities for future research, encouraging investigations into the underlying mechanisms linking genetics, diet, and gastric physiology, as an understanding of factors can lead to more effective, tailored strategies for diabetes care and improved digestive health in diverse populations.
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  • 文章类型: Journal Article
    肠道蠕虫感染引发2型免疫反应,促进以粘液分泌增加和肠道运动过度为特征的“哭泣和扫视”反应,其功能是将蠕虫从其肠道栖息地驱散。最近的研究发现,其他几种病原体通过对免疫和肠神经系统(ENS)的重大改变引起肠道动力障碍,以及它们的相互作用,在胃肠道内。然而,尚未对这些系统的参与进行蠕虫感染的调查。嗜酸性粒细胞代表由2型免疫应答募集的关键细胞类型,并且在稳态条件下改变肠运动性。我们的研究旨在调查是否改变由鼠钩虫驱动的肠道运动,巴西雪铁龙,感染涉及嗜酸性粒细胞以及ENS和肠道平滑肌如何受到影响。嗜酸性粒细胞缺乏不会影响蠕虫引起的肠道运动过度,并且运动过度不涉及ENS的总体结构或功能变化。相反,高运动性与平滑肌厚度和收缩力的急剧增加有关,延伸到另一种啮齿动物线虫的观察结果,多回螺旋体。总之,我们的数据表明,与其他病原体相比,蠕虫引起的肠道运动过度主要是由肌源性的,而不是神经性的,这种变化的改变独立于嗜酸性粒细胞而发生。(<300字)
    Intestinal helminth infection triggers a type 2 immune response that promotes a \'weep-and sweep\' response characterised by increased mucus secretion and intestinal hypermotility, which function to dislodge the worm from its intestinal habitat. Recent studies have discovered that several other pathogens cause intestinal dysmotility through major alterations to the immune and enteric nervous systems (ENS), and their interactions, within the gastrointestinal tract. However, the involvement of these systems has not been investigated for helminth infections. Eosinophils represent a key cell type recruited by the type 2 immune response and alter intestinal motility under steady-state conditions. Our study aimed to investigate whether altered intestinal motility driven by the murine hookworm, Nippostrongylus brasiliensis, infection involves eosinophils and how the ENS and smooth muscles of the gut are impacted. Eosinophil deficiency did not influence helminth-induced intestinal hypermotility and hypermotility did not involve gross structural or functional changes to the ENS. Hypermotility was instead associated with a dramatic increase in smooth muscle thickness and contractility, an observation that extended to another rodent nematode, Heligmosomoides polygyrus. In summary our data indicate that, in contrast to other pathogens, helminth-induced intestinal hypermotility is driven by largely by myogenic, rather than neurogenic, alterations with such changes occurring independently of eosinophils. (<300 words).
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  • 文章类型: Journal Article
    (1)背景:我们检查了橄榄油(EVOO)的急性给药效果,亚麻籽油(GLO),大豆油(SO),和棕榈油(PO)对大鼠胃运动和食欲的影响。(2)方法:我们评估食物摄入量,胃潴留(GR),和所有组的基因表达。(3)结果:EVOO和GLO均能提高胃潴留率,减少饥饿。另一方面,SO引起的食物摄入量减少伴随着对胃retention留的延迟作用。PO引起NPYmRNA表达的改变,POMC,和cart。尽管PO在180分钟后增加了胃retention留,它不影响食物摄入。随后证实,缺乏自主反应并没有消除EVOO在减少食物消耗方面的影响。此外,在没有副交感神经反应的情况下,接受PO的动物表现出食物消耗的显着减少,可能由较低的NPY表达介导。(4)结论:本研究发现,不同的油会对与食物消耗相关的参数产生各种影响。具体来说,EVOO主要通过对胃肠道的影响来减少食物消耗,使其成为减肥的推荐辅助手段。相反,在没有自主反应的情况下,PO的摄入限制了食物的消耗,但由于它对心脏代谢紊乱的发展有贡献,因此不建议这样做。
    (1) Background: We examined the effect of the acute administration of olive oil (EVOO), linseed oil (GLO), soybean oil (SO), and palm oil (PO) on gastric motility and appetite in rats. (2) Methods: We assessed food intake, gastric retention (GR), and gene expression in all groups. (3) Results: Both EVOO and GLO were found to enhance the rate of stomach retention, leading to a decrease in hunger. On the other hand, the reduction in food intake caused by SO was accompanied by delayed effects on stomach retention. PO caused an alteration in the mRNA expression of NPY, POMC, and CART. Although PO increased stomach retention after 180 min, it did not affect food intake. It was subsequently verified that the absence of an autonomic reaction did not nullify the influence of EVOO in reducing food consumption. Moreover, in the absence of parasympathetic responses, animals that received PO exhibited a significant decrease in food consumption, probably mediated by lower NPY expression. (4) Conclusions: This study discovered that different oils induce various effects on parameters related to food consumption. Specifically, EVOO reduces food consumption primarily through its impact on the gastrointestinal tract, making it a recommended adjunct for weight loss. Conversely, the intake of PO limits food consumption in the absence of an autonomic reaction, but it is not advised due to its contribution to the development of cardiometabolic disorders.
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  • 文章类型: Journal Article
    胃肠道(GI)是一个器官积极参与机械过程,它通过机械感觉机制检测力。机械感觉依赖于称为机械感受器的专门细胞,通过机械传感器将机械力转换为电化学信号。机械敏感性Piezo1和Piezo2在各种机械敏感性细胞中广泛表达,这些细胞通过改变跨膜离子电流来响应GI机械力,如上皮细胞,肠嗜铬细胞,和内在和外在的肠神经元。本文重点介绍了机械敏感性压电通道在胃肠道生理和病理中的最新研究进展。具体来说,关于压电通道在肠屏障中的作用的最新见解,胃肠运动性,并对肠道机械感觉进行了总结。此外,Piezo通道在胃肠道疾病发病机制中的概述,包括肠易激综合征,炎症性肠病,和胃肠道癌症,提供。总的来说,机械敏感性压电通道的存在为各种胃肠道疾病的治疗提供了有希望的新观点。
    The gastrointestinal (GI) tract is an organ actively involved in mechanical processes, where it detects forces via a mechanosensation mechanism. Mechanosensation relies on specialized cells termed mechanoreceptors, which convert mechanical forces into electrochemical signals via mechanosensors. The mechanosensitive Piezo1 and Piezo2 are widely expressed in various mechanosensitive cells that respond to GI mechanical forces by altering transmembrane ionic currents, such as epithelial cells, enterochromaffin cells, and intrinsic and extrinsic enteric neurons. This review highlights recent research advances on mechanosensitive Piezo channels in GI physiology and pathology. Specifically, the latest insights on the role of Piezo channels in the intestinal barrier, GI motility, and intestinal mechanosensation are summarized. Additionally, an overview of Piezo channels in the pathogenesis of GI disorders, including irritable bowel syndrome, inflammatory bowel disease, and GI cancers, is provided. Overall, the presence of mechanosensitive Piezo channels offers a promising new perspective for the treatment of various GI disorders.
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  • 文章类型: Journal Article
    在胃肠病学领域,目前胃肠道(GI)运动障碍和炎症性肠病(IBD)的药物治疗不足,加上它们潜在的副作用,需要新的治疗方法。神经调节,瞄准神经系统对胃肠道功能的控制,作为一个有希望的替代方案出现。这篇综述探讨了迷走神经刺激(VNS)的有希望的效果,磁神经调制,和针灸管理这些具有挑战性的条件。VNS提供胃肠道运动和炎症的靶向调节,为不能从传统药物中完全缓解的患者提供潜在的解决方案。磁神经调节,通过非侵入性手段,旨在增强神经生理过程,在改善胃肠道功能和减少炎症方面显示出希望。针灸和电针,以传统医学为基础,但又被现代科学验证,通过神经免疫内分泌机制对胃肠道生理产生综合影响,提供缓解运动和炎症症状。这篇综述强调了进一步研究以完善这些干预措施的必要性,强调他们在推进胃肠道运动障碍和IBD的患者特异性管理策略方面的前瞻性作用,从而为新的治疗范式铺平了道路。
    In the realm of gastroenterology, the inadequacy of current medical treatments for gastrointestinal (GI) motility disorders and inflammatory bowel disease (IBD), coupled with their potential side effects, necessitates novel therapeutic approaches. Neuromodulation, targeting the nervous system\'s control of GI functions, emerges as a promising alternative. This review explores the promising effects of vagal nerve stimulation (VNS), magnetic neuromodulation, and acupuncture in managing these challenging conditions. VNS offers targeted modulation of GI motility and inflammation, presenting a potential solution for patients not fully relieved from traditional medications. Magnetic neuromodulation, through non-invasive means, aims to enhance neurophysiological processes, showing promise in improving GI function and reducing inflammation. Acupuncture and electroacupuncture, grounded in traditional medicine yet validated by modern science, exert comprehensive effects on GI physiology via neuro-immune-endocrine mechanisms, offering relief from motility and inflammatory symptoms. This review highlights the need for further research to refine these interventions, emphasizing their prospective role in advancing patient-specific management strategies for GI motility disorders and IBD, thus paving the way for a new therapeutic paradigm.
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  • 文章类型: Journal Article
    小肠运动改变与肠易激综合征之间的相关性没有得到很好的评价。本研究旨在评估具有束缚应激的青少年肠易激综合征大鼠模型中的小肠和结肠过境,并确定小肠动力在肠易激综合征病理生理中的作用。
    利用约束应激来制备青少年肠易激综合征大鼠模型,对其进行临床体征评估,包括大便次数和腹泻。还评估了小肠运动和转运率。
    编码促肾上腺皮质激素释放激素的mRNA数量,肥大细胞,使用实时聚合酶链反应定量5-羟色胺(5-羟色胺)受体3a;使用免疫染色评估5-羟色胺的表达。
    限制压力显着增加了粪便颗粒输出的数量,大便含水量,青少年肠易激综合征大鼠模型的小肠运动。实时聚合酶链反应结果没有差异;然而,免疫染色分析表明,在青少年肠易激综合征大鼠模型中,小肠中5-羟色胺的表达显着增加。
    在约束应激的青少年肠易激综合征大鼠模型中,我们观察到小肠和结肠运动增加。在小肠里,远端部分的5-羟色胺分泌增强可能与增加小肠运动有关。虽然目前的研究集中在5-羟色胺,进一步研究调节肠蠕动的其他因素可能会导致建立更有效的治疗青少年肠易激综合征的方法。
    UNASSIGNED: The correlation between altered small intestinal motility and irritable bowel syndrome is not well evaluated. This study aimed to assess the small intestinal and colonic transits in an adolescent irritable bowel syndrome rat model with restraint stress and determine the role of small intestinal motility in the irritable bowel syndrome pathophysiology.
    UNASSIGNED: Restraint stress was utilized to prepare adolescent irritable bowel syndrome rat models that were evaluated for clinical signs, including stool frequency and diarrhea. The small intestinal motility and transit rate were also evaluated.
    UNASSIGNED: The amounts of mRNA encoding corticotropin-releasing hormone, mast cell, and serotonin (5-Hydroxytryptamine) receptor 3a were quantified using real-time polymerase chain reaction; the 5-Hydroxytryptamine expression was evaluated using immunostaining.
    UNASSIGNED: Restraint stress significantly increased the number of fecal pellet outputs, stool water content, and small intestinal motility in the adolescent irritable bowel syndrome rat models. There was no difference in real-time polymerase chain reaction results; however, immunostaining analysis revealed that 5-Hydroxytryptamine expression in the small intestine was significantly increased in the adolescent irritable bowel syndrome rat models.
    UNASSIGNED: In the rat model of adolescent irritable bowel syndrome with restraint stress, we observed an increase in small intestinal and colonic motility. In the small intestine, enhanced 5-Hydroxytryptamine secretion in the distal portion may be involved in increasing the small intestinal motility. Although the present study focused on 5-Hydroxytryptamine, further investigation of other factors that regulate intestinal peristalsis may lead to the establishment of more effective treatment methods for adolescent irritable bowel syndrome.
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  • 文章类型: Journal Article
    肠道运动频率(BMF)直接影响肠道微生物群,并与慢性肾病或痴呆症等疾病有关。特别是,先前的工作表明,便秘与整个生态系统从纤维发酵和短链脂肪酸生产到更有害的蛋白质发酵和毒素生产的转变有关。这里,我们分析了来自一般健康成年人的多维数据,以了解BMF如何影响他们的分子表型,在疾病前的背景下。结果显示肠道微生物属的丰度差异,血液代谢产物,以及BMF类别中生活方式因素的变化。这些差异与炎症有关,心脏健康,肝功能,和肾功能。因果介导分析表明,较低的BMF与肾功能降低之间的关联部分是由微生物衍生的毒素3-硫酸吲哚酚(3-IS)介导的。这个结果,在总体健康的背景下,表明与异常BMF相关的微生物群衍生毒素的积累先于器官损伤,并且可能是慢性,衰老相关疾病。
    Bowel movement frequency (BMF) directly impacts the gut microbiota and is linked to diseases like chronic kidney disease or dementia. In particular, prior work has shown that constipation is associated with an ecosystem-wide switch from fiber fermentation and short-chain fatty acid production to more detrimental protein fermentation and toxin production. Here, we analyze multi-omic data from generally healthy adults to see how BMF affects their molecular phenotypes, in a pre-disease context. Results show differential abundances of gut microbial genera, blood metabolites, and variation in lifestyle factors across BMF categories. These differences relate to inflammation, heart health, liver function, and kidney function. Causal mediation analysis indicates that the association between lower BMF and reduced kidney function is partially mediated by the microbially derived toxin 3-indoxyl sulfate (3-IS). This result, in a generally healthy context, suggests that the accumulation of microbiota-derived toxins associated with abnormal BMF precede organ damage and may be drivers of chronic, aging-related diseases.
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  • 文章类型: Journal Article
    在胚胎发育后期,肠道运动经历了从肌源性控制到神经源性控制的转变。这里,我们报道了肠神经系统这种转变背后的电事件,在神经c细胞衍生物中使用GCaMP6f报告基因。我们发现自发钙活性在阶段E11.5具有抗河豚毒素(TTX),但在E18.5没有。E18.5的运动性具有周期性,环形平滑肌的高频和低频交替收缩;这种频率调制被TTX抑制。神经源性运动阶段的钙成像E18.5-P3显示CaV1.2阳性神经元表现出自发的钙活性,尼卡地平和2-氨基乙氧基二苯基硼酸酯(2-APB)抑制了。我们的方案局部阻止了肌肉紧张放松,争论尼卡地平对肠神经元的直接作用,而不是间接地通过它对肌肉的放松作用。我们证明了ENS从早期阶段就对机械敏感(E14.5),并且这种行为对TTX和2-APB具有抗性。我们扩展了对成年结肠的L型通道依赖性自发活动和TTX抗性机械敏感性的结果。我们的结果揭示了在发育中的肠道中从肌源性运动到神经源性运动的关键转变,以及介导肠神经系统机电敏感性的有趣途径。重点:这项研究的中心问题是什么?在发育中的肠道中,从肌源性运动到神经源性运动转变的第一个神经电事件是什么?他们依赖什么渠道,肠神经系统是否已经表现出机械敏感性?主要发现及其重要性是什么?ENS钙活性在E18.5阶段对河豚毒素敏感,但在E11.5阶段不敏感。胎儿和成人阶段的自发电活动主要取决于L型钙通道和IP3R受体,肠神经系统表现出抗河豚毒素的机械敏感反应。附图说明机械刺激诱导E18.5小鼠十二指肠抗河豚毒素Ca2+升高。
    Gut motility undergoes a switch from myogenic to neurogenic control in late embryonic development. Here, we report on the electrical events that underlie this transition in the enteric nervous system, using the GCaMP6f reporter in neural crest cell derivatives. We found that spontaneous calcium activity is tetrodotoxin (TTX) resistant at stage E11.5, but not at E18.5. Motility at E18.5 was characterized by periodic, alternating high- and low-frequency contractions of the circular smooth muscle; this frequency modulation was inhibited by TTX. Calcium imaging at the neurogenic-motility stages E18.5-P3 showed that CaV1.2-positive neurons exhibited spontaneous calcium activity, which was inhibited by nicardipine and 2-aminoethoxydiphenyl borate (2-APB). Our protocol locally prevented muscle tone relaxation, arguing for a direct effect of nicardipine on enteric neurons, rather than indirectly by its relaxing effect on muscle. We demonstrated that the ENS was mechanosensitive from early stages on (E14.5) and that this behaviour was TTX and 2-APB resistant. We extended our results on L-type channel-dependent spontaneous activity and TTX-resistant mechanosensitivity to the adult colon. Our results shed light on the critical transition from myogenic to neurogenic motility in the developing gut, as well as on the intriguing pathways mediating electro-mechanical sensitivity in the enteric nervous system. HIGHLIGHTS: What is the central question of this study? What are the first neural electric events underlying the transition from myogenic to neurogenic motility in the developing gut, what channels do they depend on, and does the enteric nervous system already exhibit mechanosensitivity? What is the main finding and its importance? ENS calcium activity is sensitive to tetrodotoxin at stage E18.5 but not E11.5. Spontaneous electric activity at fetal and adult stages is crucially dependent on L-type calcium channels and IP3R receptors, and the enteric nervous system exhibits a tetrodotoxin-resistant mechanosensitive response. Abstract figure legend Tetrodotoxin-resistant Ca2+ rise induced by mechanical stimulation in the E18.5 mouse duodenum.
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