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首页> 外文期刊>BMC Gastroenterology >Short chain fatty acids and colon motility in a mouse model of irritable bowel syndrome
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Short chain fatty acids and colon motility in a mouse model of irritable bowel syndrome

机译：短链脂肪酸和肠易激综合征小鼠模型中的结肠运动

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Irritable bowel syndrome (IBS) is defined as a multifactorial disorder associated with visceral hypersensitivity, altered gut motility and dysfunction of the brain-gut axis. Gut microbiota and its metabolites are proposed as possible etiological factors of IBS. Short chain fatty acids (SCFAs) induce both inhibitory and stimulatory action on colon motility, however, their effects on the IBS model were not investigated. The aim of our study was to investigate the level of SFCAs in feces and their effects on colon motility in a mouse model of IBS. IBS model was induced in mice by intracolonic infusion of 1% acetic acid during the early postnatal period. Mice colon hypersensitivity was assessed by the threshold of the abdominal withdrawal reflex in response to colorectal distention. Colon contractility was studied using proximal colon specimens in isometric conditions. Transit rates were assessed by the pellet propulsion in the isolated colon. Concentrations of SCFAs in feces were measured using gas–liquid chromatography. The concentration of SCFAs in feces of IBS model mice was higher compared to the control group. Visceral sensitivity to colorectal distension and colonic transit rate were increased indicating IBS with predominant diarrhea. The frequency and amplitude of spontaneous contractions of proximal colon segments from IBS mice were higher, but carbachol induced contractions were lower compared to control. During acute application of SCFAs (sodium propionate, sodium acetate or butyric acid) dose-dependently (0.5–30?mM) decreased tonic tension, frequency and amplitude of spontaneous and carbachol-evoked contractions. In the mouse IBS group the inhibitory effects SCFAs on spontaneous and carbachol-evoked contractions were less pronounced. At the same time intraluminal administration of butyrate (5?mM) increased the transit rate in the colon of both groups, but its stimulatory effect was more pronounced in mouse IBS model group. Our data indicate that the increased transit rate in the mouse IBS model group is associated with a disbalance of activating and inhibiting action of SCFAs due to chronically elevated SCFA levels, which may impact the pathogenesis of IBS with predominant diarrhea syndrome.
机译：肠易肠综合征（IBS）被定义为与内感过敏相关的多学会障碍，改变肠杆轴的肠道运动和功能障碍。提出了肠道微生物和其代谢物作为IBS可能的病因因子。短链脂肪酸（SCFA）诱导对结肠运动的抑制和刺激作用，然而，没有研究它们对IBS模型的影响。我们的研究目的是探讨粪便中SFCA的水平及其对IBS模型模型中的对结肠运动的影响。在产后早期输注1％乙酸的1％醋酸诱导了IBS模型。通过腹部戒断反射的阈值来评估小鼠结肠超敏反应响应结直肠差异。使用近距离条件下的近端结肠标本研究结肠收缩性。通过分离的结肠中的颗粒推进来评估运输速率。使用气液色谱法测量粪便中SCFA的浓度。与对照组相比，IBS模型小鼠粪便中SCFA的浓度较高。对结肠直肠扩张和结肠传递率的内脏敏感性增加表明IBS具有主要的腹泻。来自IBS小鼠的近端结肠段的自发收缩的频率和幅度较高，但与对照相比，较低的卡酰诱导的收缩。在急性施用SCFA（丙酸钠，乙酸钠或丁酸）期间剂量 - 依赖性（0.5-30Ωmm）降低了滋补张力，频率和振幅的自发性和诱发的收缩。在小鼠IBS中，抑制作用SCFA对自发性和诱发的收缩的SCFA不太明显。同时，丁酸盐（5Ωmm）的腔内施用增加了两组结肠的过渡率，但其刺激作用在小鼠IBS模型组中更加明显。我们的数据表明，由于慢性升高的SCFA水平，小鼠IBS模型组中的转运率增加与SCFA的激活和抑制作用的分裂相关，这可能会影响具有主要腹泻综合征的IBS的发病机制。

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