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首页> 外文期刊>The Journal of Physiology >Effects of leptin on cat intestinal motility.
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Effects of leptin on cat intestinal motility.

机译:瘦素对猫肠动力的影响。

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In a previous study, we established that leptin controls food intake and immune responses by acting on intestinal vagal chemosensitive mechanoreceptors via a functional link with interleukin-1 beta (Il-1 beta). Since the control of intestinal motility is one of the main roles of the vagal afferent fibres, we investigated the effects of leptin on intestinal electromyographic (EMG) activity which reflects intestinal motility. For this purpose, the effects of locally injected leptin on small intestine spontaneous EMG activity were studied in 23 anaesthetised cats. The EMG activity was recorded using bipolar electrodes implanted in the proximal small intestine. Leptin and Il-1 beta (0.1, 1 and 10 microg), administered through the artery irrigating the upper part of the intestine 20 min after cholecystokinin (CCK, 10 microg, I.A.), had significant (P < 0.001) excitatory effects on intestinal EMG activity. The effects of both substances were blocked by the endogenous interleukin-1 beta receptor antagonist (Il-1ra, 250 microg, I.A.), by atropine (250 microg, I.A.) and by vagotomy. In the absence of CCK, leptin and Il-1 beta had no effect on intestinal electrical activity. It can therefore be concluded that: (1) leptin is effective only after the previous intervention of CCK, (2) the enhancement of the electrical activity induced by leptin involves Il-1 beta receptors and the cholinergic excitatory pathway, (3) the modes whereby the leptin-induced enhancement of EMG activity occurs strongly suggest that these effects are due to a long-loop reflex involving intestinal vagal afferent fibres and the parasympathetic nervous system.
机译:在先前的研究中,我们建立了瘦素通过与白介素-1 beta(Il-1 beta)的功能性联系,通过作用于肠迷走神经化学敏感性机械感受器来控制食物摄入和免疫反应。由于控制肠蠕动是迷走神经传入纤维的主要作用之一,因此我们研究了瘦素对反映肠蠕动的肠肌电图(EMG)活性的影响。为了这个目的,在23只麻醉的猫中研究了局部注射的瘦素对小肠自发EMG活性的影响。使用植入近端小肠的双极电极记录肌电活动。胆囊收缩素(CCK,10 microg,IA)后20分钟通过动脉灌肠上部施用的瘦素和Il-1 beta(0.1、1和10微克)对肠道具有显着(P <0.001)兴奋性作用EMG活动。两种物质的作用均被内源性白介素-1β受体拮抗剂(II-1ra,250微克,I.A。),阿托品(250微克,I.A。)和迷走神经切断术所阻断。在没有CCK的情况下,瘦素和II-1β对肠电活性没有影响。因此可以得出以下结论:(1)瘦素仅在先前的CCK干预后才有效;(2)瘦素诱导的电活动增强涉及II-1β受体和胆碱能兴奋性途径,(3)方式瘦素诱导的EMG活性增强的发生强烈表明这些作用是由于涉及肠迷走神经传入纤维和副交感神经系统的长环反射。

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